5 Minute Anesthesia Consult (2013) PDF

The
5-Minute
Anesthesia
Consult
CHIEF EDITORIAL ASSISTANT
Matthew C. Gertsch, MD
Resident Physician
Department of Anesthesia, Critical Care and Pain Medicine
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
EDITORIAL ASSISTANTS
J. Scott Bluth
Medical Student
University of Texas Medical School at Houston
Houston, Texas
Mark R. Bombulie
Medical Student
Houston, Texas
Kelly A. Bruno
Medical Student
The University of North Carolina, School of Medicine
Chapel Hill, North Carolina
N. Matthew Decker, BS
Medical Student
Loyola University Chicago Stritch School of Medicine
Maywood, Illinois
David Frey, DO
Resident Physician
Department of Anesthesiology and Pain Medicine
University of Washington Medical School
University of Washington Medical Center
Seattle, Washington
Megan Dale Henley

Medical Student
Thomas J. Hopkins, MD, MMCi

Resident Physician
Department of Anesthesiology
Duke University School of Medicine
Duke University Medical Center
Durham, North Carolina
Rachel M. Little, MPH

Medical Student
Carolyn Mohr, MD
Resident Physician
University of Colorado School of Medicine
Anschutz Medical Campus
Denver, Colorado
Olutoyosi Ogunkua, MD
Resident Physician
Department of Anesthesiology and Pain Management
University of Texas Southwestern School of Medicine
University of Texas Southwestern Medical Center at Dallas
Dallas, Texas
Michael J. Oleyar, DO
Resident Physician
The Johns Hopkins University School of Medicine
The Johns Hopkins Hospital
Baltimore, Maryland
Blake W. Perkins
Medical Student
University of Illinois College of Medicine
Peoria, Illinois
Matthew M. Peterson
Medical Student
Tulane University School of Medicine
New Orleans, Louisiana
Lauren Mai Pieczynski, MD

Resident Physician
Department of Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvaniaz
Adam M. Stuart
Medical Student
Virginia Commonwealth University School of Medicine
Richmond, Virginia
Lindsay Veit, MD
Resident Physician
Rush Medical College
Rush University Medical Center
Chicago, Illinois
CONSULTANT EDITOR
Anita Gupta
The 5-Minute
Anesthesia
Consult
Editor
Nina Singh-Radcliff, MD
Section Editor
Alan J. Kover, MD, PharmD

Clinical Assistant Professor
The Ohio State University College of Medicine
The Ohio State University Wexner Medical Center
Columbus, Ohio
Associate Editors
Kris E. Radcliff, MD
Assistant Professor of Orthopedic Surgery and Neurological Surgery
Thomas Jefferson University
The Rothman Institute
Philadelphia, Pennsylvania
Emily J. Baird, MD, PhD

Assistant Clinical Professor
Julie Scott Taylor, MD, MSc

Stanford University
Palo Alto, California
Acquisitions Editor: Brian Brown
Product Manager: Nicole Dernoski
Production Manager: Bridgett Dougherty
Senior Manufacturing Manager: Benjamin Rivera
Marketing Manager: Lisa Lawrence
Design Coordinator: Teresa Mallon
Production Service: Aptara, Inc.
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Library of Congress Cataloging-in-Publication Data
Singh-Radcliff, Nina.
The 5-minute anesthesia consult / [edited by] Nina Singh-Radcliff.
p.; cm. - (5-minute consult)
Includes bibliographical references and index.
ISBN 978-1-4511-1894-0 (alk. paper)
I. Title. II. Series: 5-minute consult.
[DNLM: 1. Anesthesia-Handbooks. 2. Perioperative Period-Handbooks. 3. Surgical Procedures, Operative-Handbooks. WO
231]
617.9’6-dc23 2012023881
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10 9 8 7 6 5 4 3 2 1
To my parents, Dilip and Madhulika Singh, for their unconditional love and support throughout my life and career and
teaching me by example about kindness, honesty, and dedication. Children cannot choose their parents, but if I had been
given the opportunity, I would choose them. I also need to give a special thanks to Carmen, my first child, who helped me
edit the book while in utero. And finally to my husband, Dr. Kris Radcliff, who served as an Associate Editor to this book.
Words cannot convey my gratitude for his contribution to, and support, with this text. I have known Kris for almost one-third
of my life and he remains the most intelligent, kind, patient, humble, and wonderful person I know. He still makes my heart
flutter when I see him. He is the best thing that has ever happened to me and I am truly blessed to be able to call him my
husband and share my life with him.
CONTRIBUTORS

Ali R. Abdullah, MBChB

Resident Physician
University of Pittsburgh School of Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania
Erik E. Abel, PharmD, BCPS

Columbus, Ohio
Benjamin Abraham, MD
The Cleveland Clinic
Cleveland, Ohio
Andaleeb Abrar Ahmed, MBBS, MD, MPH

Resident Physician
Penn State College of Medicine
Penn State Milton S. Hershey Medical Center
Hershey, Pennsylvania
Moustafa Ahmed, MD
Interim Chief, Philadelphia VA Medical Center
Jane C. Ahn, MD
Assistant Professor
Department of Anesthesiology and Perioperative Care
University of California, Irvine School of Medicine
University of California, Irvine Douglas Hospital
Irvine, California
Arun Alagappan, MD
Resident Physician
Mount Sinai School of Medicine
St. Joseph’s Hospital and Regional Medical Center
Paterson, New Jersey
Brooke Albright, MD, MAJ, MC

Assistant Professor of Anesthesiology
Critical Care Air Transport Team Physician
United States Air Force
Landstuhl, Germany
Tayab R. Andrabi
Associate Professor
Department of Anesthesiology & Perioperative Medicine
The University of Texas MD Anderson Cancer Center
Houston, Texas
Jonathan Anson, MD
Assistant Professor
John L. Ard Jr., MD

Assistant Professor
New York University School of Medicine
NYU Langone Medical Center
New York, New York
Radha Arunkumar, MD
Associate Clinical Professor
Department of Anesthesiology and Perioperative Medicine
Houston, Texas
Alan Ashworth, MBChB, FRCA, FFICM

Consultant in Cardiothoracic Anaesthesia and Intensive Care
University Hospital of South Manchester
Manchester, UK
Kalliopi Athanassiadi, MD, PhD

Senior Thoracic Surgeon
Department of Surgery
University of Athens Medical School
Athens, Greece
Joshua A. Atkins, MD, PhD

Assistant Professor
Ahmed Fikry Attaallah, MD, PhD

Assistant Professor
West Virginia University School of Medicine
Robert C. Byrd Health Sciences Center
Morgantown, West Virginia
John G. T. Augoustides, MD, FASE, FAHA

Associate Professor
Naola Austin, MD
Resident Physician
Seattle, Washington
Stephen O. Bader, MD
Assistant Professor
Sean M. Bagshaw, MD, MSc, FRCPC
Assistant Professor
Division of Critical Care
University of Alberta
Edmonton, AB Canada
Timothy R. Ball, MD
Texas A&M College of Medicine
Scott & White Memorial Hospital
Temple, Texas
Andrew L. Barker, MD
Resident Physician
Scott and White Hospital
Temple, Texas
Viachaslau Barodka, MD
Assistant Professor
Baltimore, Maryland
Amy Barulic, BS, MHS

Research Assistant
Colin Bauer, MD
Chief Resident
David Geffen School of Medicine at UCLA
Ronald Reagan Medical Center
Los Angeles, California
Shawn T. Beaman, MD
Assistant Professor
Associate Residency Program Director
John F. Bebawy, MD
Assistant Professor of Anesthesiology and Neurological Surgery
Feinberg School of Medicine, Northwestern University
Northwestern Memorial Hospital
Chicago, Illinois
A. Katharina Beckmann, MD
Fellow, Cardiac Anesthesia
Chicago, Illinois
Sascha Beutler, MD, PhD

Assistant Professor
Assistant Program Director
Department of Anesthesiology, Perioperative and Pain Medicine
Brigham and Women’s Hospital
Dmitri Bezinover, MD, PhD

Assistant Professor
Amar M. Bhatt, MD
Resident Physician
Columbus, Ohio
Shreyas Bhavsar, DO
Assistant Professor
Houston, Texas
Jeanna Blitz, MD
Assistant Professor
New York, New York
J. Scott Bluth, BS
Medical Student
Houston, Texas
Michael L. Boisen, MD
Fellow, Cardiothoracic Anesthesiology
Eric Bolin, MD
Assistant Professor
Department of Anesthesia and Perioperative Medicine
The Medical University of South Carolina
MUSC Medical Center
Charleston, South Carolina
Mark R. Bombulie, BS
Medical Student
University of Texas School of Medicine at Houston
Houston, Texas
James D. Boone, MD
Instructor
Chicago, Illinois
Mary Brady, MD, FASE

Assistant Professor
Medical Director, Post-Anesthesia Care Unit
Director, Intraoperative Transesophageal Echocardiography Program
Department of Anesthesiology and Critical Care Medicine
Baltimore, Maryland
Michelle Braunfeld, MD
Clinical Professor
Chief, Department of Anesthesiology
Greater Los Angeles Veterans Affairs Hospital
Tod A. Brown, MD
Assistant Professor
MUSC Medical Center
Charles H. Brown IV, MD

Assistant Professor
Baltimore, Maryland
Kelly Bruno, BS, MD

Medical Student
University of North Carolina School of Medicine
Ethan O. Bryson, MD
Associate Professor
Department of Anesthesiology and Psychiatry
The Mount Sinai Hospital
New York, New York
Arne O. Budde, MD, DEAA

Assistant Professor
James Cain, MD
Department of Anesthesiology and Pediatrics
Children’s Hospital of Pittsburgh of UPMC
James M. Callas, MD
Chief, Department of Radiology
King’s Daughters Clinic
Temple, Texas
Neal Campbell, MD
Assistant Professor
Department of Anesthesiology & Pediatrics
Children’s Hospital of Pittsburgh of UPMC
Elena C. Capello, MD
Universita di Torino
Dipartimento di Discipline Medico-Chirurgiche
Sezione di Anestesiologia e Rianimazione
Ospedale S. Giovanni Battista
John B. Carter, MD
Associate Professor
Oklahoma University College of Medicine
Oklahoma University Health Sciences Center
Oklahoma City, Oklahoma
Michael Carter, MD, PhD

Resident Physician
Washington University School of Medicine
Barnes-Jewish Hospital
St. Louis, Missouri
Daniel Castillo, MD
Assistant Professor
University of Florida College of Medicine
Shands Jacksonville Medical Center
Jacksonville, Florida
Davide Cattano, MD, PhD
Associate Professor
Memorial Hermann Hospital
Houston, Texas
Laura F. Cavallone, MD
Assistant Professor
St. Louis, Missouri
John T. Chalabi, MD
Vinay Chandrasekhara, MD
Instructor
Division of Gastroenterology, Department of Medicine
Jean Charchaflieh, MD, DrPH, FCCM, FCCP

Associate Professor
Yale School of Medicine
Yale-New Haven Hospital
New Haven, Connecticut
Verghese T. Cherian, MBBS, MD, FFARCSI

Assistant Professor
Jason Choi, MD
Resident Physician
Christopher G. Choukalas, MD, MS

Assistant Professor
Department of Anesthesia and Perioperative Care
University of California, San Francisco
San Francisco VA Medical Center
San Francisco, California
Jason Han Chua, MD

Theodore J. Cios, MD, MPH

Resident Physician
Carlee Clark, MD
Assistant Professor
MUSC Medical Center
Matthew D. Cohen, DO
Assistant Professor
Chief, Division of Acute Pain and Regional Anesthesia
University of Oklahoma
The University of Oklahoma Health Sciences Center
Seth R. Cohen, DO
Resident Physician
John F. Coleman, MD
Clinical Fellow
Baltimore, Maryland
Lydia A. Conlay, MD, PhD

Russell D and Mary B Sheldon Professor
Vice Chairwoman for Academic Affairs
University of Missouri School of Medicine
University of Missouri Health System
Columbia, Missouri
Craig R. Cook, MD, PhD

Resident Physician
St. Louis, Missouri
Daniel Cormican, MD
Resident Physician
Charles E. Cowles Jr., MD

Assistant Professor
Houston, Texas
Ryan Crowley, MD
Staff Physician
Legacy Good Samaritan Hospital
Portland, Oregon
William C. Culp Jr., MD, FASE
Associate Professor
Texas A&M University College of Medicine
Temple, Texas
Cristina Cunanan, MD
Resident Physician
Priti G. Dalal, MD, FRCA

Associate Professor
Patricia Dalby, MD
Associate Professor
Magee-Women’s Hospital of UPMC
Lori Dangler, MD, MBA

Assistant Professor
Houston, Texas
Nisha Dave, DO, PharmD

Resident Physician
St. Joseph’s Regional Medical Center
Alberto J. de Armendi, MD, AM, MBA

Professor
Chief, Pediatric Anesthesia
Children’s Hospital of Oklahoma
Stephen Dechter, DO
Medical Student
Loyola University Chicago Stritch School of Medicine
Maywood, Illinois
Matthew Delph, MD
Resident Physician
Jagan Devarajan, MD, FRCA

Associate Staff
Cleveland, Ohio
Anahat Dhillon, MD
Ronald Reagan Medial Center
Bradley T. Dollar, MD
Assistant Professor
Residency Program Director
Department of Radiology
Temple, Texas
Kathleen S. Donahue, DO, FAAP

Associate Professor
Associate Vice Chair, OR Management
Shawna Dorman, MD
Instructor
New York, New York
Corey C. Downs, MD
Staff Anesthesiologist
Surgical and Perioperative Careline
VA Greater Los Angeles Healthcare System
Emily L. Drennan, MD
Assistant Professor
Houston, Texas
Rebecca A. Drinkaus, MD
Assistant Professor
Peter Drocton, MD
Cedars-Sinai Medical Center
Olive View - UCLA Medical Center
Sylmar, California
Mirsad Dupanovic, MD
Assistant Professor
Kansas University School of Medicine
Kansas University Medical Center
Kansas City, Kansas
Victor Duval, MD
Ramana V. Duvvuri, MD
J. Andrew Dziewit, MD
Attending Physician
Department of Anesthesia
Crozer Chester Medical Center
Upland, Pennsylvania
Jill Eckert, DO
Assistant Professor
Nabil Elkassabany, MD
Assistant Professor
Matthew Ellison, MD
Assistant Professor
Trent Emerick, MD
Resident Physician
Thomas I. Epperson III, MD

Assistant Professor
MUSC Medical Center
Zhuang-Ting Fang, MD, MSPH

Jared Feinman, MD
Fellow, Cardiothoracic Anesthesia
Larry C. Field, MD
Assistant Professor
Medical Director, Medical/Surgical ICU
MUSC Medical Center
Robert S. Fitzgerald, LittB, STB, MA, STM, PhD

Professor
Environmental Health Sciences, Physiology, Medicine
The Johns Hopkins University
Baltimore, Maryland
Linzy Fitzsimons, MD
Resident Physician
Melissa Flanigan, DO
Assistant Professor
Andrew Fond, MD
University of Southern California
Siyavash Fooladian, MD, MPH

Fellow, Cardiothoracic Anesthesiology
Caroline Fosnot, DO, MS

Clinical Instructor
John J. Freely Jr., MD

Assistant Professor
MUSC Medical Center
Megan M. Freestone-Bernd, MD
Assistant Professor
Katy E. French-Bloom, MD
Assistant Professor
Houston, Texas
John C. Frenzel, MD
Professor
Houston, Texas
David Frey, BA
Medical Student
Ohio University College of Osteopathic Medicine
Athens, Ohio
David P. Frey, DO
Resident Physician
Seattle, Washington
Elizabeth A.M. Frost, MD

Professor of Anesthesiology
The Mount Sinai Hospital
New York, New York
Kamilia S. Funder, MD
Physician
Copenhagen University Hospital, Rigshospitalet
Copenhagen, Denmark
Jorge A. Galvez, MD
Fellow, Pediatric Anesthesiology
Children’s Hospital of Philadelphia
Wei Dong Gao, MD, PhD

Associate Professor
Baltimore, Maryland
Stephanie Gargani, MD
Resident Physician
St. Joseph’s Regional Medical Center
Andrew Geller, MD
Resident Physician
Charles Drew University of Medicine and Science
Resident Physician
Ileana Gheorghiu, MD
Assistant Professor
University of Maryland School of Medicine
University of Maryland Medical Center
Baltimore, Maryland
Brian Gierl, MD
Resident Physician
Lori Gilbert, MD
Philadelphia VA Medical Center
Ronnie J. Glavin, MB, ChB, MPhil, FRCA, FRCP (Glas)

Consultant Anesthetist
Victoria Infirmary
Glasgow, United Kingdom
Christine E. Goepfert, MD, PhD, DESA

Instructor and Visiting Professor
St. Louis, Missouri
Emily Gordon, MD
Instructor
Shannon M. Gossett-Popovich, MD
Assistant Professor
Houston, Texas
Amitabh Goswami, DO, MPH

Fellow, Pain Management
University of California, Davis School of Medicine
UC Davis Medical Center
Sacramento, California
Ori Gottlieb, MD
Assistant Professor
Department of Anesthesia and Critical Care
Pritzker School of Medicine, University of Chicago
The University of Chicago Medicine
Chicago, Illinois
Vijaya Gottumukkala, MB, BS, MD, FRCA

Professor
Houston, Texas
Basavana G. Goudra, MD, FRCA, FCARCSI

Andreas Grabinsky, MD
Assistant Professor
University of Washington School of Medicine
Harborview Medical Center
Seattle, Washington
Ashley Greene, DO
Resident Physician
Michael S. Green, DO
Assistant Professor
Interim Chair
Drexel University College of Medicine
Hahnemann University Hospital
Alina M. Grigoire, MD, MHS, FASE

Associate Professor
Director, Division of Cardiothoracic Anesthesiology
University of Maryland School of Medicine
University of Maryland Medical Center
Baltimore, Maryland
Michael Grover, MD
Resident Physician
University of Texas School of Medicine, San Antonio
University of Texas Health Science Center at San Antonio
San Antonio, Texas
Anthony H. Guarino, MD
Director, Pain Management
St. Louis, Missouri
Vadim Gudzenko, MD
Maged N. Guirguis, MD
Cleveland, Ohio
Gregory MT Hare, MD, PhD

Associate Professor
St. Michael’s Hospital
Toronto, Canada
Jagtar Singh Heir, DO

Houston, Texas
Rachel Helle, DO
Resident Physician
Columbia, Missouri
Laura B. Hemmer, MD
Assistant Professor
Chicago, Illinois
John Henao, MD
Resident Physician
Andrew Herlich, DMD, MD, FAAP

Professor
Chief, UPMC Mercy
Ibetsam Hilmi, MBChB, FRCA

Associate Professor
Institute of Clinical and Translational Sciences
Jonathan K. Ho, MD
John W. Hoffman, Jr., DO, MS

Clinical Instructor
Michael P. Hofkamp, MD
Assistant Professor
Texas A&M, -College of Medicine
Temple, Texas
Allen Alexander Holmes, MD, MS

Assistant Professor
Houston, Texas
Joe C. Hong, MD
Kimberly Howard-Quijano, MD
Clinical Instructor
Tyken C. Hsieh, MD
Staff Cardiac Anesthesiologist
Mills-Peninsula Health Services
Burlingame, California
Angela T. Hsu, MD
Attending Physician
Kaiser Permanente
Downey, California
Eric S. Hsu, MD
Clinical Professor
Allen Hu, MD
T. Kate Huncke, MD
Clinical Associate Professor
New York, New York
Catherine Ifune, MD, PhD

Associate Professor
St. Louis, Missouri
Mohamad Iravani, MD
Selma Ishag, MB, BS, MD

Assistant Professor
St. Louis, Missouri
%
Jonathan S. Jahr, MD
Clinical Professor
Ranu Jain, MD
Assistant Professor
Assistant Director, Pediatric Anesthesia
The University of Texas School of Medicine at Houston
Children’s Memorial Hermann Hospital-Texas Medical Center
Houston, Texas
Piotr K. Janicki, MD, PhD

Professor
Richard C. Jensen, MD
Resident Physician
Rongjie Jiang, MB, MS

Resident Physician
Quinn L. Johnson, MD
Columbia, Missouri
Praveen Kalra, MBBS, MD, FCCP

Assistant Professor
Mandip S. Kalsi, MD
Fellow, Regional Anesthesia
Hospital for Special Surgery
New York, New York
Valbona Kanarek, MD
Chief Resident
Mt. Sinai School of Medicine
Revati Kanekar, MD
Resident Physician
Ivan M. Kangrga, MD, PhD

Associate Professor
St. Louis, Missouri
Susan Kaplan, MD
Clinical Associate
University of Pennsylvania
Menelaos Karanikolas, MD, MPH

Assistant Professor
St. Louis, Missouri
Keyvan Karkouti, MD, FRCPC, MSc

Associate Professor
University of Toronto
Toronto, Ontario
Jeffrey Katz, MD
Chief Resident
Chicago, Illinois
Paul Kerby, MB, BS

Chief Resident
St. Louis, Missouri
Patrick Kim, MD
Resident Physician
St. Louis, Missouri
Peter H. Kim, MD
Andrew A. Klein, MD
Consultant
Anaesthesia and Intensive Care
Papworth Hospital
Cambridge, United Kingdom
Antoun Koht, MD
Professor of Anesthesiology, Neurological Surgery & Neurology
Chicago, Illinois
Iosifina Kolliantzaki, MD
Aghia Sophia Children’s Hospital
Athens, Greece
James J. Konvicka, MD
Assistant Professor
Scott and White Healthcare
Temple, Texas
Edward Kosik, DO
John D. Kot, MD
Resident Physician
Joseph Koveleskie, MD
Assistant Professor
Tulane University School of Medicine
Tulane Medical Center
New Orleans, Louisiana
Alan J. Kover, MD, PharmD

Columbus, Ohio
Kenneth F. Kuchta, MD
Chief, Vascular Anesthesiology
Anand Lakshminarasimhachar, MBBS, FRCA

Assistant Professor
St. Louis, Missouri
Daniel A. Lazar, MD
Attending Anesthesiologist
North Shore Manhasset Hospital
Manhasset, New York
Stephane Ledot, MD
Hadassah Hebrew University School of Medicine
Jerusalem, Israel
Thomas Ledowski, MD, PD, DEAA, FANZCA

University of Western Australia
School of Medicine and Pharmacology
Perth, Australia
Annie D. Lee, MD
Resident Physician
Jonathan D. Leff, MD
Assistant Professor
Chief, Cardiothoracic Anesthesiology
Albert Einstein College of Medicine
Montefiore Medical Center
Bronx, New York
Philip Levin, MD
Clinical Professor
Jinlei Li, MD, PhD

Assistant Professor
Yun Rose Li, BS

Medical Student
Jeffrey W. Lim, MD, PhD

Assistant Professor
Sharon L. Lin, MD
Attending Physician
Swedish Medical Center
Seattle, Washington
Keith E. Littlewood, MD
Associate Professor
Vice Chair for Education
Assistant Dean for Clinical Skills Education
University of Virginia School of Medicine
University of Virginia Health System
Charlottesville, Virginia
Marc A. Logarta, MD, DABA, FANZCA

Consultant Anesthetist
Campbelltown Hospital
Canterbury Hospital
Sydney, Australia
David W. Lui, DMD, MD

Assistant Professor
Department of Oral and Maxillofacial Surgery
Virginia Commonwealth University School of Dentistry and School of Medicine
VCU Medical Center
Richmond, Virginia
Calvin Lyons, MD
Resident Physician
Department of Surgery
The Methodist Hospital
Houston, Texas
Edna Ma, MD
Attending Physician
Olive View - UCLA Medical Center
Sylmar, California
Aman Mahajan, MD, PhD

Professor
Chief, Cardiothoracic Anesthesiology
Vice Chair of Anesthesiology
Victor L. Mandoff, MD
Associate Professor
The University of Arkansas College of Medicine
The University of Arkansas for Medical Sciences
Little Rock, Arkansas
Gerard R. Manecke, Jr., MD

Professor and Chair
University of California, San Diego School of Medicine
University of California, San Diego Medical Center
San Diego, California
Federica Manfroi, MD
Michael Mangione, MD
Associate Professor
Chief of Anesthesiology
VA Pittsburgh Healthcare System
Natesan Manimekalai, MD
Assistant Professor
Ana Maria Manrique-Espinel, MD

Resident Physician
Brian L. Marasigan, MD
Assistant Professor
Houston, Texas
Julie Marshall, MD
Assistant Professor
Columbia, Missouri
Jayson T. Maynes, MD, PhD

Assistant Professor
Hospital for Sick Children/SickKids Research Institute
University of Toronto
Toronto, Canada
Richard McAffee, MD
Assistant Professor
Mary E. McAlevy, MD
Assistant Professor
Russell K. McAllister, MD
Associate Professor
Assistant Dean of Quality and Patient Safety
Scott & White Memorial Hospital
Temple, Texas
Dwayne E. McClerkin, MD
Assistant Professor
MUSC Medical Center
Stephen M. McHugh, MD
Resident Physician
Julie McSwain, MD, MPH

Assistant Professor
MUSC Medical Center
Li Meng, MD, MPH

Associate Professor
Spyros D. Mentzelopoulos, MD, PhD

Assistant Professor
Department of Critical Care
University of Athens Medical School
Athens, Greece
David G. Metro, MD
Associate Professor
Berend Mets, MB, ChB, PhD, FRCA, FFASA

Eric A. Walker Professor and Chair
Tricia A. Meyer, PharmD, MS, FASHP

Associate Professor
Director, Department of Pharmacy
Temple, Texas
Agnes Miller, MD
Director, Resident Education
Maimonides Medical Center
New York, New York
Sara Miller, MD
Resident Physician
Brian Milne, MD, MSc, FRCPC

Professor
Queen’s University
Kingston General Hospital
Kingston, Ontario
Beth H. Minzter, MD, MS, FIPP

Department of Pain Management
Anesthesiology Institute
Cleveland, Ohio
Nanhi Mitter, MD
Assistant Professor
Director, Adult Cardiothoracic Anesthesiology Fellowship
Baltimore, Maryland
Kanishka Monis, MD
University of Texas School of Medicine, San Antonio
University of Texas Health Science Center at San Antonio
San Antonio, Texas
Richard C. Month, MD
Teresa L. Moon, MD
Assistant Professor
Houston, Texas
Kenneth R. Moran, MD
Columbus, Ohio
Allyson J.A. Morman, MD

Resident Physician
Juan Moya-Amor’s, PhD

Professor of Surgery
Chief, Department of Thoracic Surgery
Hospital Universitari de Bellvitge
L’Hospitalet de Llobregat
Barcelona, Spain
Daniel Mulcrone, MD
Resident Physician
Eman Nada, MD, PhD

Fellow, Neuroanesthesia
Cleveland, Ohio
Carsten Nadjat-Haiem, MD
Sharanya Nama, MD
Resident Physician
Gundappa Neelakanta, MD
Clinical Professor of Anesthesiology
Jacques Prince Neelankavil, MD

Assistant Professor
Eric W. Nelson, MD
Assistant Professor
MUSC Medical Center
Sara C. Nelson, MD
Attending Physician
Naval Medical Center San Diego
San Diego, California
Edward C. Nemergut, MD
Associate Professor of Anesthesiology and Neurosurgery
Anh-Thuy Nguyen, MD
Houston, Texas
Linh Trang Nguyen, MD

Assistant Professor
Houston, Texas
Teodora Orhideea Nicolescu, MD

Associate Professor
Chief, Division of Cardiothoracic Anesthesiology
Daniel R.C. Nieva, MD

Assistant Professor
St. Louis Children’s Hospital
St. Louis, Missouri
Dave Nisha Davendra, PharmD, DO

Mark E. Nunnally, MD, FCCM

Associate Professor
Chicago, Illinois
Satoru Ogawa, MD
Emory University School of Medicine
Emory University Hospital
Atlanta, Georgia
Olutoyosi Ogunkua, MD
Resident Physician
University of Texas Southwestern School of Medicine
University of Texas Southwestern Medical Center at Dallas
Dallas, Texas
Erik Olness, MD
Assistant Professor
Onyi Onuoha, MD, MPH

Assistant Professor
Todd M. Oravitz, MD
Associate Professor
Chief, Liver Transplantation Anesthesiology
The University o Pittsburgh School of Medicine
VA Pittsburgh Healthcare System
Pascal O. Owusu-Agyemang, MD
Assistant Professor
Houston, Texas
Nirvik Pal, MD
Clinical Instructor
St. Louis, Missouri
Edward Park, MD
Dorothea Rosenberger Parravano, MD, PhD

Associate Professor
MUSC Medical Center
Andrea Parsons, MD
Assistant Professor
St. Louis, Missouri
Parisa Partownavid, MD
Associate Director, Ambulatory Surgery Center
Mitesh Patel, MD
Chief Resident
Columbia, Missouri
Neesa Patel, MD
Shetal H. Patel, MD
Fellow, Obstetric Anesthesiology
Swati Patel, MD
Chief, Division of Pediatric Anesthesiology
Tara L. Paulose, MD
Katerina Pavenski, MD, FRCPC

Department of Laboratory Medicine
St. Michael’s Hospital, Toronto, Canada
Department of Laboratory Medicine and Pathobiology, University of Toronto Toronto, Canada
Alison R. Perate, MD
Assistant Professor
Children’s Hospital of Philadelphia
Resident Physician
Raymond M. Planisic, MD
Director, Transplantation Anesthesiology
Keyuri Popat, MD
Associate Professor
Houston, Texas
Wanda M. Popescu, MD
Associate Professor of Anesthesiology
Marek Postula, MD, PhD

Assistant Professor at the Department of Experimental and Clinical Pharmacology
Medical University of Warsaw
Senior Assistant at the Department of Noninvasive Cardiology and Hypertension
Central Clinical Hospital
The Ministry of the Interior
Warsaw, Poland
Debra Domino Pulley, MD

Associate Professor
Washington University of School of Medicine
St. Louis, Missouri
Carlos A. Puyo, MD
St. Louis, Missouri
Farooq A. Qureshi, MD
Henry Ra, MD
Resident Physician
Ronald Reagan Hospital Center
Los Angeles, California-
Fabrizio Racca, MD
S.C. Anestesia e Rianimazione Pediatrica Azienda Ospedaliera
SS Antonio Biagio e Cesare Arrigo
Alessandria, Italy
Siamak Rahman, MD
Niraja Rajan, MB, BS, FAAP

Assistant Professor
Medical Director, Hershey Outpatient Surgery Center
Sivam Ramanathan, MD
Associate Professor of Anesthesiology
Chitra Ramasubbu, MD
Baltimore, Maryland
George J. Ranier, MD
Assistant Professor
V. Marco Ranieri, MD
Universita di Torino
Dipartimento di Discipline Medico-Chirurgiche
Sezione di Anesthesiologia e Rianimazione
Ospedale S. Giovanni Battista
Torino, Italy
Srikantha L. Rao, MBBS, MS

Associate Professor
Rashmi R. Rathor, MD
Fellow, Abdominal Organ Tranplant
St. Louis, Missouri
Elizabeth Rebello, MD
Assistant Professor
Houston, Texas
Venugopal S. Reddy, MD, EDIC, FFARCS

Associate Professor
Rebecca L. Reeves, DO
Resident Physician
Baltimore, Maryland
Wendy HP Ren, MD, FAAP

Ronald Reagan UCLA Medical Center
Joseph Resti, MD
Resident Physician
Cameron J. Ricks, MD
Assistant Professor
Irvine, California
Horst Rieke, MD, PhD

Professor
MUSC Medical Center
Francisco Rivas-Doyague, MD
Medical Doctor
Department of Thoracic Surgery
Hospital Universitari de Bellvitge
L’Hospitalet de Llobregat
Barcelona, Spain
Laura L. Roberts, MD
Assistant Professor
MUSC Medical Center
Adam Romanovsky, MD
Divisions of Critical Care and Nephrology
University of Alberta
Edmonton, AB Canada
Harvey K. Rosenbaum, MD
Ronald Reagan UCLA Medical Center
Jay A. Roskoph, MD, MBA

Chief Department of Anesthesiology
UPMC-St. Margaret Hospital
Marc A. Rozner, PhD, MD

Professor of Anesthesiology and Perioperative Medicine
Professor of Cardiology
University of Texas MD Anderson Cancer Center
Houston, Texas
Daniel M. Rusu, MD
Assistant Professor
University of Kentucky College of Medicine
University of Kentucky Healthcare
Lexington, Kentucky
Ali Salehi, MD
Alain A. Salvacion, MD
Chicago, Illinois
Samuel Samuel, MD
Associate Fellowship Director of Pain Management
Cleveland, Ohio
Mona G. Sarkiss, MD, PhD

Associate Professor
Department of Pulmonary Medicine
Houston, Texas
Poovendran Saththasivam, MD
Resident Physician
Drexel University College of Medicine
Hahnemann University Hospital
Matthew V. Satterly, MD
Chicago, Illinois
Shashank Saxena, MD
Staff Anesthesiologist
VA Pittsburgh Health Care System
R. Alexander Schlichter, MD
Peter M. Schulman, MD
Assistant Professor
Oregon School of Medicine
Oregon Health and Science University
Portland, Oregon
Jeffrey J. Schwartz, MD
Associate Professor
Johanna C. Schwarzenberger, MD
Clinical Professor
Director, Pediatric Cardiac Anesthesiology
Korrin Scott, MD
Resident Physician
Jennifer Scovotti, MA
Research Associate
Khaled Sedeek, MD
Associate Professor
E. Gail Shaffer, MD, MPH

Resident Physician
Kirk H. Shelley, MD, PhD

Professor
Justin C. Shields, MD
Resident Physician
St. Louis, Missouri
Shawn T. Simmons, MD
Medical Director, Hyperbaric Medicine Service
University of Iowa Carver College of Medicine
University of Iowa Hospitals
Iowa City, Iowa
Amrik Singh, MD
Associate Professor
University of California, Davis School of Medicine
UC Davis Medical Center
Sacramento, California
Davinder Singh, MD
Assistant Professor
Irvine, California
Sukhdip Singh, MD
Resident Physician
Sumit Singh, MD
Christopher A. Skorke
Assistant Professor
Medical Director, Medical/Surgical ICU
MUSC Medical Center
Jose M. Soliz, MD
Assistant Professor
Houston, Texas
Dmitri Souzdalnitski, MD, PhD

Pain Management Department
Cleveland, Ohio
Martin M. Stechert, MD
University of California, San Francisco School of Medicine
UCSF Medical Center
San Francisco, California
Chris A. Steel, MD
Attending Physician
Director of Anesthesia Services
White River Health System
Batesville, Arizona
Jacob Steinmetz, MD, PhD

Consultant
Copenhagen University Hospital
Rigshospitalet, Copenhagen
Jochen Steppan, MD
Baltimore, Maryland
Joel Stockman, MD
William David Stoll, MD

Assistant Professor
MUSC Medical Center
Bradley A. Stone, MD
Attending Anesthesiologist
Mission Hospital
Asheville, North Carolina
Suzanne Strom, MD
Irvine, California
Adam M. Stuart, MD
Medical Student
Virginia Commonwealth University School of Medicine
Richmond, Virginia
Mariya Svilik, MD
Staff Physician
Rajeshwary Swamidurai, MD
Attending Physician
Lodi Memorial Hospital
Lodi, California
Kenichi A. Tanaka, MD, MSc

Associate Professor
Emory University School of Medicine
Atlanta, Georgia
Rob C. Tanzola, MD, FRCPC

Assistant Professor
Queen’s University
Kingston General Hospital
Kingston, Ontario
Vijay Tarnal, MBBS, FRCA

The University of Texas Medical Branch School of Medicine at Galveston
The University of Texas Medical Branch at Galveston
Galveston, Texas
Adam Thaler, DO
Resident Physician
Ilka Theruvath, MD, PhD

Assistant Professor
MUSC Medical Center
Svjetlana Tisma-Dupanovic, MD
Assistant Professor
Department of Cardiology
Kansas University School of Medicine
Kansas University Medical Center
Kansas City, Kansas
Catherine Dawson Tobin, MD

Assistant Professor
MUSC Medical Center
Lan Chi Tran, MD

Resident Physician
St. Louis, Missouri
Timothy T. Tran, MD
Resident Physician
St. Louis, Missouri
Ravi S. Tripathi, MD
Columbus, Ohio
Angela Truong, MD
Associate Professor
Houston, Texas
Dam-Thuy Truong, MD
Professor
Houston, Texas
January Y. Tsai, MD
Houston, Texas
Judith A. Turner, MD, PhD

Kalpana Tyagaraj, MD
Director, Obstetric Anesthesiology
Maimonides Medical Center
New York, New York
Shital Vachhani, MD
Assistant Professor
Houston, Texas
Dierk A. Vagts, MSc, DEAA, EDIC

Professor
Department of Anesthesiology and Intensive Care Medicine, Emergency Medicine, Pain
Therapy and Palliative Care
Academic Teaching Hospital of Johannes Gutenberg University
Mainz, Neustadt Weinstrasse, Germay
Sonia Vaida, MD
Professor of Anesthesiology, Obstetrics and Gynecology
Elizabeth Valentine, MD
Assistant Professor
Andrea Vanucci, MD, DEAA

Assistant Professor
St. Louis, Missouri
Swarup S. Varaday, MBBS, FRCA, FCARSI

Assistant Professor
St. Louis, Missouri
Malina M. Varner, MD
Instructor
Aditya Venkataraman, MD
Chief Resident
St. Louis, Missouri
Thomas Verbeek, MBChB

Assistant Professor
Bruce Vrooman, MD
Department of Pain Management
Cleveland Clinic
Cleveland, Ohio
Samuel H. Wald, MD
Clinical Professor
Cynthia Wang, MD
Ellen Y. Wang, MD
Stanford University
Lucile Packard Children’s Hospital
Palo Alto, California
Steve Wang, MD
Assistant Professor
University of Texas MD Anderson Cancer Center
Houston, Texas
Izabela M. Wasiluk, MD
Assistant Professor
Huafeng Wei, MD, PhD

Assistant Professor
Jiadong Wei, MD
Yoram G. Weiss, MD, MBA, FCCM

Associate Professor in Anesthesiology and Critical Care Medicine
Hadassah Hebrew University School of Medicine
Jerusalem, Israel
Adjunct Associate Professor
University of Pennsylvania
Gregory E. R. Weller, MD, PhD

Assistant Professor
Joseph R. Whiteley, DO
Assistant Professor
MUSC Medical Center
J. Aaron Williams, MD
Assistant Professor
Columbia, Missouri
Sylvia H. Wilson, MD
Assistant Professor
MUSC Medical Center
Stephen P. Winikoff, MD
Professor
Jeremy Wong, MD
Christopher Wray, MD
Assistant Professor
Jennifer Wu, MD, MBA

Assistant Professor
Houston, Texas
Sulin G. Yao, MD
Attending Physician
Atlanticare Regional Medical Center
Pomona, New Jersey
Peter K. Yi, MD
Assistant Professor
Dirk Younker, MD
Russell D and Mary B Sheldon Professor of Anesthesiology
Vice Chairman for Clinical Affairs
Columbia, Missouri
Zdravka Zafirova, MD
Assistant Professor
Chicago, Illinois
Alan P. Zaggy, MD
Assistant Professor
Columbia, Missouri
Mark Zakowski, MD
Associate Professor of Anesthesiology, Adjunct
Chief, Obstetric Anesthesiology
Sherif Zaky, MD, PhD

Assistant Professor of Anesthesiology
Cleveland, Ohio
Sessunu M. Zemo, MD
Resident Physician
Baylor College of Medicine
Ben Taub Hospital
Houston, Texas
Fei Zheng, MD, MPH, MS

Resident Physician
Baltimore, Maryland
Dayna Zimmerman, BS
Research Assistant
Keren Ziv, MD
Zachary M. Zumbar, MD, MPH

Attending Physician
Midwest Pain Physicians
Uniontown, Ohio
FOREWORD

I t is a pleasure to introduce the 5 Minute Anesthesia Consult to readers around the globe.
This concise compendium of topics pertinent to modern anesthesiology practice will be
useful as a rapid reference for busy anesthesiology clinical practitioners, anesthesiology
residents, medical students and others in training, nurse anesthetists, anesthesiology
assistants, perioperative nurses, post-operative intensive care personnel, and other allied
health professionals caring for patients before and after anesthetic administration. The
contents are offered in both text format as well as applications for smart devices, to be readily
at hand in any clinical situation in any clinical location.
The editor has drawn from a wide spectrum of expert authors from multiple institutions to
compile approximately 480 two-page chapters, in template formats for easy-to-retrieve
information. The content is organized into sections on important topics in physiology,
pertinent issues for major co-existing diseases/co-existing conditions, key information for
important surgical procedures, and guidance for managing a variety of complications
encountered in anesthetic practice. In addition, the 5 Minute Anesthesia Consult contains a
drug section in a condensed, easily accessible format with current information about
anesthetic drugs and adjuvants, chronic medications that patients may be taking in the
perioperative period, and medications used to treat complications encountered in the peri-
anesthetic period.
As anesthesiology care is extending to encompass the spectrum from early evaluation and
optimization/management of pre-procedural risk factors, through post-procedural care to
minimize subsequent complications and/or re-admission, every practitioner can benefit from
timely access to a “one-stop” content source to support evidence-based anesthesiology care, a
source that concisely presents the most important concepts on a topic in an accessible
manner.
I look forward with enthusiasm to the broad distribution and availability of the 5 Minute
Anesthesia Consult to support high quality patient outcomes on an international basis.
PATRICIA A. KAPUR, MD
Professor and Chairwoman
Los Angeles, California, USA
April 2012
PREFACE

T he 5 Minute Medicine Consult was amongst the medical texts and references that
lined my mother’s bookshelf when I was in high school. I was drawn to the unique style
that made it “easy to read,” even at my level. The topic-specific and highly templated
format was the first of its kind amongst medical references. Years later, I have been given the
amazing opportunity to add to The 5 Minute Consult Series.
The goal of The 5 Minute Anesthesia Consult is to emulate that style by creating an
evidence-based, focused, and practical textbook that will be relevant to students, trainees,
nurse anesthetists, and physicians. The 480 topics are presented alphabetically, but are
presented in a second table of contents organized in four sections: Physiology, Co-Existing
Disease, Surgical Procedure, and Management. Each topic follows a two-page outline format
that is consistent with the section and easy to read. Additionally, we have provided a focused
Drug section.
The chapters in the Physiology section were specifically written to simplify complex topics
and then extrapolate them to pathophysiologic processes and apply them to relevant
perioperative matter.
The Surgical Procedures section describes key surgical steps, followed by anesthetic
considerations for preoperative preparation, intraoperative care, and postoperative concerns.
The goal of this section is to “involve” the anesthesia practitioner in the surgical procedure by
providing an understanding of, and appreciation for, our surgical colleagues’ work.
The chapters in the Co-Existing Disease Section describe basic pathophysiology concepts,
followed by key considerations to optimizing and managing patients throughout the
perioperative period.
The Management Section covers a comprehensive list of perioperative complications that
can arise in anesthetic practice. For example, the author of the Anaphylaxis chapter had a
patient who “crumped” after being exposed to medication. Despite appropriately treating the
patient with epinephrine and following ACLS protocol, the patient remained unresponsive to
therapy. The author saved her patient’s life by administering glucagon, which she describes in
her chapter as the treatment for refractory anaphylaxis that may be seen in patients who are
beta-blocked.
Each chapter provides a list of additional complementary topics that are available within
the book to allow readers the opportunity to supplement their knowledge of a given topic.
I sincerely hope that the practical nature and quality of this text will contribute to your
learning and benefit our patients in the ever-growing field of anesthesia. I welcome feedback
and suggestions at fiveminuteanesthesia@aol.com.
ACKNOWLEDGEMENTS

T he completion of this text would not have been possible without a number of special
people. The authors have given their time and expertise to prepare, revise, and re-revise
their chapters to attain the overarching vision for this textbook. I enjoyed the
opportunity to meet (and learn from) so many talented and enthusiastic practitioners and
teachers, as well as work with so many of my close friends, colleagues, former attendings, and
mentors. I would like to express my utmost gratitude for their quality contributions; their
work has resulted in what I believe is one of the best anesthesia texts out there.
My Publisher, Brian Brown, Senior Product Manager, Nicole Dernoski, and Lippincott
Williams & Wilkins/Wolters Kluwer Health provided me with mentorship, a team of high-
level professionals, and invaluable resources. I would like to thank them for providing me
with this tremendous opportunity to expand the highly successful 5 Minute Consult Series.
Thank you Drs. Patricia A. Kapur, Randy Steadman, Sam Wald, Rima Matevosian, Susan
Chan, Jordan Miller, Aman Mahajan, Barbara Van de Wiele, Phil Levin, Victor Duval, Nir
Hoffman, Carsten Nadjat-Haiem, Keren Ziv, Eric Hsu, Kenneth Kuchta, Michael Ferrante,
Michelle Braunfeld, Zhuang Fang, Swati Patel, Mitchell Lin, Michael Sopher, Ali Salehi,
Siamak Rahman, Parisa Partownavid and the UCLA Department of Anesthesiology for
teaching me to think critically, being patient, and serving as role-models. Your efforts,
dedication, and love for teaching and your patients have had far-reaching influences on me.
12 LEAD EKG
Elizabeth Valentine, MD
BASICS
DESCRIPTION
• The 12-lead EKG is a noninvasive test that provides information on the electrical function of
the heart and aids in the diagnosis of pathophysiologic processes.
• Serves as a baseline for perioperative changes and as a screening tool to identify cardiac
abnormalities.
• Continuous 3- or 5-lead EKG is an American Society of Anesthesiologists (ASA) standard
monitor used for general anesthesia and monitored anesthesia care.
PHYSIOLOGY PRINCIPLES
• P wave (80 ms): Denotes atrial depolarization. Myocardial depolarization is normally
initiated by spontaneous sinoatrial (SA) node depolarization. The signal is quickly and
efficiently conducted along a specialized conduction pathway. In the atria, this pathway is
via interatrial tracts (anterior, middle, and posterior); they begin by depolarizing the right,
followed by the left, atria. The conduction cells depolarize adjacent myocardial cells, which
have a different histology.
• QRS (80–120 ms): Denotes the varying stages of ventricular depolarization. The Q wave is
the initial negative deflection and results from septal depolarization. The R wave follows
and is the first positive deflection. It results from depolarization of the larger, more
muscular left ventricle; right ventricular depolarization is normally obscured. The S wave is
the final negative deflection caused by lateral wall depolarization.
• T wave: Denotes ventricular repolarization. The beginning of the wave represents a period
of absolute refractoriness, where a subsequent depolarization (no matter how strong) cannot
initiate a aberrant rhythm. The latter portion of the wave is a time of relative refractoriness,
where a strong enough depolarization can result in a runaway rhythm.
• PR interval (120–200 ms): Time from the start of atrial depolarization to atrioventricular
(AV) nodal conduction to conduction through the His-Purkinje system.
• QRS width: Represents the time for ventricular depolarization
• J point: Describes the intersection between the QRS complex and ST segment. When the
heart rate is increased, atrial repolarization may be observed at the very end of the QRS
complex as J point depression.
• ST segment: Denotes the end of depolarization to the beginning of repolarization and is
usually isoelectric
• QT interval (QTc <440 ms): Beginning of ventricular depolarization to the end of
ventricular repolarization. Time for ventricular repolarization is heart rate dependent; thus,
the QT is usually corrected for heart rate (QTc).
• Rate: Typically measured between sequential R waves; the RR interval (0.6–1.2 s) is useful
due to its prominent wave that allows for easy detection. A rate <60 bpm is bradycardia; a
rate >100 bpm is tachycardia.
• Rhythm: The location of regular P waves preceding each QRS suggests an atrial rhythm. The
relationship between the P wave and QRS complex provides information about underlying
conduction defects or dissociation.
• Axis: The average direction of the various complexes determines the axis. The normal QRS
axis is between 0 and 100° in the frontal plane. Left or right axis deviation can suggest
underlying pathophysiology.
ANATOMY
• A total of 12 leads allows for “visualizing” the electrical function from different angles
through the heart. Considering the leads in different combinations can aid in clinical
diagnosis.
• Standard limb leads (I, II, III): Form the points of Einthoven’s triangle, an equilateral
triangle whose vertices lie at the left and right shoulders and the pubic region and whose
center corresponds to the vector sum of all electric activity occurring in the heart at any
given moment. This allows for the determination of the electrical axis.
• Augmented limb leads (aVR, aVL, aVF): Together with the standard limb leads, record the
electrical activity along the frontal plane.
• Precordial leads (V1, V2, V3, V4, V5, V6): Record the electrical activity along the horizontal
plane.
• Anterior leads (V3 and V4): Allow evaluation and assessment of the electrical function of the
anterior wall of the heart. Usually supplied by the left anterior descending artery.
• Inferior leads (II, III, and aVF): Allow evaluation and assessment of the electrical function of
the inferior heart muscle. The inferior wall is usually supplied by the right coronary artery.
DISEASE/PATHOPHYSIOLOGY
• ST segments: Ischemia or infarct may present as either elevation or depression of the ST
segment. A routine preoperative EKG may appear normal if a patient is not experiencing
active ischemic symptoms. Thus, a high index of suspicion must be maintained for patients
at risk for coronary ischemia.
• Axis deviation: Common conditions associated with left axis deviation include left bundle
branch block or left anterior hemiblock, inferior MI, or left ventricular hypertrophy.
Common causes of a right axis deviation include right ventricular hypertrophy, chronic lung
disease, right bundle branch block, or lead reversal.
• Bundle branch blocks: A prolonged QRS suggests either a right (RBBB) or a left bundle
branch block (LBBB). They are described as either partial (QRS <120 ms) or complete (QRS
>120 ms). Although a RBBB can represent pulmonary or right heart disease, it is more
commonly benign. Alternatively, a LBBB is more likely to indicate underlying cardiac
pathology (CAD, CMO, valvular disease). A new onset LBBB should prompt a thorough
cardiac workup. The anterior or posterior fascicle of the left bundle may be blocked in
isolation (termed hemiblock). A nonspecific intraventricular conduction delay describes a
nonpathologic widening of the QRS complex that does not meet the criteria for either LBBB
or RBBB.
• AV blocks: Impaired conduction between the atria and ventricles of the heart are described
as first, second, and third degree. First-degree AV block is defined as a PR interval >0.2 s.
Second-degree AV block may be Type 1 (Mobitz 1, Wenckebach), defined as progressive
prolongation of the PR interval with eventual dropped QRS; or Type II (Mobitz 2), where
the PR remains unchanged prior to the sudden failure of conduction of a P wave and a
dropped ventricular beat. In third-degree AV block, there is no association between P waves
and QRS complexes. While first-degree and Mobitz I AV block are generally benign
conditions, Mobitz II (can progress to complete heart block) and third-degree AV blocks are
indications for cardiac pacing.
• P waves: Abnormal P wave morphology may indicate an ectopic atrial rhythm, whereas a
changing P wave morphology may suggest either a wandering atrial pacemaker or
multifocal atrial tachycardia. An irregular rhythm with no clear P waves suggests atrial
fibrillation. A regular “saw tooth” pattern may suggest atrial flutter.
• Arrhythmias: A narrow QRS suggests a supraventricular (above the ventricles) rhythm while
a wide QRS suggests either a ventricular source or aberrant conduction of a supraventricular
rhythm.
• QT prolongation: Prolonged QTc is a risk factor for developing ventricular arrhythmias
(Torsades de Pointes) and is an independent risk factor for sudden cardiac death. QTc may
be prolonged due to genetic causes (long QT syndrome), drugs (haloperidol, methadone), or
diseases (hypothyroidism).
• Delta waves: Describes a slurred upstroke of the QRS complex and is found in patients with
Wolff–Parkinson–White (WPW) syndrome. WPW is caused by the bypass of the AV node via
an accessory pathway called the bundle of Kent. This accessory pathway does not have the
rate-slowing property of the AV node, thus allowing for extremely fast heart rates and
potential hemodynamic instability. The combination of cardiac arrhythmias and an
accessory pathway may degenerate into ventricular fibrillation.
• R on T phenomenon: The beginning of the T wave is a time of absolute refractoriness; the
latter portion of the wave is a time of relative refractoriness. An abnormal depolarization
signal (aberrant pacemaker, PAC, PVC, cardioversion) cannot depolarize the entire ventricle
during the absolute refractory period; however, it may potentially do so during the relative
refractory period. This can result in degeneration into ventricular tachycardia or fibrillation.
• Artificial pacemaker: May be identified by tell-tale “pacer spikes” on EKG or telemetry. May
be atrial, ventricular, or sequentially paced. QRS will appear widened if ventricularly paced.
• Medication toxicities:
– Digoxin: Characteristic downward sloping of the ST segment. May also see an increased
PR and decreased QTc interval.
– Tricyclic antidepressants (TCAs): Characteristic rightward change in the frontal plane QRS
vector. A large R wave in aVR is quite sensitive for TCA toxicity; may also see an
increased QRS and QTc interval.
• Electrolyte abnormalities:
– Hypokalemia: EKG changes result from delayed ventricular repolarization. May include T
wave flattening and/or inversion, ST segment depression, prominent U wave, increased P
wave amplitude, and prolonged PR interval. Increased myocardial cell automaticity may
predispose to atrial or ventricular arrhythmias.
– Hyperkalemia: EKG changes are due to delayed depolarization and hastened
repolarization. Changes commonly progress in order from symmetrically peaked T waves
→ widened QRS → prolonged PR interval → loss of P wave → loss of R wave → ST
depression → EKG that resembles sine wave → ventricular fibrillation → asystole.
– Hypocalcemia: QTc prolongation and cardiac irritability leading to arrhythmias
– Hypercalcemia: Shortened ST segment and QTc interval
– Hypomagnesemia: PR and QT interval prolongation, cardiac irritability
– Hypermagnesemia: May see PR prolongation and QRS widening
PERIOPERATIVE RELEVANCE
• Intraoperative bovie, electrical interference, patient shivering, tremors, or movement may
closely resemble an intraoperative arrhythmia. Close inspection may reveal the QRS
“marching through” the interference; other times, it may be indistinguishable from a true
arrhythmia. Close evaluation of other monitors (blood pressure, pulse oximetry or arterial
plethysmograph, verification of palpable peripheral pulses) may provide clues in this
circumstance.
• Malpositioning of leads may result in the appearance of ST changes. Thus, it is good practice
to place leads in proper position if it does not interfere with the surgical field and to note
baseline abnormalities in the EKG tracing.
• Body habitus: Large breasts or obesity may result in low-voltage EKG.
• Pulmonary artery catheters and central lines: For patients with LBBB, there is a risk of
complete heart block with insertion. In this circumstance, it is prudent to have pacing
capabilities readily available. Similarly, in patients with WPW, the pulmonary artery
catheter or a wire for central line placement can induce a hemodynamically intolerable
tachyarrhythmia.
• Extracorporeal shock wave lithotripsy: Older machines time shocks to be delivered during
the R wave to prevent R on T phenomenon.
• Cardioversion: Machines synchronize the delivery of electrical discharge to the R wave to
prevent R on T phenomenon.
GRAPHS/FIGURES
FIGURE 1. EKG waves, segments, and intervals

FIGURE 2. The 12 leads allow for assessment of the electrical function of the three-dimensional heart.
REFERENCES
1. Correll DJ, Hepner DL, Chang C, et al. Preoperative electrocardiograms: Patient factors
predictive of abnormalities. Anesthesiology. 2009;110(6):1217–1222.
2. Eagle KA, Berger PB, Calkins H, et al. Practice advisory for preanesthesia evaluation: An
updated report by the American Society of Anesthesiologists Task Force on Preanesthesia
Evaluation. Anesthesiology. 2012;116:522–538.
ADDITIONAL READING
• ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac
surgery. Circulation. 2002;105:1257–1267.
• Guidelines for electrocardiography: A report of the American College of
Cardiology/American Heart Association Task Force on assessment of diagnostic and
therapeutic cardiovascular procedures. J Am Coll Cardiol. 1992;19:473–481.
See Also (Topic, Algorithm, Electronic Media Element)
• Myocardial ischemia
• QT prolongation
• Wolff–Parkinson–White (WPW) syndrome
• Cardiac action potentia
• Coronary arteries
CLINICAL PEARLS
• The axis of lead II is parallel to that of atrial depolarization; thus, it has the largest P wave
and helps to determine rhythm. Lead II also represents the inferior wall of the left ventricle,
which is typically supplied by the right coronary artery. EKG abnormalities in this area may
suggest ischemia or disease in this distribution.
• Lead V5 is most sensitive for detecting ST segment changes when a single lead is monitored
(detects abnormalities in 75% of cases). The combination of monitoring leads V5 and II
increases sensitivity to 80% and leads V4 and V5 increases sensitivity to 90% for detecting
intraoperative ST changes (1).
• Preoperative guidelines: The ASA Task Force on Preanesthesia Evaluation does not support
the ordering of any routine preoperative testing; instead, preoperative tests should be
ordered on a selective basis based on patient history, exam, and surgical risk factors (2).
– Important clinical factors that may make preoperative EKG evaluation useful include
cardiovascular diseases (CAD, CHF, significant valvular disease), respiratory diseases
(COPD, OSA, lung cancer), or highly invasive procedures.
– While age >65 years old is an independent predictor for significant preoperative EKG
abnormalities, there was no consensus minimum age for asymptomatic patients
undergoing low-risk procedures, or in low-risk patients.
• Preoperative EKG may be useful in risk-stratification in intermediate-risk and high-risk
surgical patients for predicting cardiovascular death. An abnormal EKG in patients with
documented CAD or at high risk for CAD and undergoing major noncardiac surgery was
shown to predict long-term outcome.
ABDOMINAL AORTIC ANEURYSM
Adam M. Thaler, DO
BASICS
DESCRIPTION
• The normal aortic diameter is approximately 20 mm (2 cm). The aorta is considered
widened, dilated, or aneurismal when it increases to 1.5 times the normal diameter.
• Patients may present perioperatively for aneurismal repair as well as for nonvascular
surgeries with a known (or unknown) diagnosis of an abdominal aortic aneurysm.
EPIDEMIOLOGY
Incidence
• 12–19% of patients with an AAA have a first-degree relative with a history of AAA.
• Total incidence in the adult population: 2–4%
Prevalence
• Approximately 90% of AAAs that are found incidentally on screening are <3.5 cm.
• Most common age 65–75 years
• Male:female 7:1
• Infrarenal aneurysms comprise ∼90% of AAAs.
Mortality
• Mortality: Ruptured AAA is the 13th leading cause of death in the US, causing an estimated
15,000 deaths per year.
• AAA rupture is usually fatal (70–80%) and only 50% present to the hospital alive.
ETIOLOGY/RISK FACTORS
• Chronic smokers (4 times more likely than nonsmokers) (1)
• Male gender
• Atherosclerosis
• Hypertension
• Marfan syndrome, Ehlers–Danlos syndrome, syphilis, trauma, mycotic infection (rare causes)
PATHOPHYSIOLOGY
• The extracellular matrix is comprised of elastin and collagen, which provides tensile
strength. Tensile strength is defined as the maximum stress that a material can withstand
while being stretched or pulled before being deformed or broken. Thus, they provide a
necessary function to the aorta—to endure the pulsatile, high pressures of blood being
ejected from the left ventricle.
• The pathogenesis of aneurysms involves alterations in the connective tissue of the aortic
wall. It has been proposed that adventitia elastin degradation is a primary, and hallmark,
event that leads to AAA formation; collagen disruption is the ultimate cause of rupture.
• Inflammation is believed to play a role with macrophages and T lymphocytes capable of:
– Producing proteolytic enzymes that can cause protein degradation
– Causing smooth muscle apoptosis
– Releasing pro-inflammatory cytokines
• Degradation that results in weakening of the aortic wall and aneurysmal development can
result from a number of different causes:
– Arteriosclerosis most commonly affects the abdominal aorta (compared to the thoracic). It
is also more likely to result in aneurysm (compared to stenosis in the infrarenals).
– Infection
• Laplace’s law states that T = (R × ΔP)/H, where T is tension, R is radius, ΔP is change in
pressure, and H is wall thickness. Thus, vessel diameter widening, increased arterial
pressures, and decreased wall thickness result in increased tension; the increased tension
can serve to further exacerbate the size of the aneurysm.
• Morphology: A fusiform aneurysm has a fairly uniform shape, with symmetrical dilation that
involves the full circumference of the aortic wall. Saccular aneurysms have a localized
dilation that appears as an outpouching of only a portion of the aortic wall. A
pseudoaneurysm is not an aneurysm, but instead, is a well-defined collection of blood and
connective tissue outside the vessel wall.
ANESTHETIC GOALS/GUIDING PRINCIPLES
• Patients with a diagnosis of AAA often have comorbid cardiovascular conditions such as
cerebrovascular, coronary, or renal disease.
• Both the size and rate of growth of aneurysm are important when determining the need for
intervention.
PREOPERATIVE ASSESSMENT
SYMPTOMS
• Usually asymptomatic
• Expanding AAA may present with abdominal or back pain (due to pressure on surrounding
tissues) or pain in the legs (due to disturbed blood flow).
• Ruptured AAA: Classic triad (hypotension, back pain, pulsatile abdominal mass) presents in
only 1/2 of patients.
History
• How and when the AAA diagnosed; any change in size, current plan of treatment
• Risk factors
• Comorbid conditions; patients are considered “vasculopaths” and disease in other vessels
should be considered until proven otherwise.
Signs/Physical Exam
Presence of an abdominal bruit or lateral propagation of the aortic pulse wave offers subtle
clues and may be more frequently found than a pulsatile mass.
MEDICATIONS
• No medical therapy has been found to be effective at decreasing the growth rate or rupture
rate of asymptomatic AAAs. There may be some protective effects with ACE inhibitors, beta-
blockers, and statins.
– Beta-blockers can reduce cardiac morbidity and mortality and should be continued
perioperatively. HR control and decreased contractility result in less systolic pressure
generated against the aneurysm wall.
– Statins’ pleiotropic effects have been shown to decrease postoperative cardiac, cerebral,
and renal morbidity in patients undergoing major vascular surgery; should be continued
perioperatively.
DIAGNOSTIC TESTS & INTERPRETATION
Labs/Studies
• Electrolytes, CBC, BUN/CR, PT/PTT
• 12-lead EKG
• Echocardiography, stress testing, and coronary angiography may be indicated to evaluate
the myocardium.
• Carotid ultrasound if bruits are present, especially if history of stroke or TIA.
• Ultrasound report should be reviewed even in patients presenting for nonvascular surgery.
• CT scan with contrast or MRA is typically performed when patients present for repair;
provides information on the position, diameter, and involvement of the mesenteric vessels.
• Type and crossed units for open AAA repair
CONCOMITANT ORGAN DYSFUNCTION
• Aortic disease is indicative of other atherosclerotic diseases including coronary, cerebral,
peripheral vascular, and renal diseases.
• Chronic obstructive pulmonary disease
• Diabetes mellitus
CIRCUMSTANCES TO DELAY/ CONDITIONS
• In patients presenting for nonvascular surgery, symptomatic and large aneurysms (i.e., >5.5
cm in diameter) as well as growth >1 cm/year should be considered for endovascular or
surgical repair.
• Acute coronary or cerebral event
CLASSIFICATIONS
• There are many classification systems in determining the risk of AAA rupture which take
into account the rate of increase, size, comorbid factors, etc (2).
• Biggest predictors of risk of rupture (annually) are diameter of the aneurysm and rate of
expansion.
– <4.0 cm in diameter = <0.5%
– 4.0–4.9 cm in diameter = 0.5–5%
– 5.0–5.9 cm in diameter = 3–15%
– 6.0–6.9 cm in diameter = 10–20%
– 7.0–7.9 cm in diameter = 20–40%
– >8.0 cm in diameter = 30–50%
TREATMENT
PREOPERATIVE PREPARATION
Premedications
• Anxiolytics as needed; anxiety may increase BP and the risk of AAA rupture.
• Beta-blockers may be titrated to heart rate goals, particularly if taking chronically.
• Perioperative statin therapy initiation may be indicated for their pleiotropic effects.
INTRAOPERATIVE CARE
Choice of Anesthesia
• Non vascular procedures: Based on the type of surgery, patient comorbidities, and physical
exam
• Open AAA repair: Neuraxial techniques may be appropriate; however, traumatic placement
may necessitate the delay of surgery (patients are heparizined intraoperatively).
Monitors
• Standard ASA monitors
• Non vascular procedures: Additional monitoring depends on the surgery and patient
comorbidities.
• Open AAA repair:
– 2 large-bore peripheral IVs or a central introducer sheath for possible rapid fluid and
blood administration
– Arterial line to assess rapid hemodynamic changes and the potential for hypotension and
MI; may be placed pre-induction.
– Pulmonary artery catheter may be indicated when pulmonary vascular resistance, cardiac
output, and mixed venous oxygen saturation can help guide therapy.
– TEE may be indicated to evaluate myocardial function and detect regional wall motion
abnormalities.
Induction/Airway Management
• A slow, controlled induction is necessary to ensure an adequate depth of anesthesia and
minimize hemodynamic changes. Hypotension can impair perfusion, while hypertension can
result in aneurysmal rupture (transluminal pressures, coughing, bucking, etc.).
• Short-acting agents, such as esmolol and nitroglycerin, may be necessary to blunt the
patient’s response to tracheal intubation and the subsequent increased tension against the
aneurysmal wall that could result in rupture.
Maintenance
• Maintenance agents (non vascular and AAA repairs): Balanced volatile or intravenous
techniques may be utilized.
• Hemodynamics (non vascular and AAA repairs): Close titration of intravenous and
inhalation agents with an emphasis on reducing tension against the aneurysmal wall.
Maintaining HR and MAP within 20% of baseline is generally appropriate (3).
– Short-acting drugs permit a rapid termination of effect, if desired, and allow for enhanced
titration.
– Opioids, beta-blockers, and vasodilating drugs can be used to control pain and BP. Esmolol
has ultra-short action and organ-independent elimination making it particularly useful.
• Aggressive fluid replacement may cause dilutional and hypothermic coagulopathy. This can
result in secondary clot disruption from increased blood flow, increased perfusion pressure,
and decreased blood viscosity thereby exacerbating bleeding.
Extubation/Emergence
• Standard extubation criteria; special attention to blood loss, hemodynamics, and
normothermia. Consider postoperative intubation in complicated AAA repairs or with
significant comorbidities.
• Smooth extubation (avoid coughing and bucking)
• Control of hypertension and tachycardia is important; consider beta-blockers and/or
vasodilators.
POSTOPERATIVE CARE
BED ACUITY
• Non vascular repair: Depends on surgery, comorbidities, intraoperative course
• AAA repair: ICU or monitored setting, given the high risk of cardiac complications. (MI
occurs more frequently postoperatively than intraoperatively). The postoperative period is
marked by increased myocardial oxygen demand, increased catecholamine levels, hypoxia,
hypercoagulability, and large fluid shifts. Consider supplemental oxygen (nasal cannula,
face mask), incentive spirometry and deep breathing, and early mobilization.
COMPLICATIONS
In AAA procedures, cardiac complications, such as myocardial ischemia or infarction are most
commonly seen. Additionally, hemorrhage or coagulopathy, peripheral embolization, and
aortocaval or aortoduodenal fistula can occur.
REFERENCES
1. Hatch C. Abdominal aortic aneurysm repair. In: Manual of anesthesia practice.
Charlottesville, VA: Unbound Medicine, 2011.
2. Leonard A, Thompson J. Anaesthesia for ruptured abdominal aortic aneurysm. Contin Educ
Anaesth Crit Care Pain. 2008;8(1):11–15.
3. CDC Aortic Aneurysm Factsheet. Available at:
http://www.cdc.gov/dhdsp/data_statistics/fact_sheets/docs/fs_aortic_aneurysm.pdf
ADDITIONAL READING
• Abdominal aortic aneurysm on UpToDate
• http://emedicine.medscape.com/article/463354-overview
• Thoracic aneurysm
• Endovascular aneurysm repair
• Abdominal aortic aneurysm, infrarenal
• Abdominal aortic aneurysm, supraceliac
CODES
ICD9
441.4 Abdominal aneurysm without mention of rupture
ICD10
I71.4 Abdominal aortic aneurysm, without rupture
CLINICAL PEARLS
• Preoperative preparation should involve a careful assessment of the disease and
comorbidities.
• The US Preventive Services Task Force recommends screening for AAA using ultrasound
imaging one-time for men aged 65–75 years who have ever smoked, even if they have no
symptoms. Men aged ≥60 years with a family history of AAA may also be tested.
ABDOMINAL AORTIC ANEURYSM RUPTURE
John W. Hoffman, Jr., DO, MS
Shawn T. Beaman, MD
BASICS
DESCRIPTION
• The abdomen is the most common site for an aortic aneurysm.
– Abdominal aortic aneurysms (AAA) are most commonly located between the inferior
mesenteric and renal arteries.
– Approximately two-thirds of all AAAs extend into the iliac arteries
• Ruptured AAA (rAAA) is a surgical emergency.
EPIDEMIOLOGY
Incidence
• AAA is present in 5–10% of patients >65 years old (1)[C].
• Estimated to occur in 7.7 to 26.8 per 100,000 person-years in recent large European study
(remarkable variation was noted across countries).
Morbidity
• Respiratory insufficiency (5–10%)
• Myocardial infarction (10–15%)
• Renal insufficiency (2–5%)
• GI complications (3–4%)
• Lower extremity ischemia (2–5%)
Mortality
• rAAA is the 13th leading cause of death in the US, with up to 15,000 deaths annually.
• 30–50% of patients with a rAAA do not survive transport to a hospital.
• Operative mortality after rupture ∼ 50%
• Risk factors associated with AAA rupture (6)[C]:
– Anteroposterior aneurysm diameter >5 cm
– Elevated diastolic pressure
– Obstructive pulmonary disease
• Causes of AAA:
– Atherosclerosis (most common) (2–5)[C]
– Connective tissue diseases (e.g., Marfan syndrome, Ehlers–Danlos syndrome, and cystic
medial necrosis) (2)[C]
– Infectious etiologies are uncommon (e.g., syphilis, salmonellosis, brucellosis, tuberculosis)
(2)[C].
• Risk factors associated with presence of AAA:
– Smoking: Duration (years) of tobacco exposure is more important than absolute number of
cigarettes (2)[C].
– Age >65 years old
– Male gender: Incidence is 4 times higher in men; women have delayed development of
AAA by ∼10 years compared with men.
– Hypertension
– Presence of peripheral arterial aneurysms (e.g., popliteal or femoral arterial aneurysm)
– Family history of AAA (first-degree relative)
– Decreased serum high-density lipoprotein
– Caucasian ethnicity
PATHOPHYSIOLOGY
• Collagen and elastin fibers provide most of the tensile strength of the aortic wall. An
imbalance between aortic wall matrix metalloproteinases and their inhibitors, chronic
inflammatory infiltrates, smooth muscle apoptosis, and increased production of pro-
inflammatory cytokines contribute to aneurysm formation.
• The average rate of growth of a AAA is 0.4 cm/year
• Risk of rupture is proportional to wall stress/tension, which increases as the AAA expands
(Laplace’s law).
• Intravascular volume replacement
• Inotropic support of cardiac output
• Maintenance of adequate tissue oxygenation
• Immediate surgical control of rupture
SYMPTOMS
Back, chest, or abdominal pain
History
• Comorbidities are common.
– Atherosclerosis associated with coronary artery disease, stroke, peripheral vascular
disease, and renal insufficiency
– Smoking associated with obstructive pulmonary disease
• Presence of connective tissue disease
• Medical optimization is not feasible due to the emergent nature of the surgery.
Signs/Physical Exam
• Pulsatile abdominal mass
• Hypotension
TREATMENT HISTORY
Pre-existing vascular grafts or repairs
MEDICATIONS
• Vasodilators (nitroglycerin and/or nitroprusside)
• Short acting beta blockers (e.g. esmolol) are utilized to decrease the heart rate.
Labs/Studies
• Baseline and serial cardiac biomarkers, BUN/Cr, CBC with platelets, coagulation profile, and
TEG if available
• ECG may be normal or show nonspecific ST segment or T wave changes, left ventricular
hypertrophy, ischemia, or infarction.
• Chest radiograph may suggest concomitant pulmonary disease.
• CT angiography is quick, highly sensitive, and specific; 64-slice multidetector CT with
cardiac gating may allow for simultaneous evaluation of pulmonary and coronary arteries.
• TEE allows rapid evaluation of cardiac function, volume status, and valvular integrity.
• MRI/MRA has high sensitivity and specificity, avoids radiation, and iodinated contrast; but
is more time-consuming and contraindicated with metallic implants.
• Cardiovascular: Coronary artery disease (30–40%), hypertension, peripheral vascular disease
• Neurologic: Cerebrovascular disease
• Pulmonary: Chronic obstructive pulmonary disease (COPD), smoking history
• Renal: Chronic renal insufficiency
• Endocrine: Diabetes mellitus
None; rAAA has a mortality that exceeds 80% if not repaired.
CLASSIFICATIONS
• Anterior intraperitoneal rupture (20%): Rapid bleeding into the peritoneal cavity usually
results in exsanguination and death before the patient arrives at the hospital (1)[C].
• Retroperitoneal rupture (80%): Tamponade effect limits internal hemorrhage. Associated
with a lower mortality rate (1)[C].
TREATMENT
Premedications
• Analgesia: Small incremental doses of opioids
• Sedation: Avoid in hemodynamically unstable patients
• Bronchodilators: Symptomatic patients with COPD
• Antihypertensive/anti-anginal: Continued until time of surgery if hemodynamically stable
• Blood products: pRBCs, platelets, FFP, cryoprecipitate
Special Concerns for Informed Consent
• May not be possible in emergency
• Blood consent
INTRAOPERATIVE CARE
• General endotracheal anesthesia
• Continuous epidural anesthesia may be considered if rupture is contained and coagulation
status is normal. However, placement should not occur in hemodynamically unstable
patients or if it will delay surgery.
Monitors
• ECG with ST-segment analysis
• Arterial line: Pre-induction placement in radial artery is commonly performed. Femoral
artery insertion may permit monitoring of distal perfusion pressures.
• Central venous access is appropriate for monitoring pressures and administration of
vasoactive medications.
• TEE facilitates continuous evaluation of intravascular volume, valvular integrity, and
ventricular function.
• Pulmonary artery catheterization provides SvO2, SVR, CO, PAP.
• Temperature (central and peripheral sites if bypass is to be used)
• Foley catheter
• Cell salvage, rapid infuser
• Slow, controlled titration of induction medications: In patients at risk for pulmonary
aspiration, the decision to proceed with an RSI should be balanced against the potential for
hypertension.
– Control of hypertensive response to laryngoscopy and intubation can be accomplished
with moderate-dose narcotics.
– Avoid hypotension which may contribute to cardiac ischemia and further deterioration of
peripheral perfusion.
• Single-lumen endotracheal tube is sufficient for surgery contained to the abdominal cavity.
Lung isolation with a double-lumen tube or bronchial blocker is preferred for procedures
extending into the thorax.
• Positive pressure ventilation may decrease venous return and further decrease cardiac
output and peripheral perfusion.
Maintenance
• Position: Supine with transperitoneal approach; the lateral decubitus position and
retroperitoneal approach may be preferred in certain situations.
• Thermoregulation: Forced air and fluid warming systems are necessary due to significant
heat loss with open procedures.
• Fluid management: Maintenance of intravascular volume may be challenging due to
significant hemorrhage and evaporative losses; no specific colloid or crystalloid strategy has
emerged as superior.
• Coagulation: Consumption and dilution of coagulation factors and platelets may be
significant; replacement is guided by conventional coagulation studies as well as TEG, if
available.
• Renal protection: Maintenance of renal blood flow and urine output is essential. IV sodium
bicarbonate, mannitol, and fenoldapam may decrease the risk of kidney injury (mannitol
and fenoldapam should not be used in hemodynamically unstable patients).
• Placement of aortic cross-clamp
– Increase in left ventricle (LV) afterload and potential for cardiac collapse. Acute increases
in systemic vascular resistance (SVR) can be mitigated with vasodilators (nitroprusside,
nitroglycerin, calcium channel blockers, propofol).
– Decrease in venous return: Gentle administration of IV fluids may augment preload.
– Suprarenal clamping decreases renal perfusion. Consider administration of mannitol
(0.25–0.5 g/kg) prior to clamping.
• Removal of aortic cross-clamp
– Release of vasoactive metabolites into the central circulation can lead to hypotension and
cardiac arrhythmias.
– Decreases in the SVR are mitigated with IV fluids and vasopressors (phenylephrine or
epinephrine). Profound, unresponsive hypotension can be temporarily treated with re-
instigation of the aortic clamp.
• Ongoing cardiac or pulmonary instability, bleeding, hypothermia, or neurologic injury may
necessitate continued mechanical ventilation; otherwise patients may be extubated at the
conclusion of the procedure.
• Pain, hypertension, and tachycardia should be anticipated and addressed.
POSTOPERATIVE CARE
BED ACUITY
• Intensive care unit
• Monitoring of BP, HR, and LV function
• Analgesia with intravascular or neuraxial opioids
• Continued assessment of graft patency and peripheral perfusion
COMPLICATIONS
• Hemorrhage
• Coagulopathy
• Myocardial ischemia/infarction
• Renal failure
• Incision and/or graft infection
• Spinal cord ischemia, paralysis
• Impotence
• Bowel ischemia
• Embolism
• Lower extremity ischemia
• Pneumonia, respiratory insufficiency
• Hypothermia
REFERENCES
1. Assar A, Zairians C. Ruptured abdominal aortic aneurysm: A surgical emergency with many
clinical presentations. Postgrad Med J. 2009;85:268–273.
2. rattheim BJ, Elkemo TA, Altreuther M, et al. Regional disparities in incidence, handling
and outcome of patients with symptomatic ruptured abdominal aortic aneurysms in
Norway. Eur J Endovasc Surg. 2012.
3. ozniak F, LaMuraglia GM, Musch G, et al. Anesthesia for open abdominal surgery. Int
Anesth Clin. 2005;43(1):61–78.
4. Thompson R, Geaghty P, Lee J. Abdominal aortic aneurysms: Basic mechanisms and
clinical implications. Curr Probl Surg. 2002;39:110–130.
5. Adam van der Vliet J, Boll A. Abdominal aortic aneurysms. Lancet. 1997;349:863–866.
6. Bernstein E, Chan E. Abdominal aortic aneurysm in high risk patients: Outcome of selective
management based on size and expansion rate. Ann Surg. 1984;200(3):255–263.
7. Falk J, Rackow EC, Blumenberg R, et al. Hemodynamic and metabolic effects of abdominal
aortic cross-clamping. Am J Surg. 1981;142:174–177.
8. Subramaniam B, Singh N, Roscher C, et al. Innovations in treating aortic diseases: The
abdominal aorta. J Cardiothorac Vasc Anesth. 2011 (article in press).
9. Gelman S. The pathophysiology of aortic cross clamping and unclamping. Anesthesiology.
1995;82(4):1026–1060.
• Abdominal aortic aneurysm
• Abdominal aortic aneurysm dissection
CODES
ICD9
441.3 Abdominal aneurysm, ruptured
ICD10
I71.3 Abdominal aortic aneurysm, ruptured
CLINICAL PEARLS
• rAAA is a surgical emergency. Mortality exceeds 80% without intervention; with repair it
can decrease to ~50%.
• Patients often present with significant cardiac, cerebral, and/or renal vascular disease.
• Application of the aortic cross-clamp leads to an abrupt increase in afterload and may
precipitate cardiac collapse.
• Removal of the aortic cross-clamp causes a decrease in SVR and release of vasoactive
metabolites into the central circulation.
ABDOMINOPERINEAL RESECTION (APR)
Vijaya Gottumukkala, MB, BS, MD, FRCA
BASICS
DESCRIPTION
General
• Ernest Miles (1869–1947) devised the approach in the 1930s as a curative procedure for all
rectal cancers. It involves resection of the anus, rectum, and a portion of the sigmoid colon,
as well as a wide perineal and lymph node dissection.
• Abdominoperineal resection (APR) is now reserved for conditions where the rectum needs to
be removed and there is involvement of the primary sphincter complex or tumors in the
lower third of the rectum that do not have adequate clearance for sphincter preservation. It
requires a permanent colostomy.
• Laparoscopy-assisted APR and low anterior resection (LAR) are more commonly performed
today. LAR is a modified technique that allows for sphincter preservation.
Position
• Modified lithotomy
• Trendelenburg, as needed
Incision
Midline abdominal and perineal
Approximate Time
5–10 hours
EBL Expected
500–1,500 mL
Hospital Stay
7–10 days
Special Equipment for Surgery
• 2 table set-up (abdominal and pelvic sets)
• Long pelvic instruments, stapling devices
• Cystoscopy set with ureteric stents
EPIDEMIOLOGY
Incidence
• Colorectal cancer is the 4th most common cancer and the second leading cause (10%) of all
cancer-related deaths.
• From 2003 to 2007, the median age at diagnosis for colorectal cancer was 70 years of age.
At diagnosis, about 20% had distant metastasis.
• 5–10% of all colorectal cancers are associated with a familial colorectal cancer syndrome,
and an additional 15–20% are associated with a familial disposition.
• Risk for colorectal cancer increases with age (90% of cases occur in patients >50 years),
and with a diet rich in red meat and animal fat.
• Aspirin, NSAIDs, and COX-2 inhibitors have been reported to have protective effects against
colorectal cancer.
Prevalence
• As of January 1, 2007, in the US there were approximately 1,112,493 men and women alive
with a history of colon and/or rectal cancer.
• Based on rates from 2005 to 2007, 5.12% of men and women born today will be diagnosed
with cancer of the colon and/or rectum during their lifetime.
• High incidence of local recurrence despite margin-free resection
Mortality
• The overall 5-year relative survival in the US for 1999–2006 was 65.0%; for high-risk
patients it is 20%.
• Hormone replacement therapy has been shown to significantly reduce mortality in women
with colorectal cancer.
• Patient population with sequelae related to the primary pathology and significant medical
comorbidities (age, smoking, diabetes, hypertension, atherosclerosis, coronary artery
disease, malnutrition). Optimize preoperative comorbid burden for optimal postoperative
recovery.
• Maintenance of tissue oxygenation, perfusion, and euvolemia. Patients are often placed on a
clear liquid diet 1–3 days prior to surgery, combined with bowel prep (laxative, enemas,
whole gut irrigation with saline via a nasogastric tube, polyethylene glycol electrolyte
lavage, or mannitol solution).
• Effective analgesia (epidural preferred for open procedures)
• Extubation at the end of surgery
• Postoperative monitoring in a high-dependency unit for 48 hours
SYMPTOMS
• Symptomatic, depending on the size and location of the tumor
• Change in bowel habits and pencil stools
• Rectal or lower abdominal pain, spotting of blood in stool, lower GI bleeding, hematochezia,
and tenesmus
• May be acutely or chronically ill depending on the primary pathology (Crohns disease,
ulcerative colitis)
History
• Inflammatory bowel diseases (Crohns disease, ulcerative colitis), inherited colon cancers
(familial adenomatous polyposis, Gardner syndrome, Peutz–Jeghers syndrome, juvenile
polyposis, and hereditary non-polyposis colon cancer)
• Careful assessment of the sequelae and complications of the primary colonic/rectal
pathology, medical comorbidities, nutritional and functional status
Signs/Physical Exam
• Systemic signs of inflammatory bowel disease (IBD)
• Anemia, weight loss, fever of unknown origin
• Abdominal wall and/or internal colonic fistulae
• Palpable mass in the recto-sigmoid on examination
MEDICATIONS
• Therapy for IBD: Antidiarrheals, aminosalicylates (5-ASA), corticosteroids,
immunomodulators (azathioprine and 6-mercaptopurine, cyclosporine), antibiotics, and
pain medications
• Patient may have recently completed adjuvant chemoradiation prior to surgery and/or
planned for after surgery.
• Chemotherapy for colorectal cancer is 5-FU and leucovorin based. Irinotecan or oxaliplatin
is added in metastatic disease.
• Medications for the comorbidities (antihyperglycemics, antihypertensives, anticholesterol
medications, aspirin, etc.)
Labs/Studies
• CBC, PT/PTT, creatinine, prealbumin, and LFTs
• Electrolytes if on diuretics, ACE I, renal insufficiency
• Colonoscopic evaluation (location, size, and number of masses)
• CT scan (tumor location, size, perirectal and vascular involvement, peritoneal and liver
metastasis)
• Other tests (TEG, ECG, CXR, cardiac echocardiogram, exercise stress test, PFTs) as indicated
• Anemia from bleeding or occult blood loss
• Metastasis: Abdominal pain (hepatomegaly) and liver dysfunction from hepatic metastasis;
skeletal pain from bony metastasis; ascites from peritoneal dissemination; bladder
dysfunction, sacral or sciatic neuropathy, and vaginal discharge and bleeding from pelvic
metastasis
• Obesity/malnutrition
• Inflammatory bowel disease and its associated sequelae
• Age-related morbidities: Diabetes, hypertension, coronary artery disease
TREATMENT
Premedications
• Anxiolytic and analgesic medications, as needed
• Gastric volume reducing and acid-neutralizing medications, if indicated
• Continue appropriate medications (antibiotics, anti-inflammatory/immunomodulators,
antihypertensives, antiarrhythmics, and others) as needed
• There is an increasing trend to use alvimopan to hasten recovery of bowel function.
• Blood consent for possible transfusion
• Consent for epidural catheter for postoperative analgesia
• Potential for postoperative intubation and intensive care
Antibiotics/Common Organisms
• Prophylactic cefotetan or cefoxitin; metronidazole plus an aminoglycoside may be used for
cephalosporin allergy.
• Gram-negative aerobes and anaerobic bacteria
• Mechanical bowel preparation decreases fecal bulk, but does not decrease the concentration
of bacteria in the stool.
INTRAOPERATIVE CARE
• General anesthesia with ETT
• Epidural catheter for postoperative analgesia: Need to rule out contraindications, review
medication list (herbals, clopidogrel, low-molecular-weight heparin, or other drugs that
alter coagulation), consider preoperative PT/PTT/INR or other advanced coagulation tests
as needed (TEG, PFA). Not contraindicated with usual thromboprophylaxis for postoperative
DVT (heparin 5,000 U SQ BID).
Monitors
• ASA standard monitors
• Arterial line (beat-to-beat blood pressure monitoring, systolic pressure variation [SPV] to
evaluate intravascular volume status, blood draws for lab work); consider placing the
arterial line pre-induction for high-risk patients.
• 2 large-bore IVs for volume resuscitation if needed. Central line access is not usually
necessary unless there is poor IV access or a need for postoperative TPN.
• Foley catheter: Ureteric stents are placed preoperatively to identify ureters during the
resection.
Standard induction technique and strategies to maintain hemodynamic stability and full
stomach precautions if indicated
Maintenance
• Avoid nitrous oxide. Air–oxygen mixture with an FiO2 of 0.5 will help identify oxygenation
issues early.
• Continuous epidural infusion of local anesthetic/narcotic mixture may be used for analgesia
throughout the procedure.
• Nasogastric tube placement may be requested.
• Volume: APR is a major procedure with complex bowel resection; bleeding may be
encountered from the presacral venous plexus. Additionally, insensible fluid losses can
result. Intravascular volume status and maintenance of organ perfusion should be closely
monitored.
• Surgeon may request intraoperative indigo carmine to rule out injury to the ureters; it may
temporarily result in a decrease in the pulse oximeter reading.
• Blood glucose, serum electrolytes, ABG, ACT and other coagulation parameters as may be
checked needed.
• Standard extubation criteria
• Post-extubation sensory–motor exam and evaluation of epidural puncture site for
effectiveness and complications
POSTOPERATIVE CARE
BED ACUITY
• High-dependency unit or ICU for 48 hours
• May need monitoring of invasive hemodynamic parameters to guide fluid volume/blood
product transfusion
ANALGESIA
• Epidural: Follow ASRA guidelines for maintenance and removal of epidural catheters
• Multimodal approach involving IV PCA if epidural contraindicated or laparoscopic
procedure
COMPLICATIONS
• Intra-abdominal abscess, wound infections (10%), anastomotic leaks (15%)
• Postoperative ileus
• Injury to the ureters, hypogastric or parasacral nerve plexus
• Postoperative fever and leukocytosis are not uncommon.
• Adverse cardiac events (hypotension, hypertension, arrhythmias, ischemia, infarct, and CHF)
• Postoperative delirium in elderly
• Postoperative neuropathies from positioning
• Epidural site infection or hematoma (very rare)
PROGNOSIS
• Overall local recurrence is 30% after a margin-free resection.
• The best prognosis in patients with locally advanced rectal cancer appears to be after
preoperative chemoradiation, maximal surgical resection (margin free), and localized
intraoperative radiation therapy (IORT) in selected cases.
REFERENCES
1. Ferg BW, Berger DH, Fuhrman GM. Cancer of the colon, rectum and anus. In: Chang G,
Feig BW. The M.D. Anderson surgical oncology handbook, 4th ed. Philadelphia, PA:
Lippincott Williams & Wilkins, 2006:261.
2. Lindholm ML, Träff S, Granath F, et al. Mortality within 2 years after surgery in relation to
low intraoperative bispectral index values and preexisting malignant disease. Anesthes
Analges. 2009;108(2):508–512.
3. Green D, Paklet L. Latest developments in the peri-operative monitoring of the high risk
surgical patient. Int J Surg. 2010;8(2):90–99.
4. Kimberger O, Arnberger M, Brandt S, et al. Goal-directed colloid administration improves
the microcirculation of healthy and perianastomotic colon. Anesthesiology.
2009;110(3):496–504.
ADDITIONAL READING
• Cancer Facts and Figures 2010. Atlanta, GA: American Cancer Society, 2010.
• Surveillance, Epidemiology and End Results (SEER) Program of the National Cancer Institute
• Insensible fluid losses
• International normalized ratio
• Partial thromboplastin time
• Prothrombin time
CLINICAL PEARLS
• Major bowel resection surgery can require significant blood products and fluid resuscitation
in the perioperative period.
• There exists a risk for positioning and surgery-related neuropathies.
• Patients are prone to the occurrence of late DVTs.
ACE INHIBITORS AND HYPOTENSION
John B. Carter, MD
BASICS
DESCRIPTION
• Significant hypotension has been reported after the induction of general anesthesia in
patients on angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor
blockers (ARBs).
• At this time, guidelines have not been established regarding preoperative management
(withdrawal or continuation) of ACEI or ARBs. Large randomized controlled studies are
lacking and most information stems from retrospective studies:
– Elective, noncardiac surgical patients who have taken ACEI or ARBs on the morning of
surgery appear to have an increased risk of moderate hypotension (systolic blood pressure
[SBP] <85 mm Hg) (1) and vasopressor requirement (2).
– Vascular surgical patients who have taken ACEI or ARBs on the morning of surgery appear
to have an increased incidence of hypotension and level of severity (3).
– Cardiac surgical patients who withhold ACE inhibitors before surgery appear to maintain a
greater MAP and require less vasopressors while on bypass. Additionally, they may
require more vasodilator therapy post-bypass and do not incur hypotension at the time of
anesthesia induction (4).
EPIDEMIOLOGY
Incidence
• ACEI/ARBs are frequently prescribed for antihypertensive therapy with particular
advantages in:
– Renal protection in diabetes mellitus (DM) and hypertension (HTN)
– Prevention of cardiac remodeling after myocardial infarction (MI)
• Lower risk of cerebrovascular accident (CVA) and MI (4)
Prevalence
Approximately 50 million individuals in the US (and 1 billion worldwide) have HTN.
Morbidity
In addition to causing hypotension, ACEI/ARBs can also cause renal impairment and
hyperkalemia. They are contraindicated in renal artery stenosis and should be used with
caution in hypovolemia.
Concurrent use of diuretics with ACEI/ARBs has been associated with a higher risk of
hypotension during anesthesia (2).
PHYSIOLOGY/PATHOPHYSIOLOGY
• The physiology of the renin-angiotensin-aldosterone system (RAAS) plays an essential role in
the short-term regulation of blood pressure and long-term regulation of intravascular
volume.
– Angiotensinogen is an inactive glycoprotein produced in the liver.
– Renin is secreted by the kidneys into the bloodstream when pressure receptors sense low
blood volume. Renin is highly specific in cleaving angiotensinogen to angiotensin I.
– Angiotensin converting enzyme (ACE) is a nonspecific enzyme in the vascular
endothelium which converts angiotensin I to angiotensin II. ACE also inactivates
bradykinin, a potent vasodilator.
– Angiotensin II can cause immediate vasoconstriction of arterial and venous vessels, with a
resultant increase in the systemic vascular resistance (SVR) and venous return. It
constricts renal efferent arterioles during moderate decreases in perfusion pressure in
order to preserve the glomerular filtration rate (GFR). Small amounts are also produced
independently of ACE.
– Aldosterone is produced by the adrenal glands in response to angiotensin II and
hyperkalemia. It plays a role in sodium retention and increasing the blood volume; it has
a slower response and longer duration (5).
• Blood pressure regulation is also maintained by other systems.
– The sympathetic nervous system maintains vascular tone, heart rate, and contractility;
however, induction of anesthesia results in a reduction of sympathetic tone in both the
arterial and venous vessels. This results in a lower SVR as well as decreases in effective
blood volume and preload.
– Vasopressin (antidiuretic hormone) is an important compensatory mechanism in
hypovolemia.
• Refractory hypotension: ACEI and ARBs impair the RAAS; general anesthesia impairs the
sympathetic nervous system. Thus, the combination leaves the vasopressin system as the
main mechanism of maintaining blood pressure.
• Other:
– Genetics may influence which patients are susceptible to hypotension following induction.
– Neuraxial blocks: Whether ACEI or ARBs cause refractory hypotension in patients
receiving an epidural or spinal is unclear.
PREVENTATIVE MEASURES
• Patients may be asked to withhold their ACEI/ARB on the day of surgery.
• If they are not withheld, cancellation of surgery is not necessarily warranted. Consider
volume administration, the use of an induction agent other than propofol (or lower doses),
and having vasopressors including vasopressin available.
DIAGNOSIS
Despite intraoperative hypotension being an independent predictor of mortality in the first
year after surgery (12), no standard definition exists.
• A common practical approach is to establish the patient’s baseline from several readings and
attempt to stay within 20% (6).
• However, the lowest “safe” blood pressure will vary with an individual’s comorbidities such
as aortic stenosis or cerebrovascular insufficiency.
• Adequate cerebral perfusion has been cited as a MAP >70 mm Hg (7), with higher MAPs
often necessary in chronic HTN. MAPs <70 mm Hg may be tolerated for a short time in
hypertensive patients. Cerebral ischemia resulting in stroke was not noted in these studies.
DIFFERENTIAL DIAGNOSIS
Hypotension, in general, may be seen in ∼9% of patients in the first 10 minutes following the
induction of anesthesia (8). The following predictors were found:
• ASA III-V
• Age >50
• Baseline MAP <70 mm Hg
• Use of propofol for induction
• Increased doses of fentanyl
• Chronic HTN
• Hypovolemia
TREATMENT
• Volume infusion
• Sympathomimetics such as ephedrine or phenylephrine as first-line treatment. One study
showed that doses of ephedrine and phenylephrine did not usually exceed 20–25 mg and
200 mcg, respectively (3).
• Vasopressin may be helpful in refractory cases. It is usually administered as an infusion for
vasodilatory shock; bolus therapy is off label. It may have a more sustained effect than other
pressors.
• Terlipressin, an AVP analog, may also be useful (9).
• Methylene blue has been reported in the treatment of refractory hypotension. The
mechanism of action is an in inhibition of cGMP in the endothelium.
REFERENCES
1. Comfere T, Spring J, Kumar M, et al. Angiotensin system inhibitors in a general surgical
population. Anesth Analg. 2005;100:636–644.
2. Pigott DW, Nagle C, Allman K, et al. Effect of omitting regular ACE inhibitor medication
before cardiac surgery on haemodynamic variables and vasoactive drug requirement. Br J
Anesth. 1999;83:715–720.
3. Bertrand M, Gilles G, Meersschaert K, et al. Should the angiotensin II antagonists be
discontinued before surgery. Anesth Analg. 2001;92:26–30.
4. White W. Angiotensin-converting enzyme inhibitors in the treatment of hypertension: An
update. J Clin Hypertens. 2007;9:876–882.
5. Colson P, Ryckwaert F, Coriat P. Renin angiotensin system antagonists and anesthesia.
Anesth Analg. 1999;89:1143–1155.
6. Howell SJ, Sear JW, Foex P. Hypertension, hypertensive heart disease, and perioperative
cardiac risk. Br J Anaesth. 2004;92:570–583.
7. Drummond JC. The lower limit of autoregulation: Time to revise our thinking?
Anesthesiology. 1997;86:1431–1433.
8. Reich D, Hossain S, Baez B, et al. Predictors of hypotension after induction of general
anesthesia. Anesth Analg. 2005;101:622–628.
9. Meersschaert K, Brun L, Gourdin M, et al. Terlipressin-ephedrine versus ephedrine to treat
hypotension at the induction of anesthesia in patients chronically treated with angiotensin
converting-enzyme inhibitors: A prospective, randomized, double-blinded, crossover study.
Anesth Analg. 2002;94:835–840.
10. Hohne C, Meier L, Boemke W, et al. ACE inhibition does not exaggerate the blood
pressure decrease in the early phase of spinal anaesthesia. Acta Anaesthesiol Scand.
2003;47:891–896.
11. heterpal S, Khodaparast O, Shanks A, et al. Chronic angiotensin-converting enzyme
inhibitor or angiotension receptor blocker therapy combined with diuretic therapy as
associated with increased episodes of hypotension in noncardiac surgery. J Cardiothoracic
Vasc Anesth. 2008;22:180–186.
12. Monk TG, Saini V, Weldon BC. Anesthetic management and one-year mortality after
noncardiac surgery. Anes Analg. 2005;100:4–10.
ADDITIONAL READING
• Augoustides J. Angiotensin blockade and general anesthesia: So little known, so far to go. J
Cardiothoracic Vasc Anesth. 2008;22:177–179.
• Smith I, Jackson I. Beta-blockers, calcium channel blockers, angiotensin receptor blockers:
Should they be stopped or not before ambulatory anaesthesia. Curr Opin Anesth.
2010;23:687–690.
• Angiotensin
• Hypotension
• Renin
CODES
ICD9
458.8 Other specified hypotension
ICD10
I95.2 Hypotension due to drugs
CLINICAL PEARLS
• Hypertensive patients often demonstrate very labile blood pressures. Excessive drops in MAP
cause concern for a possible increase in morbidity and possibly mortality.
• Following induction of anesthesia in association with use of ACEI/ARBs, there appears to be
an increased incidence of hypotension due to a reduction in vascular tone, especially on the
venous return. The angiotensin II system is unable to compensate for the hypotension;
therefore, these patients are more volume sensitive to maintain preload.
• Arguments against discontinuing ARBs and ACEI include: Neuroprotection, as well as
improved hemodynamic stability, decreased ischemia–reperfusion injury, and renal
protection.
ACLS ANESTHETIC MANAGEMENT
Mark E. Nunnally, MD, FCCM
BASICS
DESCRIPTION
• The American Heart Association’s Advanced Cardiac Life Support (ACLS) course is evidence-
based consensus products to assist practitioners with emergency scenarios, in particular
cardiac arrest. They are intentionally broad in scope (1).
• Algorithms treat distinguishable syndromes to specify care. These are often cardiac rhythm
based (e.g., asystole vs. ventricular tachycardia).
• ACLS guidelines, however, may not fit the most common arrest scenarios seen in the
operating room (OR).
– ACLS treats probabilities; these are not specific to the surgical setting.
– There is no provision in ACLS for a previously ventilated patient.
– Arrest in the OR is witnessed, usually evolves over minutes, and can be treated with a
broad range of resources.
EPIDEMIOLOGY
Incidence
• Data for arrest or near arrest in the OR are difficult to assess. Best estimates are 4.3–19.7
cardiac arrests per 10,000 anesthetics for adults (approximately 10% of these are directly
attributed to anesthesia) and 2.6–11 per 10,000 for children (much higher in infants) (2,4).
• Arrest during neuraxial anesthesia is estimated at 1.8 per 10,000 anesthetics and is more
common with spinal anesthesia than epidural anesthesia (4).
• Most available data on intraoperative cardiac arrest come from registries or closed-claims
databases. These are useful tools for studying rare events but cannot be trusted for accurate
incidence data.
Prevalence
• Arrest is an incident phenomenon, but there are many prevalent factors in the OR that
influence the risk and type of arrest.
– Intraoperative hypovolemia is common and an important cause of shock.
– Patient comorbidities contributing to arrest include cardiac and thromboembolic disease.
– Anesthetic agents are potent and their overdose accounts for the majority of arrests
attributable to anesthesia. Induction drugs and volatile anesthetic agents are potent
vasodilators and negative inotropes.
– Arrest at induction has declined while arrest during maintenance or emergence has
remained the same. Esophageal intubation and airway loss are less common since the use
of capnography and pulse oximetry became routine (8).
– Complications of intravascular access (e.g., hemorrhage, pneumothorax, tamponade) are
rare but serious causes.
• The frequency of arrhythmias under anesthesia is different. The most common arrhythmias
include (7):
– Bradycardia followed by asystole (45%)
– Unknown (33%)
– Ventricular tachycardia/ventricular fibrillation (14%)
– Pulse-less electrical activity (7%)
Morbidity
• Hypoxic neurologic injury is the salient morbidity of cardiac arrest. It is a prominent factor
in closed-claims data, associated with some of the highest payments.
• Pancreatitis, hepatic dysfunction, renal failure, and the multiple organ dysfunction
syndrome (MODS) can follow prolonged shock after cardiac arrest.
Mortality
• Estimated mortality from an intraoperative arrest ranges from 20% to 50%, compared with
84–97% for out-of-hospital cardiac arrest (US data) (5).
• In one large series from the Mayo Clinic, in-hospital mortality was 21% from arrests directly
attributable to anesthesia, versus 71% in those that were not. Other smaller series suggest
higher mortality in anesthesia-attributable arrest (up to 80%) (6).
• Factors associated with mortality include: ASA patient status, emergency surgery, diabetes
mellitus, end-stage organ failure, protracted hypotension or use of vasopressors prior to
arrest, invasive monitoring, and type of surgery (cardiac surgery worst).
• Unlike other patient populations, asystole is associated with good survival (80% in one
series), suggesting it is mediated by autonomic or drug effects, and is therefore reversible in
many cases.
• Mortality differences suggest that the combination of different etiologies, witnessed arrest,
and timely availability of advanced resuscitation techniques make intraoperative arrest
different from community arrest.
• Arrest in the OR is multifactorial.
• Ischemic heart disease and conduction abnormalities share etiologies with causes of arrest
outside the OR.
• Patient comorbidities are the most likely contributors to cardiac arrest, followed by surgical
and anesthetic factors.
• Anaesthetists cannot prepare for every emergency the same way. Training in arrest
management should target 4 specific cause groups:
– Events specific to anesthetic intervention (e.g., pneumothorax, high spinal)
– Reactions to specific agents (e.g., local anesthetic systemic toxicity, malignant
hyperthermia)
– Factors that occur more frequently, even though they do not always cause arrest, such as
hypovolemic shock and hypoxemia
– Relatively “common” rare causes (somewhere between 0.1 and 1 in 10,000 anesthetics)
• Some causes of arrest in the OR that result from direct intervention include:
– Hypoxemia
– Hemorrhage
– Vagal stimulation
– Emboli (e.g., venous air embolism)
– Over-ventilation/auto-PEEP
– Drug reactions (anaphylaxis, malignant hyperpyrexia)
• Since arrest data come from retrospective sources, only correlation can be ascertained.
Causation must be speculative.
– Preload (hemorrhage, capillary leak, hypovolemia)
– Afterload (vasoplegia, drug effect)
– Pump function (right heart, left heart, contractility, dysrhythmia)
– Impaired filling (tamponade, auto-PEEP, abdominal compartment syndrome)
• Retrospective evaluation of arrests suggests a correlation with preclinical signs.
– Hypotension
– Tachycardia
– Abrupt drops in end-tidal CO2 are particularly ominous.
• MOST of what anaesthetists do involves avoiding arrest scenarios. Skilled anaesthetists
proactively avoid disaster before signs of deterioration become apparent.
• The time between a problem becoming detectable and arrest can be short as problems
escalate.
• Rapid treatment is most likely to improve outcomes.
DIAGNOSIS
• Disaster evolves quickly; thus, diagnosis and rescue treatment should occur simultaneously.
• Monitor failures are far more common than arrest, but must be addressed quickly and arrest
scenarios should always be ruled out first.
• Factors associated with arrest include:
– Change in ECG to pulse-less rhythm
– Loss of palpable pulse or arterial waveform pulsatility
– Loss of end-tidal CO2 (very specific, values <10 mm Hg are associated with severe loss of
cardiac output and the need for chest compressions).
– Loss of plethysmograph waveform
• Do not spend more than 10 seconds seeking a pulse before beginning chest compressions.
Return of spontaneous circulation (ROSC) is associated with preserved myocardial oxygen
tension, which depletes rapidly without CPR.
• Screening for specific risks helps identify sources of arrest (e.g., history of allergy/adverse
drug reactions, obstructive airway disease, aortic stenosis, prolonged QT syndrome).
• Pulse pressure variation >15%, with a tidal volume of 8–10 mL/kg, predicts fluid
responsiveness. In a population at high risk for hypovolemia, this can be very useful.
• If available, a focused, rescue transesophageal echocardiography can aid with diagnosis
(comparative chamber size, wall motion abnormalities, and signs of embolic phenomena).
• Chest radiography may aid with ruling out probable complications of central venous
cannulation (e.g., hemorrhage, pneumothorax).
• Pathophysiologic mechanisms are a useful way to organize etiologies and treatments.
• Anesthetic causes: Drug overdose, high neuraxial block, local anesthetic systemic toxicity,
malignant hyperthermia, drug swap, anaphylactic reaction
• Respiratory causes: Hypoxemia, auto-PEEP, hypoxemia, bronchospasm, tension
pneumothorax
• Cardiovascular causes: Hemorrhage, hypovolemia, acute coronary syndrome, pulmonary
hypertension, right heart failure, pulmonary embolism (thrombus, air, fat, etc.), long QT
syndrome (Torsades de Pointes), pacemaker failure, oculocardiac syndrome, tamponade,
increased intra-abdominal pressure, inferior vena cava (IVC) compression (e.g., flex
position, gravid uterus)
• Metabolic causes: Electrolyte imbalance (hyperkalemia), transfusion reaction
TREATMENT
• CPR should be initiated quickly (allow no more than 10 seconds to find a pulse in suspected
arrest) [C].
• Compression rate should be 100/minute and each compression should be at last 51 mm in
depth (1).
• Respiratory rate should be no more than 10 breaths/minute (1).
• Local anesthetic systemic toxicity: Intralipid™ rescue is associate with ROSC (1) and good
outcomes have been reported even after 60 minutes of CPR (7).
• Fluid responsiveness should be immediately assessed. Fluids are beneficial in most cases (7).
• Amiodarone is a first-line agent in ventricular tachycardia and ventricular fibrillation (1).
• Consider pacing for hemodynamically significant bradycardia (1).
• In right heart failure, physiologic considerations include adequate filling, perfusion pressure
(both systolic and diastolic systemic pressures), and inotropic support (7).
• Embolic arrests, including venous air embolism, should be treated as right heart failure (7).
• Wide-complex bradycardia and asystole are consistent with hyperkalemia. Early treatment
with an IV calcium chloride bolus is indicated (7).
• Emergency pacing is indicated for:
– Bradycardia unresponsive to chronotropes (7)
– Escape rhythms, drug overdose, acidosis, electrolyte abnormalities (7)
– Significant sinus node dysfunction, Mobitz type II 2nd degree, 3rd degree heart block,
alternating bundle branch block, or bifascicular block (1).
– Overdrive pacing of tachycardias (supraventricular tachycardia or ventricular tachycardia)
(7).
FOLLOW-UP
• During post-arrest care, one should consider: Targeted temperature management
(therapeutic cooling) (1) and avoidance of hyperoxia (PaO2 >100 mm Hg) (7).
• Patients surviving anaphylaxis or malignant hyperthermia, or those with a difficult airway,
should be given documentation they can bring for future operative encounters (7).
CLOSED CLAIMS DATA
• Death or brain damage was associated with induction of anesthesia in 62% of cases during
1985–1992, versus 35% of cases from 1993 to 1999 (8).
• Caplan et al. describe 14 cases of high spinal, suggesting that bradycardia is an important
early warning sign and that epinephrine is associated with ROSC (3).
Pregnancy Considerations
• The gravid uterus can compress the aorta and IVC after the 20th week of gestation.
• Resuscitation of the mother may not be possible until the fetus is delivered by emergency
hysterotomy.
• During arrest, hysterotomy should be performed at the bedside since there is insufficient
time to transport the patient to the OR.
Pediatric Considerations
• CPR recommendations in pediatric patients vary by the patient’s age.
• Resuscitation drugs should be dosed according to the patient’s weight.
• Intravenous access can be uniquely difficult in pediatric patients. Intraosseous lines are a
method to get quick reliable access to the circulation.
• Cardiac output in children frequently depends on heart rate (rather than on contractility),
making the treatment of bradycardia an important part of pediatric resuscitation.
REFERENCES
1. American Heart Association. ACLS Provider Manual, 2010.
2. Newland MC, Ellis SJ, Lydiatt CA, et al. Anesthetic-related cardiac arrest and its mortality:
A report covering 72,959 anesthetics over 10 years from a US teaching hospital.
3. Zuercher M, Ummenhofer W. Cardiac arrest during anesthesia. Curr Opin Crit Care.
2008;14:269–274.
4. Peterson GN, Domino KB, Caplan RA, et al. Management of the difficult airway: A closed
claims analysis. Anesthesiology. 2005;103:33–39.
5. Gabrielli A, O’Connor MF, Maccioli GA. Anesthesia-centric ACLS. Available at:
http://www.asahq.org/For-Members/Publications-and-Research/
∼/media/For%2520Members/Publications/Other/Anesthesiology-CentricACLS.ashx.
6. Nichol G, Thomas E, Callaway CW, et al. Regional variation in out-of-hospital cardiac
arrest incidence and outcome. JAMA. 2008;300:1423–1431.
7. Sprung J, Warner ME, Contreras MG, et al. Predictors of survival following cardiac arrest in
patients undergoing noncardiac surgery: A study of 518,294 patients at a tertiary referral
center. Anesthesiology. 2003;99:259–269.
8. Caplan RA, Ward RJ, Posner K, et al. Unexpected cardiac arrest during spinal anesthesia: A
closed claims analysis of predisposing factors. Anesthesiology. 1988;68:5–11.
ADDITIONAL READING
• Cheney FW. The American Society of Anesthesiologist closed claims project: What have we
learned, how has it affected practice, and how will it affect practice in the future?
• Cheney FW, Posner KL, Lee LA, et al. Trends in anesthesia-related death and brain damage:
A closed claims analysis. Anesthesiology. 2006;105:1081–1086.
CODES
ICD9
427.5 Cardiac arrest
ICD10
I46.9 Cardiac arrest, cause unspecified
CLINICAL PEARLS
• Cardiac arrest associated with anesthesia is different; good recovery is frequent with timely
intervention.
• Hypovolemia is a common cause of arrest and vigilance is important. Pulse pressure
variation >15% can be an important clue to volume responsiveness.
• Take no more than 10 seconds to find a pulse before starting compressions.
• Bradycardia and asystole are often related to reversible factors.
ACROMEGALY
Adam Thaler, DO
BASICS
DESCRIPTION
• The term acromegaly comes from the Greek words for “extremities” and “enlargement.”
• Acromegaly is a condition caused by an abnormal overproduction of growth hormone (GH)
from the anterior pituitary, usually by a pituitary tumor. The result is an overgrowth of
skeletal, soft, and connective tissues. Enlargement is seen in:
– Major organs including the heart, lungs, liver, and kidney
– Hands, feet, jaw, and tongue
– Airway anatomy including the tongue, epiglottis, mandible, and generalized soft tissue
(making airway management potentially difficult)
EPIDEMIOLOGY
Incidence
• Annual new patient incidence: 3–4 per million per year
• In the US: 1:20,000 persons
Prevalence
• Most common age at diagnosis is 40–45 years.
• All ethnic groups and gender are affected equally.
Morbidity
• Increased prevalence of cardiovascular risk factors
• Difficult airways are seen in 10–43% of patients (compared to 3.6% in the general
population). Mallampati Class I and II may present with airway difficulty in up to 20% of
patients.
Mortality
• Premature death can occur twice as frequently when GH concentration is >10 ng/mL.
• Cardiovascular causes are the most frequent cause of death in untreated acromegaly; the
majority of patients die before the age of 50 years.
• Survival in patients with uncontrolled disease is reduced by an average of 10 years
compared with age-matched controls.
• No major risk factors
• Weak risk factors include:
– MEN type I syndrome
– McCune–Albright syndrome
– Isolated familial acromegaly
– Carney complex
– Family history of aryl hydrocarbon-receptor interacting protein (AIP) mutation
PATHOPHYSIOLOGY
• Hypothalamus: Growth hormone-releasing hormone (GHRH) is produced and secreted by
the hypothalamus via the hypophyseal tract to the anterior pituitary gland (as is
somatostatin).
• Pituitary gland: GHRH stimulates the anterior pituitary gland to produce and secrete GH
into the bloodstream, whereas somatostatin inhibits GH production and secretion.
• Tissues: GH travels to and stimulates the liver to produce another hormone called insulin-
like growth factor 1 (IGF-1). IGF-1, in turn, promotes growth of bone and other tissues.
• “Feedback loop”: Normally, levels of GHRH, GH, somatostatin, and IGF-1 are tightly
controlled by each other. Levels are affected by: Sleep, exercise, stress, food intake, and
blood sugar levels.
• Excessive GH results from pituitary adenomas in >95% of cases. Secretion of GH by a
pituitary tumor is not controlled by the feedback loop resulting in excessive IGF-1 with
subsequent abnormal tissue growth.
– Carbohydrate and fat processing is affected causing diabetes and high levels of fats in the
blood. This, in turn, can lead to atherosclerosis and heart disease.
– Myocardial growth can result in conduction disturbances.
– Hepatomegaly
– Kidneys: Positive fluid balance may be due to chronic hypertension, causing
vasoconstriction, preoperative hypovolemia, lower cardiac output, fluid volume
dysautoregulation, and/or renal dysfunction.
– Lungs: Lower arterial pH
– Tumors can also grow to considerable size and cause problems by pressing on and
invading surrounding tissues.
• Gigantism is the term used when acromegaly occurs in children.
• Patients with acromegaly may have glottic or subglottic stenosis, nasal turbinate
enlargement, vocal cord thickening, or recurrent laryngeal nerve involvement. Be aware of
the potential for a difficult airway, perform a careful exam, and consider having backup
airway devices available.
• Address comorbid conditions including diabetes, hypertension, and cardiac disease.
SYMPTOMS
• May be divided into 2 groups: Tumor compression of surrounding tissues or those caused by
excess GH and IGF-1 in the blood. Compression of surrounding tissues can present as
headaches or partial loss of vision in one or both eyes. Bitemporal hemianopsia is due to
pressure on the optic chiasm.
• Pituitary tumors also can damage the pituitary gland itself, disrupting hormone production.
Hormone imbalances are responsible for symptoms such as impotence, low sex drive, and
changes in the menstrual cycle.
• Symptoms due to excess GH or IGF-1 include increase in ring size or tightness of rings
(“sausage-like” fingers), shoe size, sweating, jaw prominence, as well as coarseness or
thickening of facial features (especially the nose), macroglossia, or skin tags.
History
• Onset: The average time from onset to symptoms to diagnosis is 12 years.
• Snoring may suggest obstructive sleep apnea; present in 75% of patients. If on CPAP,
establish settings.
• If the patient has diabetes mellitus, assess blood sugar control; present in 25% of patients.
Signs/Physical Exam
• Musculoskeletal:
– Prognathism
– Osteoarthritis
– Osteoporosis
– Kyphosis
– Skeletal muscle weakness
• Airway:
– Macroglossia
– Vocal cord thickening with hoarseness
– Thickening of the laryngeal and pharyngeal soft tissues: Leading to subglottic narrowing
– Enlarged epiglottis
– Hypertrophy of the periepiglottic folds
– Calcinosis of the larynx
– Recurrent laryngeal nerve injury
• Endocrine:
– Peripheral neuropathy
– Thyroid nodule; goiter (25%): May compress trachea
• Cardiovascular:
– Increased prevalence of valvular heart disease
Significant AI (30%)
Significant MR (5%)
– Hypertension (46%)—volume overload
Cardiomegaly
Dysrhythmias (40%)
LV dysfunction: EF ∼ 42%
CHF (3–10%)
MEDICATIONS
• Octreotide is a somatostatin analog that inhibits GH secretion. It is capable of causing GI
side effects such as nausea, bloating, and gas in up to 30% of patients.
• Dopamine agonists, bromocriptine and cabergoline, work at the level of the pituitary to
reduce GH and subsequent IGF-1 secretion.
• Pegvisomant is a GH receptor blocker and a new category of drugs. Studies have shown that
it normalized IGF-1 levels in >90% of people treated. Side effects include reaction at the
injection site, sweating, headache, and fatigue.
Labs/Studies
• GH and IGF-1 levels
• GH suppression test is a confirmatory test measured before and after drinking 75 g of
glucose. The inability to sufficiently suppress serum GH confirms the diagnosis.
• ECG changes, such as ST-segment depression, T-wave abnormalities, and conduction defects,
are noted in >50% patients.
• Chest radiography can show bone thickening.
• CT or MRI of the head to confirm that an adenoma is in the pituitary gland.
• CT scans of the abdomen/pelvis and chest look for tumors of the pancreas, adrenal glands,
ovaries, or lung that might secrete GH or GHRH.
• Hypertension
• Arthritis
• Colonic polyps
• Coronary artery disease
• Conduction disturbances
• Severe symptoms such as CHF or critical aortic stenosis
• Returning GH levels to normal can reduce the incidence of upper respiratory tract
complications. Regression of the mucosal hyperplasia and thickening could be achieved
preoperatively.
CLASSIFICATIONS
• Biochemical criteria:
– Elevated age- and sex-matched plasma IGF-1, random plasma GH >0.4 mcg/L, and lack of
GH suppression below 1 mcg/L following an oral glucose load
– Severity is judged according to GH levels, which correlate with the tumor mass.
• Imaging criteria: Severity of pituitary adenoma judged according to:
– Pituitary tumor volume
– Suprasellar extension and compression of neural structures
– Invasion of sphenoid bone and cavernous sinuses
• Pathology criteria: Positive GH immunostaining confirms the diagnosis of a pituitary GH-
secreting adenoma. On the basis of the number of cytoplasmic granules, somatotroph
adenomas are divided into 2 types:
– Densely granulated
– Sparsely granulated (more aggressive)
TREATMENT
Premedications
• Antihypertensive medications, as needed
• Insulin, as needed
INTRAOPERATIVE CARE
Regional blocks may be considered to avoid airway instrumentation; however, in the event of
a complication, or failed block, it would require airway instrumentation in less than ideal
conditions or emergently.
Monitors
• Arterial line may be considered in patients with poorly controlled hypertension or diabetes,
or with coronary artery disease.
• Foley catheters may be placed to carefully monitor fluid management; patients may be
1,200–1,500 mL overloaded.
• Preparations should be made for a potential difficult airway.
– Larger face mask may be required because of prognathism.
– Smaller ETT may be needed because of subglottic narrowing and distortion.
– If direct laryngoscopy is difficult, fiberoptic intubation can also be challenging.
Maintenance
• Balanced anesthetics with volatiles and intravenous agents have been utilized.
• Hypertension may be seen intraoperatively, especially after the nasal septum is prepped
with cocaine, epinephrine, or phenylephrine.
• In patients with aortic regurgitation, “fast and loose” describes providing afterload reduction
and higher heart rates. Bradycardia and increases in SVR increase the regurgitant volume in
patients with aortic regurgitation.
• Glucose monitoring may be necessary in long cases or in poorly controlled diabetics.
• Fluid regulation may be altered: Urine output is significantly lower in acromegalic patients
resulting in greater positive fluid balance.
Patients are at increased risk for airway obstruction and may have difficult airways; ensure
that the patient is fully awake and following commands before extubating.
POSTOPERATIVE CARE
BED ACUITY
• Consider supplemental oxygen (nasal cannula, face mask)
• Prepare for the potential backward displacement of the already large tongue post-extubation
that may cause respiratory compromise.
COMPLICATIONS
• Airway difficulties
• Mild perioperative metabolic problems occur with respect to blood glucose and fluid
balance.
REFERENCES
1. Nemerget EC, Dumont AS, Barry UT, et al. Perioperative management of patients
undergoing transsphenoidal pituitary surgery. Anesth Analg. 2005;101:1170–1181.
2. Seidman PA, Kofke WA, Policare R, et al. Anaesthetic complications of acromegaly. Br J
Anaesth. 2000;84(2):179–182.
3. Hakala P, Randell T, Valli H. Laryngoscopy and fiberoptic intubation in acromegalic
patients. Br J Anaesth. 1998;80(3):345–347.
4. Scacchi M, Cavagnini F. Acromegaly. Pituitary. 2006;9(4):297–303.
5. Nabarro JD. Acromegaly. Clin Endocrinol (Oxf). 1987;26(4):481–512.
ADDITIONAL READING
• Katznelson L, Atkinson JL, Cook DM, et al. American Association of Clinical
Endocrinologists medical guidelines for clinical practice for the diagnosis and treatment of
acromegaly-2011 update: Executive summary. Endocr Pract. 2011;17(4):636–646.
• Cushing syndrome
• Difficult airway
CODES
ICD9
253.0 Acromegaly and gigantism
ICD10
E22.0 Acromegaly and pituitary gigantism
CLINICAL PEARLS
• Greater than 50% of patients develop cardiac complications: Cardiomyopathy with
arrhythmias, left ventricular hypertrophy, decreased diastolic function, hypertension
• Greater than 60% of patients develop respiratory complications: Upper-airway obstruction
with sleep apnea, associated with soft-tissue laryngeal airway obstruction and central sleep
dysfunction
ACUTE ADRENAL INSUFFICIENCY
Cristina Cunanan, MD
Anahat Dhillon, MD
BASICS
DESCRIPTION
• Also called adrenal crisis, acute adrenal insufficiency is a life-threatening condition
secondary to inadequate adrenal steroid production not matching increased demands during
stress (e.g., infection, surgery) (1).
• Manifestations result from mineralocorticoid deficiency, in association with prostaglandin
excess, and decreased responsiveness to norepinephrine and angiotensin II (2):
– Severe hypotension
– Circulatory collapse
– Hypothermia
– Altered mental status
– Hypoglycemia
• Primary adrenal insufficiency (PAI) (3):
– All 3 layers of the adrenal cortex are affected.
– Involves glucocorticoid, mineralocorticoid, and adrenal androgen deficiencies
– Seen with autoimmune adrenalitis, adrenal hemorrhage, adrenalectomy, AIDS, and
tuberculosis
• Secondary adrenal insufficiency (SAI) (2):
– Results from disorders of the hypothalamic–pituitary–adrenal (HPA) axis that may involve
tumors, irradiation, trauma, surgery, exogenous glucocorticoid therapy (most common),
enzyme inducers that enhance the clearance of synthetic glucocorticoids (rifampin and
carbamazepine), or drugs that inhibit cortisol synthesis (ketoconazole, etomidate) (3)
– These conditions can cause a deficiency in adrenocorticotropic hormone (ACTH) or
corticotropin-releasing hormone (CRH), leading to atrophy of the adrenal zona fasciculata
where glucocorticoids are synthesized.
– Mineralocorticoid function is better maintained, and hence, less likely to cause an adrenal
crisis.
• Initiation of thyroxine replacement in patients with hypothyroidism may induce adrenal
crisis due to increased cortisol metabolism (4).
EPIDEMIOLOGY
Incidence
3.3–6.3 adrenal crisis per 100 patient years (4,5)
Prevalence
• Of PAI, 93–140 per million; age of diagnosis peaks in the 4th decade of life; women more
frequently than men (5).
• Of SAI, 150–280 per million; age of diagnosis peaks in the 6th decade of life; women more
frequently than men (5).
Morbidity/Mortality
• Data regarding morbidity and mortality in patients with adrenal insufficiency are scarce (6).
• The risk ratio for death is more than 2-fold higher in patients with PAI; it is attributed to
malignancy and cardiovascular and infectious diseases (7).
• In patients with PAI, mean age at death for females is 75.7 years, and for males mean age is
64.8 (this is 3.2 and 11.2 years less than the estimated life expectancy, respectively) (8).
• In children with PAI, there is a 3- to 4-fold increase in mortality compared with the general
population (8).
• Risk of adrenal crisis is higher in:
– PAI compared to SAI (3.3–6.6 per 100 vs. 2.5–5.8 per 100)
– Women compared to men (4.4 per 100 vs. 1.6 per 100 years) (4,5)
• In SAI patients, there is a higher risk of adrenal crisis in female patients and with the
presence of diabetes insipidus.
• Precipitating factors for adrenal crisis include (5):
– Infectious disease (particularly GI infections)
– Surgery
– Strenuous physical activity
– Cessation of glucocorticoid replacement
– Psychic distress
– Heat
– Pregnancy
• HPA axis is vital to the body’s ability to cope with severe stress, such as that induced by
natural or iatrogenic trauma or infection.
• Adrenal cortex produces glucocorticoids (mainly cortisol) and mineralocorticoids (mainly
aldosterone); these hormones are required for the maintenance of metabolic control, blood
volume, and normal cardiovascular function.
• Surgery, anesthesia, trauma, and severe illness result in elevated ACTH and cortisol levels,
from a normal cortisol secretion rate of 10 mg/d to 75–150 mg/d during stress; and this
response is absent in patients with adrenal insufficiency.
• Mineralocorticoids are produced by the zona glomerulosa under the control of the renin–
angiotensin system:
– Facilitates sodium and potassium homeostasis and the maintenance of intravascular
volume
– Primary target is the kidney, where it stimulates reabsorption of sodium and secretion of
potassium and hydrogen ions.
– Deficiency results in salt wasting and volume depletion.
• Glucocorticoids have multiple effects on body tissues including:
– Increased gluconeogenesis
– Increased angiotensin synthesis by the liver
– Increased vascular reactivity to vasoconstrictors
– Decreased capillary permeability
– Decreased production and activity of nitric oxide
– Alteration of kinin and prostaglandin systems
– Facilitate conversion of norepinephrine to epinephrine in the adrenal medulla
• Glucocorticoid deficiency, therefore, results in decreased vascular responsiveness to
angiotensin II and norepinephrine, decreased synthesis of renin substrate, and increased
prostacyclin production which can aggravate the circulatory collapse seen in
mineralocorticoid deficiency.
• Chronic use of exogenous corticosteroids given in supraphysiologic doses leads to the
development of SAI, and the amount of adrenal suppression depends on the dose, duration,
frequency, time and route of administration and can occur as early as 1 week after
commencing therapy (3).
• Anesthetic plan should avoid the use of drugs that inhibit cortisol synthesis (e.g., etomidate)
in patients at risk.
• Controversy remains over whether supplemental perioperative steroids are required for
patients on maintenance doses of corticosteroids who undergo surgery (9). A 2009 Cochrane
review of randomized controlled trials of supplemental perioperative steroids concluded
that there is inadequate evidence to support or refute the use of supplemental perioperative
steroids, but it is likely that the administration of daily maintenance steroid dose may be
sufficient and supplemental doses are not required.
• While this topic is controversial and the optimal dose and duration of perioperative
glucocorticoid coverage have also not been established, the following recommendations are
based on a review of expert opinion and clinical experience (3):
– For minimal stress procedures (<1 hour under local anesthesia), continue usual
replacement corticosteroid dose.
– For minor stress procedures (colonoscopy, inguinal hernia repair), administer IV
hydrocortisone 25 mg or equivalent at the start of the procedure, followed by usual
replacement doses after the procedure.
– For moderate stress procedures (open cholecystectomy, joint replacement, lower limb
revascularization, abdominal hysterectomy), administer IV hydrocortisone 75 mg/d on the
day of the procedure (25 mg q8h), then taper over the next 1–2 days to usual replacement
doses.
– For severe stress procedures (cardiothoracic, Whipple, liver resection), administer IV
hydrocortisone 150 mg/d (50 mg q8h), then taper over the next 2–3 days to the usual
replacement dose.
DIAGNOSIS
• History/physical exam
– If PAI is undiagnosed and suspected, elicit symptoms such as chronic fatigue, weakness,
lethargy, anorexia, weight loss, postural hypotension, recurring abdominal pain, loss of
libido, loss of axillary and pubic hair, and hyperpigmentation (2).
– All of the above may be present in SAI, except for hyperpigmentation, and hypotension
may be less prominent (2).
– Any patient who has received the equivalent of 20 mg/d of prednisone for >5 days is at
risk for suppression of the HPA axis; if on therapy for 1 month, HPA axis suppression can
last up to 6–12 months after cessation of therapy (10).
– Other modes of steroid administration should be noted, such as topical, inhaled, and
regional (10).
• Maintain a high level of suspicion for adrenal crisis in cases of unexplained hypotension
refractory to catecholamines, especially in patients with increased risk (e.g., prior
glucocorticoid therapy, autoimmune disease, AIDS) (2).
• ACTH stimulation test involves the administration of cosyntropin 250 mcg IV (synthetic
ACTH hormone), followed by serum cortisol measurements at 30 minutes and 60 minutes.
Plasma cortisol values:
– <3 mcg/dL (80 nmol/L) is highly suggestive of adrenal insufficiency.
– <10 mcg/dL (275 nmol/L) requires further adrenal evaluation.
– >20 mcg/dL (550 nmol/L) makes adrenal insufficiency highly unlikely (2).
• Morning plasma cortisol levels
– 10–20 mcg/dL is normal.
– <3 mcg/dL is highly suggestive of adrenal insufficiency (2).
• Other tests:
– Elevated plasma corticotropin levels in PAI
– Decreased aldosterone levels
– Hyperreninemia
– Hyponatremia
– Hyperkalemia
– Hypoglycemia
– Eosinophilia
– TSH
• Cardiogenic shock
• Anaphylactic shock
• Hypovolemic shock
TREATMENT
• Immediate administration of hydrocortisone 100 mg IV followed by 100–200 mg IV per 24

hours
• IV fluids
• Electrolyte replacement
• Improvement in response to glucocorticoids is usually seen within 12 hours (2).
• If diagnostic screening demonstrates basal or post-ACTH cortisol levels >20 mcg/dL, stop
further hydrocortisone therapy unless the patient is still critically ill.
FOLLOW-UP
• If hemodynamic stability is recovered after administration of glucocorticoid, may consider

continuing with surgical procedure.
• Final confirmation of adrenal insufficiency and evaluation of its etiology, if unknown, may
be appropriate after resolution of the acute crisis.
REFERENCES
1. Hahner S, Allolio B. Therapeutic management of adrenal insufficiency. Best Pract Res Clin
Endocrinol Metab. 2009;23(2):167–179.
2. Bouillon R. Acute adrenal insufficiency. Endocrinol Metab Clin North Am. 2006;35(4):767–
775.
3. Jung C, Inder WJ. Management of adrenal insufficiency during the stress of medical illness
and surgery. Med J Aust. 2008;188(7):409–413.
4. Hahner S, Loeffler M, Bleicken B, et al. Epidemiology of adrenal crisis in chronic adrenal
insufficiency: The need for new prevention strategies. Eur J Endocrinol. 2010;162(3):597–
602.
5. Arlt W, Allolio B. Adrenal insufficiency. Lancet. 2003;361:1881–1893.
6. Schulman D, Palmert MR, Kemp SF, et al. Adrenal insufficiency: Still a cause of morbidity
in childhood. Pediatrics. 2007;119:e484–e494.
7. Bergthorsdottir R, Leonsson-Zachrisson, M, Oden A, et al. Premature mortality in patients
with Addison’s disease: A population-based study. J Clin Endocrin Metab. 2006;91:4849–
4853.
8. Erichsen M, Løvås K, Fougner KJ, et al. Normal overall mortality rate in Addison’s disease,
but young patients are at risk of premature death. Eur J Endocrinol. 2009;160:233–237.
9. Yong SL, Marik P, Esposito M, et al. Supplemental perioperative steroids for surgical
patients with adrenal insufficiency. Cochrane Database Syst Rev. 2009;7(4).
10. Kohl B, Schwartz S. Surgery in the patient with endocrine dysfunction. Anesthesiol Clin.
2009;27:687–703.
• Cortisol
• Ulcerative colitis
• Rheumatoid arthritis
CODES
ICD9
255.41 Glucocorticoid deficiency
ICD10
• E27.2 Addisonian crisis
• E27.40 Unspecified adrenocortical insufficiency
CLINICAL PEARLS
• Risk of adrenal crisis is significantly higher in PAI than in SAI.
• The body makes approximately 10 mg/d of cortisol. During extreme stress 75–150 mg/d can
be made.
• Any patient who receives >20 mg/d of prednisone equivalent for >5 days is at risk for SAI.
• There is inadequate evidence to support empiric use of supplemental corticosteroids in
patients with risk factors for SAI.
ACUTE NORMOVOLEMIC HEMODILUTION
Teresa L. Moon, MD
BASICS
DESCRIPTION
• Acute normovolemic hemodilution (ANH) is a strategy that may be implemented to decrease
the need for blood transfusions and their associated risks; it is a form of autologous blood
transfusion. Other commonly utilized techniques include preoperative autologous donation
and cell salvage.
• The process of ANH entails the controlled removal of whole blood from the patient prior to
incision and blood loss and simultaneous replacement with an appropriate volume of
crystalloid or colloid (non-red cell containing), in order to maintain normovolemia and
avoid hypotension.
• The goal is to decrease the loss of red cell mass (as well as other blood cells and proteins)
during surgical bleeding. ANH has the following advantages:
– No risk of transfusion error
– No risk of disease transmission
– Simple
– Inexpensive
– Minimal use of collective resources
– Stored in the operating room
– Whole blood with all components is returned to the patient; minimal loss of coagulation
factors and platelets secondary to limited storage time.
– Does not require significant coordination with the patient and blood bank (unlike
autologous blood donation)
• Transient intraoperative anemia is achieved by removing whole blood to a target hematocrit
while concurrently administering crystalloid or colloid to maintain normovolemia. By
decreasing the hematocrit, there is a reduced loss of erythrocyte mass during surgical
bloodshed.
• Hemodynamics during dilutional anemia
– Combination of decreased blood viscosity and local vasoregulatory factors. The
endothelium senses changes in intraluminal blood flow, shear stress, and the chemical
environment that result from hemodilution and changes in cardiac output; it appears to
respond by releasing NO and causing vasodilation. Additionally, studies have suggested
that hemodilution may decrease the blood’s ability to scavenge and inactivate NO (results
in increased levels). Autonomic nervous system-mediated vasodilation does not appear to
play a significant role.
– Cardiac output is increased (stroke volume) secondary to decreased viscosity (decreased
afterload/tension of the left ventricle); the myocardium is capable of ejecting more
volume.
– Mean arterial pressure is usually maintained within the limits of normal, secondary to the
compensatory increase in cardiac output.
– Heart rate may increase with profound anemia.
• Critical red cell mass: A concept that describes the lower limit of hemoglobin that is capable
of maintaining effective oxygen delivery. Below this threshold, ischemia and anaerobic
metabolism/lactate production can result.
• Unlike techniques such as deliberate hypotension, ANH does not directly decrease surgical
blood volume loss.
ANATOMY
• Phlebotomy may be performed via a:
– Large vein in the periphery; newly placed or pre-existing large-bore IV catheter or one-
time stick
– Central line
– Arterial line
• Decreased blood oxygen carrying capacity occurs secondary to hemodilution. Studies have
demonstrated that tissue oxygenation is usually not sacrificed if normovolemia is
maintained.
• Cardiac ischemia: Usually presents with tachycardia and ECG changes as a result of
decreased oxygen delivery
• Edema may be present postoperatively if large volumes of crystalloid and/or colloids are
used to maintain normovolemia.
• Indications:
– Spinal surgery
– Prostatectomy
– Hysterectomy
– Hip arthroplasty
– Major liver resections: The reported rate of blood transfusion is rarely <30% and patients
normally require 1–2 units. One study demonstrated that the use of ANH did not result in
adverse cardiac, renal, or neurologic outcomes. Benefit were particularly pronounced in
patients who had significant blood loss that exceeded 800 mL.
• Contraindications:
– Pre-existing anemia
– Unstable angina
– Coronary artery disease with significant stenosis or recent myocardial infarction in the last
6 months
– High-grade aortic stenosis or carotid stenosis
– Renal impairment
– Bacteremia
• Invasive monitors may be needed to closely monitor the effects of anemia, including volume
status and frequent blood draws in order to monitor oxygen delivery, confirm EBL, and
electrolytes. The extent of monitoring should factor in comorbidities, the extent of
hemodilution, and expected blood loss.
• Collection:
– Phlebotomy: Whole blood is collected immediately prior to, or during, the initial stages of
surgery (ideally prior to any blood loss).
– Fluid replacement: May be done with either crystalloid or colloid to maintain
normovolemia
– Storage: Whole blood is collected into blood-collection bags with a predetermined
anticoagulant (usually CPD) and kept in the operating room. Agitation of the bags
throughout the case can decrease clotting.
• Considerations:
– Patient becomes unstable during hemodilution: May be evidenced by unexplained
tachycardia or ECG changes despite normal intravascular volume. Phlebotomy should be
halted and blood returned to the patient in order to avoid any acute cardiac events.
– Patient becomes unstable intraoperatively: The removed blood may need to be transfused
to treat severe anemia. Should be administered prior to donated blood.
– May be utilized with cell salvage techniques; however, should not be combined with
deliberate hypotension.
• Determining the amount of blood to be collected:
– Safe hematocrit: A standard, agreed-upon post-hemodilution value does not exist. Target
levels usually range from 20% to 28% and are dependent upon myocardial oxygenation
needs, as well as comorbidities (in particular cardiac and cerebral disease).
– Red cell mass: Dependent on starting hematocrit and total blood volume. Healthy patients
with normal and high hematocrits and men have a greater amount of red cells that can be
collected (compared to those who are chronically ill, anemic, or women).
– Anticipated surgical blood loss
• Efficacy of ANH is dependent upon:
– Volume removed: Patients that can tolerate a large volume of blood removal will likely
have a higher final hematocrit once surgical bleeding has stopped and the blood is
returned. Whereas patients who are unable to donate as much blood will clearly not
receive as much red blood cell mass when blood is returned.
– Effectiveness of hemodilution: Inadequate volume repletion, initially or intraoperatively,
can result in hemoconcentration and increased red blood cell mass.
– Timing of autologous blood replacement: If the collected blood is returned after surgical
bleeding is complete, the patient will have less absolute red cell losses.
EQUATIONS
• Estimated blood volume (EBV)
– Male: 70 mL/kg
– Female: 60 mL/kg
• Blood volume to be withdrawn = EBV × (Hctinitial – Hcttarget)/Hctaverage
• For a 70 kg man with a starting Hct of 40%
•
• ?> and target Hct 28%: [(70 mL/kg × 70 kg) × (40 − 28)]/[(40 + 28)/2] = 1,729 mL
• For a 70 kg man with starting Hct of 35%: [(70 mL/kg × 70 kg) × (35 − 28)]/[(35 +
28)/2] = 1,089 mL
• Volume replacement with appropriate amounts of crystalloid (3 × volume withdrawn) or
colloid (1 × volume withdrawn)
REFERENCES
1. Doss DN, Estafanous FG, Ferrario CM, et al. Mechanism of systemic vasodilation during
normovolemic hemodilution. Anesth Analg. 1995;81:30–34.
2. Epstein NE. Bloodless spinal surgery: A review of the normovolemic hemodilution
technique. Surg Neurol. 2008;70:614–618.
3. Matot I, Scheinin O, Jurim O, et al. Effectiveness of acute normovolemic hemodilution to
minimize allogenic blood transfusion in major liver resections. Anesthesiology.
2002;97:794–800.
4. Monk TG. Acute normovolemic hemodilution. Surg Infect. 2005;6(Suppl 1):S9–S15.
5. Murray D. Acute normovolemic hemodilution. Eur Spine J. 2004;13(Suppl 1):S72–S75.
6. Pape A, Habler O. Alternatives to allogenic blood transfusions. Best Pract Res Clin
Anesthesiol. 2007;21(2):221–239.
• Cell salvage
• Autologous blood transfusion
• Anemia
• Myocardial oxygen supply
• Blood oxygen carrying capacity
CLINICAL PEARLS
• Normovolemic hemodilution is a technique that can help prevent or decrease the need for
allogenic blood transfusion in patients who can sustain moderate anemia intraoperatively.
• In comparison to autologous or homologous blood transfusions, normovolemic hemodilution
eliminates the need for blood bank storage or testing. Since the collected blood remains in
the operating room with the patient, transfusion errors and disease transmission are
eliminated.
• The amount of whole blood collection is directly related to the preoperative hematocrit. Safe
post-hemodilution hematocrits depend upon surgical blood loss and comorbidities.
• The efficacy of ANH has produced conflicting results, which have been attributed to the
heterogeneity of the surgeries it is used for, differences in study protocol, as well as the
definition of outcome variables.
• During cardiopulmonary bypass grafting, when ANH was implemented in lieu of
homologous blood transfusion, significantly lower bilirubin levels were observed. However,
it may be associated with increased postoperative bleeding.
ACUTE RESPIRATORY DISTRESS SYNDROME
Carlos A. Puyo, MD
BASICS
DESCRIPTION
• Acute respiratory distress syndrome (ARDS) is a form of noncardiogenic pulmonary edema.
It results from lung inflammation and presents as acute hypoxemia and bilateral pulmonary
infiltrates.
– Acute lung injury (ALI) is a milder form of ARDS.
– Hyaline membrane disease is a pediatric form of ARDS (caused by a decrease in
surfactant).
• Causes stem from either pulmonary or extrapulmonary sources.
• Histologically, affected alveolar units are filled with protein-rich edematous fluid and
cellular debris; this occurs in a heterogenous manner.
• Diagnosis is based on the history, ABG, and chest radiography.
• Treatment consists of supportive measures (supplemental oxygen, mechanical ventilation)
while the lungs heal.
EPIDEMIOLOGY
Incidence
In the US, approximately 200,000 cases per year
Morbidity
• Can lead to multiorgan failure syndrome, GI ulcers, cardiac dysfunction, acute renal failure,
malnutrition, and chronic issues such as myopathy and psychiatric problems
• Lung function recovers significantly 6–12 months after initial injury.
Mortality
Estimated 25–40%, but is influenced by a variety of coexisting conditions such multisystem
organ failure
• Lung dysfunction due to direct lung injury:
– Pneumonia (frequent cause, high mortality)
– Aspiration
– Mechanical ventilation
– Lung contusion
– Inhalational injury
– Near drowning
• Extrapulmonary sources:
– Sepsis (frequent cause, high mortality; elderly patients are more susceptible)
– Trauma
– Pancreatitis
– Polysubstance abuse: Cocaine, opioid
– Massive blood transfusions
– Ischemia-reperfusion injury
– CNS injury
– Air/fat embolism
– Cardiopulmonary bypass
• Early: “Exudative phase” translates into ventilation/perfusion mismatch (shunting) and
hypoxia, decreased lung compliance, and increased work of breathing. It is associated with
the following:
– Diffuse alveolar and capillary endothelial injury
– Influx of protein-rich fluid into alveoli
– Release of tumor necrosis factor, interleukin-1, and interleukin-8
– Procoagulant activity as protein C and S levels fall and levels of tissue factor and
plasminogen activator inhibitor-1 increase
– Pneumocyte type 1 apoptosis with resultant accumulation of necrotic cellular debris in the
alveolar lumen. Pneumocyte type 2 dysfunction reduces surfactant production.
• Late: Fibroproliferative changes occur later and are characterized by:
– Chronic inflammation resulting from the proliferation of pneumocyte type 2 and
macrophages, and neutrophils filling the alveolar space.
– Fibrosis (associated with increase mortality).
– Neovascularization
• Pneumonia should be diagnosed and treated aggressively.
• Identify patients at risk for pulmonary aspiration (e.g., full stomach, reflux disease, active
vomiting, recent oral contrast for radiological study, altered mental status) and implement
appropriate maneuvers to reduce risk (gastric tube suctioning, prokinetic agents, reverse
Trendelenburg, rapid sequence induction).
• Mechanical ventilation should be weaned as tolerated.
• Prevention of multiorgan dysfunction:
– Diagnose and treat sources of infection aggressively (e.g., urinary tract infection in the
elderly) to avoid sepsis.
– Limit blood transfusions, as appropriate. Consider blood salvaging techniques, blood
filters, and collection from donors without multiple HLA exposures.
DIAGNOSIS
• The diagnosis of ARDS can coexist with other (extrapulmonary) diagnoses.
– History: Acute dyspnea or hypoxemia related to trauma, sepsis, drug overdose, massive
transfusion, aspiration, or acute pancreatitis
– Physical examination: Tachypnea and tachycardia are nonspecific. Auscultation may
reveal bilateral rales. Cyanosis, fever, hypothermia.
– ABG: PaO2/FiO2 ratio <200; a ratio <300 suggests ALI. Initially a respiratory alkalosis is
seen. If ARDS is secondary to sepsis, the ABG may reveal a respiratory acidosis with or
without respiratory compensation.
– CXR is initially patchy and located peripherally; it progresses rapidly to diffuse bilateral
involvement with a ground-glass appearance.
– PCWP ≤18 mm Hg with no clinical evidence of cardiac failure.
– TEE may be helpful to determine pulmonary artery pressures and intravascular volume
status.
– CT scan: Heterogeneous alveolar involvement
• Interstitial/idiopathic pulmonary fibrosis
• Lymphangitic carcinoma
• Veno-occlusive pulmonary disease
• Intravascular fluid overload
• Pneumonia and respiratory failure: Ventilator-associated pneumonia, viral, bacterial
• Pulmonary hemorrhage
• Near drowning
• Drug reaction toxicity: Heroin, salicylate
• Cardiac disease: Left ventricle failure, mitral stenosis
• Toxic shock syndrome
• Tumor lysis syndrome
TREATMENT
• Nonpharmacologic interventions are supportive and consist of intubation and mechanical

ventilation:
– Tidal volume (6 mL/kg) using predicted body weight and plateau pressures of ≤30 cm
H2O (Level I evidence per the ARDS Network trial)
– Positive end-expiratory pressure (PEEP); higher PEEP levels do not negatively impact low-
VT strategy.
– Prone positioning can improve oxygenation and mortality (Level I evidence).
– Permissive hypercarbia allows for decreased minute ventilation with consequent decreases
in shear injury that is imposed on the alveoli with positive pressure ventilation. The pH
should be maintained at ≥7.20.
– Extracorporeal membrane oxygenation and extracorporeal carbon dioxide removal; no
outcome improvement has been demonstrated with these techniques.
– Recruitment maneuvers expand atelectatic areas and improve ventilation/perfusion
matching. However, they are ineffective in providing sustained oxygen concentration.
– Pressure–volume curve to set VT and PEEP; has uncertain clinical value.
– Open-lung strategy applying high-pressure ventilation (55 cm H2O) for 5–10 minutes and
PEEP of 16 cm H2O has uncertain value.
– High-frequency oscillatory ventilation and bilevel ventilation improve oxygenation
transiently with no benefit in mortality.
• Pharmacologic interventions:
– Fluid management: A conservative or restrictive strategy can improve oxygenation. It has
been associated with decreased morbidity and mortality.
– Inhaled nitric oxide (INO): Provides short-term reduction of pulmonary artery pressures
and oxygen improvement (Level I evidence)
– N-acetylcysteine and procysteine have some benefit in improving lung injury score.
– Corticosteroids and methylprednisolone have been used with benefit in ALI/ARDS patients
diagnosed with Pneumocystis carinii pneumonia or at high risk for fat emboli. High doses
may benefit patients with unresolved ARDS of more than 7 days duration.
– Nutritional support: Diets with high-fat content and antioxidant nutrition. The use of
eicosapentaenoic acid (EPA) and gamma-linoleic acid (GLA) appears to decrease
inflammation mediated by arachidonic acid metabolites. Evidence exists to support the
use of EPA and GLA in ARDS.
– Surfactant: Evidence demonstrates that there is a lack of improvement in oxygenation,
ventilator- free days, or mortality.
– Partial liquid ventilation appears to reduce inflammation and disease progression, but has
no obvious benefit in ventilator dependency and mortality.
– Ibuprofen and NSAIDs do not control inflammation mediated by sepsis and are likely of no
benefit in ARDS.
– Ketoconazole, pentoxifylline, lisofylline: Studies have not demonstrated a benefit.
• Diagnose and provide supportive therapy for extrapulmonary manifestations:
– Renal: Monitor for acute tubular necrosis
– Hepatic: Monitor liver function test for abnormalities such as cholestasis and
hepatocellular injury
– Hematologic: Monitor for thrombocytopenia, disseminated intravascular coagulation, and
changes in Von Willebrand factor
FOLLOW-UP
After resolution of the acute phase, mechanical ventilation and respiratory therapy should be
administered to regain muscle strength.
REFERENCES
1. Bernard GR. Acute respiratory distress syndrome. Am J Respir Crit Care Med.
2005;172:798–806.
2. Briel M, Meade M, Mercat A, et al. Higher versus lower positive end-expiratory pressure in
patients with acute lung injury and acute respiratory distress syndrome: Systematic review
and meta-analysis. JAMA. 2010;303(9):865–873.
3. Kallet RH. Evidence-based management of acute lung injury and acute respiratory distress
syndrome. Resp Care. 2004;49(7):793–809.
4. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as
compared with traditional tidal volumes for acute lung injury and the acute respiratory
distress syndrome. N Engl J Med. 2000;342(18):1301–1308.
• Aspiration
• Noncardiogenic pulmonary edema
• Burns
• Pressure volume loops
• Respiratory system compliance
• Positive end expiratory pressure (PEEP)
CODES
ICD9
518.82 Other pulmonary insufficiency, not elsewhere classified
ICD10
J80 Acute respiratory distress syndrome
CLINICAL PEARLS
• Frequent evaluation of respiratory and hemodynamic status
• Since sepsis is the most common risk factor for ARDS, infectious sources must be sought
aggressively.
• If transportation is required, consider maintaining respiratory ventilation with an ICU
ventilator.
ADRENALECTOMY
Joe C. Hong, MD
BASICS
DESCRIPTION
General
• Adrenalectomy is indicated for any malignant lesion, suspicious lesion, or hormone-
secreting lesion of the adrenal gland.
• The laparoscopic approach is considered when the lesion is nonmalignant and has the
benefit of reduced pain, faster recovery, and fewer complications.
• Open adrenalectomy is indicated for large or malignant tumors where en bloc resection and
local dissection may be necessary. It can be performed via an anterior, posterior, or
thoracoabdominal approach.
– The anterior approach allows access to the entire peritoneal cavity and the ability to treat
bilateral adrenal disease or other intra-abdominal pathology. However, it is a major
laparotomy with the potential for prolonged ileus, pulmonary dysfunction, and pain.
– The posterior approach allows avoidance of the thoracic and peritoneal cavities; this
reduces bowel injury or pulmonary problems. However, it is limited to tumors <5 cm and
precludes exploration of metastases or other intra-abdominal pathologies.
– The thoracoabdominal approach allows wide direct exposure for larger tumors and en bloc
resection of a single adrenal gland. However, it limits intraperitoneal exploration, and if
the other gland needs to be removed, it requires repositioning and a second incision.
Position
• Laparoscopic: Lateral decubitus position with the operative side up. The table is flexed at
the waist with the patient in a slight reverse Trendelenburg position to facilitate placement
of the laparoscopic ports.
• Open adrenalectomy: Supine position
Incision
• Laparoscopic: 4 laparoscopic ports, 2 cm below the respective costal margin and spaced no
less than 5 cm apart
• Open: Either a unilateral subcostal, bilateral subcostal, or midline incision is used.
Approximate Time
• Laparoscopic: Typically 2.5–3.5 hours
• Open: Typically 2–3 hours with additional time when local invasion of nearby structures is
present
EBL Expected
• Laparoscopic: 50 mL
• Open: 100–200 mL
Hospital Stay
• Laparoscopic: Routine cases in relatively healthy patients can be discharged within 24
hours. Longer in-hospital stay is dependent on patient comorbidities, need for blood
pressure monitoring, or adjustment of steroid replacement therapy.
• Open: Postoperative in-hospital stays of 4–5 days are typical.
• Laparoscopic instruments and ultrasonic or bipolar coagulator
• Invasive monitoring and possibly a transesophageal echocardiogram for management of
patients with pheochromocytoma
EPIDEMIOLOGY
Incidence
• Incidental finding on abdominal CT scan ranges from 0.6% to 1.3% (1).
• Autopsy finding in patients who had no evidence of adrenal disease: 1.4–9%
Prevalence
• Nonfunctional adrenocortical adenomas: 70% (2)
• Adrenal metastasis: 21%
• Pheochromocytomas: 11%
• Cortisol-producing adenomas: 2–15%
• Aldosteronomas: 2%
• Adrenocortical carcinomas: 1.2%
Morbidity
• Depends on the nature of the adrenal mass
• Aldosteronomas may have marked hypertension, hypokalemia, and metabolic alkalosis.
• Cortisol-producing adenomas may have labile diabetes in addition to marked hypertension,
hypokalemia, and metabolic alkalosis.
• Pheochromocytoma may have significant cardiac morbidity induced by long-standing
catecholamine excess, hypertension, arrhythmias, dilated and hypertrophic cardiomyopathy,
and congestive heart failure.
Mortality
Dependent on the nature of the adrenal mass
• Understanding the physiologic implications of the hormonally active adrenal mass is vital to
appropriate anesthetic management.
• Patients with aldosteronoma should have their antihypertensive medication (most
commonly spironolactone) maintained up to the time of surgery. Careful cardiac assessment
is necessary since these patients have increased cardiac comorbidity. Serum sodium and
especially serum potassium should be checked prior to surgery. Severely hypokalemic
patients should have their potassium replaced preoperatively.
• Patients with Cushing syndrome must have their diabetes, blood pressure, intravascular
volume status, and electrolytes optimized prior to surgery. Their Cushingoid habitus
(central obesity, moon facies, buffalo hump) may present an airway challenge.
Hydrocortisone supplementation at the time of surgery is needed since they are at increased
risk of developing acute glucocorticoid deficiency postoperatively.
• Patients with pheochromocytoma must be adequately alpha-blocked, volume resuscitated,
and concomitant organ dysfunctions identified and optimized prior to surgery.
Phenoxybenzamine is the alpha-blocker of choice. Intraoperatively, hypertension is
expected during tumor manipulation whereas hypotension is expected after ligation of the
tumor’s venous drainage (3).
• Nonfunctional masses are relatively straightforward with anesthetic goals geared toward
each patient’s comorbidities.
SYMPTOMS
Due to mass effect and/or physiologic effects of excess hormone production
History
Based on the nature of the adrenal mass. In patients with hormone-producing adrenal lesions,
a careful history of the medical management of the endocrinopathy is necessary. This
includes the type and dosage of medication, clinical response to therapy, and relevant
comorbidities.
Signs/Physical Exam
• Cortisol-producing adenoma: Steroid encephalopathy, central obesity, moon facies, thick
neck, muscle wasting, osteoporosis, virilization and infertility, glucose intolerance,
hypertension, hypokalemia, alkalosis, easy bruising, poor wound healing (2)
• Aldosteronoma: Hypertension, hypokalemia, alkalosis, hypernatremia, left ventricular
hypertrophy (4)
• Pheochromocytoma: Hypertension, arrhythmias, cardiomyopathy, congestive heart failure,
glucose intolerance (3)
MEDICATIONS
• Cortisol-producing adenoma: Hypoglycemic agents, potassium supplements,
antihypertensives
• Aldosteronoma: Spironolactone, potassium supplements, antihypertensives
• Pheochromocytoma: Alpha-adrenergic antagonists
Labs/Studies
• Evaluation of hormonal function is based on concomitant signs and symptoms.
• Cortisol-producing adenoma: Dexamethasone suppression test, plasma ACTH, urine-free
cortisol
• Aldosteronoma: Potassium level, aldosterone:renin ratio
• Pheochromocytoma: 24-hour urine catecholamine and metanephrines
Cardiac dysfunction in the form of left ventricular hypertrophy is common in patients with
aldosteronoma and pheochromocytoma. In addition, cardiac comorbidity induced by long-
standing catecholamine excess is prominent in patients with pheochromocytoma. These
include hypertension, arrhythmias, dilated and hypertrophic cardiomyopathy, and congestive
heart failure.
TREATMENT
Premedications
• Standard anxiolytic titrated to comfort
• In patients undergoing adrenalectomy for pheochromocytoma, benzodiazepines and opioid
premedication are helpful for awake arterial line placement.
• Patients with cortisol-producing tumors and those undergoing bilateral adrenalectomy must
receive perioperative intravenous hydrocortisone.
If planned, risks specific to central venous and epidural catheter placement should be
discussed.
• First-generation cephalosporin, such as cefazolin, is recommended prior to surgical skin
incision.
• Clindamycin is an alternative for a cephalosporin allergy.
INTRAOPERATIVE CARE
• General endotracheal anesthesia is the technique of choice.
• Epidural analgesia for postoperative pain may be helpful for patients undergoing open
adrenalectomy.
Monitors
• Invasive monitoring is dictated by patient comorbidities.
• Pheochromocytoma: Arterial line for hemodynamic monitoring and a central line for
infusion management and vasoactive medications. Pulmonary artery catheter or TEE may be
needed if significant catecholamine-induced cardiomyopathy is present (3).
• Induction and airway management is dictated by preoperative airway assessment.
• Pheochromocytoma: A deep plane of general anesthesia is needed prior to attempted
laryngoscopy and intubation.
• Cortisol-producing adenomas: Cushingoid habitus (central obesity, moon facies, buffalo
hump) may complicate airway management.
Maintenance
• Inhalational anesthesia with opioid supplementation is suitable.
• Nitrous oxide should be avoided because bowel distension may limit the visibility of the
surgical field in both laparoscopic and open adrenalectomy. The increased incidence of
pneumothorax after open adrenalectomy also makes nitrous oxide relatively
contraindicated.
General extubation criterion can be used.
POSTOPERATIVE CARE
BED ACUITY
• For routine uncomplicated procedures, a standard floor bed is usually adequate.
• Patients with pheochromocytoma with persistent labile blood pressure requiring
postoperative infusion of vasoactive medications should be monitored in the ICU.
ANALGESIA
• Laparoscopic adrenalectomy is well tolerated. Patients are typically able to convert from
intravenous to oral analgesics on postoperative day 1.
• Epidural analgesia provides excellent pain relief for open adrenalectomy.
• Patient-controlled analgesia (PCA) may be used for patients undergoing open adrenalectomy
without epidural analgesia.
COMPLICATIONS
• Intraoperative complications include massive bleeding due to the proximity of the renal
artery, renal vein, vena cava, and aorta.
• Hypertensive, as well as hypotensive crises, can occur during adrenalectomy for
pheochromocytoma. Postoperatively, these patients may be at risk for hypotension and
hypoglycemia.
• Acute adrenal insufficiency can occur after resection of a cortisol-producing adrenal mass or
after bilateral adrenalectomy. Perioperative hydrocortisone 100 mg IV q8h is recommended.
• Injury to pancreas resulting in pancreatitis
• Injury to diaphragm and pneumothorax
• Conversion from laparoscopic approach to open adrenalectomy
• Peritoneal carcinomatosis
PROGNOSIS
Dependent on the type, malignant nature, and degree of local and distant invasion
REFERENCES
1. Brunt LM, Moley JF. Adrenal incidentaloma. World J Surg. 2001;25(7):905–913.
2. Cook DM. Adrenal mass. Endocrinol Metab Clin North Am. 1997;26(4):829–852.
3. Kinney MA, Narr BJ, Warner MA. Perioperative management of pheochromocytoma. J
Cardiothorac Vasc Anesth. 2002;16(3):359–369.
4. Young WF Jr. Adrenal causes of hypertension: Pheochromocytoma and primary
aldosteronism. Rev Endocr Metab Disord. 2007;8(4):309–320.
ADDITIONAL READING
• Graham GW, Unger BP, Coursin DB. Perioperative management of selected endocrine
disorders. Int Anesthesiol Clin. 2000;38(4):31–67.
• Lampe GH, Roizen MF. Anesthesia for patients with abnormal function of the adrenal cortex.
Anesthesiol Clin North Am. 1987;5:245–268.
• Pheochromocytoma
• Aldosterone
• Cortisol
CODES
ICD9
CLINICAL PEARLS
• Understanding the physiologic implications of the hormonally active adrenal mass is vital to
appropriate anesthetic management.
• Patients undergoing bilateral adrenalectomy will need perioperative stress dose steroids.
Postoperatively, they will need glucocorticoid and mineralocorticoid replacement.
• Patients with cortisol-producing adrenal lesions also need perioperative stress dose steroids.
The quiescent contralateral adrenal gland will be unable to produce enough cortisol in the
immediate postoperative period.
• Patients with pheochromocytoma must be adequately alpha-blocked prior to adrenalectomy.
• Pneumothorax should be considered if the patient develops postoperative respiratory
distress.
AFTERLOAD
BASICS
DESCRIPTION
• Left ventricular (LV) afterload is the force against which the heart must work to generate
pump work (eject blood out of the heart into the aorta).
• In the purest form, afterload is defined as wall stress, which are the forces opposed to
ventricular fiber shortening. Afterload or wall stress provides the most accurate indication
of cardiac energy expenditure. However, clinically true afterload or wall stress cannot be
measured.
• Ventricular afterload is comprised of a static and dynamic component; elevation in either
component may result in increased afterload.
– Static component of the LV is comprised of the systemic vascular resistance (SVR) or
outflow of blood into resistance arterioles. Under normal physiologic circumstances and in
healthy (compliant) vasculature, the SVR is the main determinant of LV afterload.
Small arteries and arterioles are referred to as resistance vessels since they are the
principal site of SVR. The autonomic nervous system provides constant regulation on a
short time scale (seconds to minutes).
SVR; Normal 800–1400 dyne-s/cm5. SVR can be calculated from MAP, CVP, CO; SVR =
[(MAP – CVP) × 80]/CO. The pressures are measured from the “beginning” of the
circuit to the “end” of the circuit. For example, if the CO is 5 L/min, the BP is 120/80
mm Hg (MAP is 93.3 mm Hg), and the CVP is 12 mm Hg, then SVR = [(93.3–12) ×
80]/5 = 1396 dyne-s/cm5.
The static component of the right ventricle (RV) is composed of the pulmonary vascular
resistance (PVR); normal 80–120 dyne-s/cm5. The blood flow (CO) through the left and
right sides of the heart are equal; however, the afterload for the RV is significantly less.
The main component of RV afterload is PVR, which is around 10 times lower than SVR.
The formula to calculate is: PVR = [(Mean PAP – wedge pressure) × 80]/CO. The
pressures are measured from the “beginning” of the circuit to the “end” of the circuit.
For example, if the PA pressures is 25/10 mm Hg (Mean PAP is 15 mm Hg), the wedge
pressure is 8 mm Hg, and CO is 5 L/min, then PVR = [(15–8) × 80]/5 = 112 dyne-
s/cm5.
– Dynamic pulsatile component: Consists of 2 phasic elements; one is the compliance-related
forward pulse wave and the second is the reflected pulse wave. The pulsatile component
contributes significantly to total LV afterload in stiff vessels. Central arterial vessels are
the principal site of the pulsatile component.
• Despite the clinical use of SVR to determine LV afterload, it is best measured as systolic wall
stress. Stress (or tension) is defined as the force, or load, per unit cross-sectional area. Wall
stress/tension is the product of transmural pressure and chamber radius divided by the wall
thickness. For the LV: S = PR/2h; where S is the LV wall stress, P is the LV cavity pressure,
R is the radius of the LV, and h is the myocardial thickness (also known as LaPlace’s Law).
– LV cavity pressure
During systole, the LV generates pressure. That pressure should be higher than pressure
seen by the LV in the ascending aorta at each point in time during ejection to promote
forward blood flow. Pressure in the ascending aorta will depend on the peripheral
resistance, compliance of the arterial tree, and contributions of wave reflections.
Aortic valve: Any obstruction to flow from the LV cavity to the ascending aorta will
cause additional resistance and a necessary increase in the LV cavity pressure to
overcome it. Clinically, the most common causes are aortic stenosis and hypertrophic
obstructive cardiomyopathy which can cause up to 100 mm Hg extra LV pressure over
what is needed to pump blood into aorta.
Blood viscosity contributes to the resistance to blood flow, such that increased viscosity
leads to increased resistance. The blood viscosity depends, for the most part, on the
hematocrit.
– Radius: Wall stress (afterload) is dependent on the geometry of the LV itself. During
systole, the ventricular wall thickens and the radius decreases as the ventricle pumps
blood out (and reduces LV wall stress). Preload or LV end diastolic volume affects the
initial radius and, hence, wall stress during isovolemic contraction.
– Myocardial thickness: In cases of pressure overload, and resultant increases in wall stress,
the heart muscles compensate by becoming hypertrophic (wall stress is inversely related
to wall thickness, thus myocardial hypertrophy decreases wall stress). Increased muscle
mass requires less force per unit area.
– Wall stress or afterload varies over time since the LV pressure, radius, and wall thickness
are continuously changing throughout the cardiac cycle. As a result, afterload can be
calculated at the instant of aortic valve opening, at the end of ejection, or at any instant
throughout systole. Clinical investigators use peak systolic stress, end-systolic stress, or
mean systolic wall stress as indices of afterload.
• Determinants/regulation of vascular resistance (and hence afterload)
– Neurohumoral responses (long-term regulation, over days and weeks)
Renin–angiotensin axis: Juxtaglomerular cells in the kidneys secrete renin directly into
the blood. The secreted renin then converts angiotensinogen (released by the liver) to
angiotensin I. Angiotensin I is subsequently converted to angiotensin II by the enzyme
angiotensin-converting enzyme (produced by the lungs). Angiotensin II is a potent
vasoactive peptide that causes blood vessels to constrict, resulting in increased SVR.
Vasopressin (antidiuretic hormone) is secreted into the blood by the neurohypophysis. It
activates specific vasopressin receptors on the VSMC and causes vasoconstriction.
– Nitric oxide (NO) is produced by endothelial cells, diffuses into the media, and relaxes the
VSMC by activating cyclic guanylate cyclase. Hence, NO is called endothelium-derived
relaxation factor. Smoking, hypercholesterolemia, oxidative stress, or limited physical
exercise can result in endothelial dysfunction; consequently, there is a decrease in NO
production (increase in SVR).
– Hydrogen sulfide has been recently recognized as endothelium-derived hyperpolarizing
factor. Similar to nitric oxide, hydrogen sulfide causes relaxation of resistance arterioles,
vasodilation, and decreases the SVR.
ANATOMY
• The mean pressure decreases by only 1–2 mm Hg between the ascending aorta and
peripheral arteries in compliant and healthy vasculature, indicating low resistance at this
portion of the vascular tree.
• A major drop of pressure occurs over small arterioles and they constitute the major site of
resistance.
• Increased afterload:
– Aortic stenosis: The LV needs to generate increased force to overcome the resistance of the
stenosed aortic valve and eject blood into the aorta. This results in increased LV wall
tension and stress (increased afterload). The LV usually compensates with a hypertrophic
response to return the wall stress to normal. The thickened LV, in conjunction with
increased force, however, increases the myocardial oxygen demand (increased muscle
mass working harder) and decreases the myocardial oxygen supply, especially to the
endocardium. Blood flows from the epicardium into the endocardium; additionally, it
takes more time for blood to flow across a thickened LV wall to reach the endocardium.
– Chronic hypertension: Essential hypertension in the young and middle-aged population is
frequently characterized by increases in DBP. This is the result of vasoconstrictory
responses predominating over vasodilatory responses at the level of the arterioles in the
periphery. In the elderly, the predominant form of hypertension is systolic hypertension,
while DBP is low to normal (the SVR in isolated systolic hypertension is usually normal or
even decreased). However, there is a marked increase in vascular sclerosis, stiffness, and
arterial impedance. The increased resistance is to the pulsatile (dynamic) component of
blood flow. In either case, untreated or poorly controlled hypertension requires the heart
to work harder, increases afterload, and often elicits a compensatory hypertrophic
response in the LV to return wall stress to normal.
– Hemoconcentration: Analogous to the reservoir bag on the anesthesia machine; if the bag
was filled with water or jelly as opposed to air, it would require more energy to compress
or squeeze the bag.
– Increased LV radius: A dilated LV, as with cardiomyopathy or heart failure, causes
increases in wall tension due to decreased myocardial thickness as well as increased radius
( = increase in afterload). This is analogous to the reservoir bag overfilled; more energy
would be required to empty the bag, compared to a partially or normally filled bag.
– Cor pulmonale: Elevated PVR requires the RV to squeeze harder to generate more force to
eject blood ( = increased afterload for the RV). Elevations in the PVR over prolonged time
lead to compensatory RV hypertrophy to decrease wall tension and normalize the
afterload.
• Decreased afterload
– Sepsis: Mostly due to loss of SVR
– Anaphylaxis: Mostly due to loss of SVR
– High-output cardiac failure: Due to arteriovenous shunts
– Anemia: Due to both a decrease in viscosity and lowered SVR (decreased BP)
– Hypovolemia: There is less blood to stretch the LV and, hence, less force is needed to eject
blood. To counteract for reductions in the stroke volume (and maintain BP), the
sympathetic tone is increased (increase in SVR and heart rate).
• Increased afterload
– Sympathetic stimulation with intubation and surgery
– Vasopressors:
Preferential alpha-1 agonists have the most profound effect on increasing the afterload
(phenylephrine and norepinephrine).
Vasopressin
Ephedrine and epinephrine will increase afterload in addition to increasing contractility.
• Decreased afterload
– An increasing depth of anesthesia with either volatile agents or IV anesthetics (e.g.,
propofol) causes a decrease in sympathetic tone (vasorelaxation) with resultant decreases
in the SVR and BP. Increased depth should be avoided in hypovolemia or hypotensive
patients.
– Neuraxial techniques: Both spinal and epidural blocks interrupt conduction of nerve
impulses through sympathetic fibers at the level of their spread. This leads to a decrease
in sympathetic tone, SVR, and preload (pooling of blood in veins). To counteract this
response, volume resuscitation and pressors may be administered as needed. In
hypovolemic or hemorrhaging patients, neuraxial techniques should not be used; they
block compensatory increases in SVR and heart rate.
– NO donors (nitroglycerin, nitroprusside) cause relaxation of both resistance arterioles and
veins and, hence, a decrease in SVR and preload. They are used for tight BP control in
procedures such as AAA and CEA.
– Inhaled NO is used to alleviate increased pulmonary artery pressures. It has minimal
systemic effects.
– Calcium channel blockers cause arterial smooth muscle relaxation and decrease
myocardial contractility.
– Phosphodiesterase inhibitors increase cardiac contractility while relaxing resistance
arterioles, decreasing SVR, and causing hypotension. They are mostly used in heart
failure, but may also require simultaneous administration of alpha-agonists to counteract
pronounced hypotension.
– Positive end expiratory pressure (PEEP). LV dysfunction with pulmonary edema results in
decreased pulmonary volume and compliance. Greater negative inspiratory pressures (and
hence transmural pressures) are required to expand the lungs. PEEP can partially offset
this.
EQUATIONS
• SVR = [(MAP – CVP) × 80]/CO; MAP = mean arterial pressure (mm Hg), CVP = central
venous pressure (mm Hg), CO = cardiac output (liters/minute)
• PVR = [(mPAP – wedge pressure) × 80]/CO; mPAP = mean pulmonary artery pressure
(mm Hg), CO = cardiac output (liters/minute)
• Tension = (ΔP × R)/H × 2; ΔP = change in pressure, R = radius, H = wall thickness
O’Rourke M, Nichols W. McDonald’s blood flow in arteries. Hodder Arnold, 2006.
REFERENCES
1. Thiele RH, Nemergut EC, Lynch C. The physiologic implications of isolated alpha1
adrenergic stimulation. Anesth Analg. 2011;113(2):284–296.
2. Thiele RH, Nemergut EC, Lynch C. The clinical implications of isolated alpha1 adrenergic
stimulation. Anesth Analg. 2011;113(2):297–304.
• Pulmonary artery catheter waveforms
• Anaphylaxis
• Hypertension
• Aortic stenosis
CLINICAL PEARLS
• The SVR is considered by most professionals as equivalent to afterload and is substituted for
it; SVR is calculated from MAP and CO (SVR = MAP/CO). SVR is an oversimplified
quantification of the true resistance force against which the heart works. It has an
underlying assumption that flow is constant.
AIRWAY FIRE
Charles E. Cowles, Jr., MD
BASICS
DESCRIPTION
• Surgical fires can occur either on the patient or in the patient’s airway (1). They are most
commonly observed during procedures that involve the open delivery of oxygen near an
ignition source, like electrocautery or laser.
• Airway fires are defined as either within the airway or within the breathing circuit. Many
fires occur during relatively minor procedures of the head and neck which involve the use
of a cautery device and a simple facemask or nasal cannula.
• As with operating room (OR) fires, airway fire prevention depends on:
– An understanding of how triad elements (ignition, fuel, oxidizers) interact to create a fire
– Recognizing how standard OR equipment, materials, and supplemental oxygen can
become one of those elements
– Vigilance for circumstances that bring fire triad elements into close proximity (2)
EPIDEMIOLOGY
Prevalence
• Occurs in about 650 cases per year (1:87,646) (3,4)
• Actual incidence is likely higher, but surgical fires are under-reported.
Morbidity
20–30 serious injury cases per year (3)
Mortality
2–3 deaths per year (3)
• High-risk procedure: Use of an ignition source in close proximity to an oxidizer (oxygen and
nitrous oxide) (1). Fires have been reported during head and neck procedures including
tracheostomies, adenotonsillectomies, endoscopic airway surgeries, and cutaneous surgeries
of the head and neck.
• Monitored anesthesia care (MAC)/sedation cases, especially when there is/are:
– Open delivery of oxygen at a FiO2 >30%
– Drapes and towels configured in a manner to “trap” oxygen underneath drapes and allow
for significant accumulation.
– Patients with obstructive sleep apnea or other diseases (decreased functional residual
capacity) that cannot tolerate sedation without oxygen supplementation
– Surgeries that involve the head and neck or are above the xiphoid process
• Laser use in or near the airway
• Prep solution and drapes:
– Adequate drying time is not observed when using alcohol-based preps or if pooling of prep
has occurred.
– Flammable prep solutions are used in hairy locations or crevasses of the body or if large-
sized sponge containers (26 mL) are used for head and neck cases.
• Fire occurs when elements of the fire triangle are combined (3):
– Ignition source
Electrosurgical units (ESU), cautery, lasers, and light sources
Usually controlled by the surgeon
– Fuel
Alcohol-based preps, towels, and drapes
Usually controlled by the OR nurse
– Oxidizers
Oxygen and nitrous oxide
Usually controlled by the anesthesia provider
• Fires which occur in oxygen-enriched environments may result in a sudden flash fire where
the burn injuries occur in a matter of seconds (too quickly for extinguishment).
• Often, fires are the result of a lack of communication among surgical team members.
• Injury and damages commonly occur when the response to the fire is uncoordinated and
haphazard.
• Assess the fire risk prior to every surgical procedure; this is especially important for cases
involving the head and neck or cases performed under MAC.
– Perform fire risk assessment during surgical “time out”
– Assign specific tasks for each OR team member to perform in case of a fire
• MAC/sedation cases with increased fire risk
– Do not use supplemental oxygen unless clinically necessary
– Allow sufficient time for oxidizer levels to drop before using an ignition source. This may
take several minutes.
– If an FiO2 >30% is required:
Communicate with the surgical team.
Titration of the FiO2 can be accomplished with the use of an oxygen blender or by using
the common gas outlet found on some anesthesia machines.
Consider using an ETT or supraglottic device such as the laryngeal mask airway (LMA) to
eliminate the open flow of oxygen, especially in cases above the xiphoid
Configure drapes to prevent accumulation of oxygen and to facilitate open ventilation.
• Prep solution and drapes
– Allow flammable surgical preps such as alcohol-based solutions to dry fully before the
application of surgical drapes or barriers
– Assess for pooling as a routine part of the time-out process
– Avoid 26 mL applicators in head and neck cases
• General anesthetics, particularly for procedures above the xiphoid
– Use cuffed tracheal tubes when possible
– FIO2 <30% may reduce the risk of fire, particularly for intraoral cautery.
– Decreasing the electrocautery wattage may reduce the incidence of airway fires (5).
• Laser procedures
– Use an appropriate laser tube for the type and frequency of the laser
– Use an indicator dye such as methylene blue in the distal cuff of laser tubes to detect
inadvertent rupture
– Moisten gauze or sponges if used to pack the airway
– Participate in OR-specific fire drills which include the practice of patient evacuation
methods and involvement of all team members, including surgeons and anaesthetists
• Know the location of fire extinguishers and gas cut-off valves before the case begins
• Consider assembling a cart for high-risk procedures which includes saline or water bottles,
fire extinguishers, and placards to guide response
• By index of suspicion and investigation of any smell of smoke, hearing loud “pop,” or seeing
smoke or flames
• Excessive movement of the patient during MAC
• Alcohol burns with a nearly invisible flame which becomes increasingly difficult to see
under bright surgical lights.
TREATMENT
The following steps should be carried out as soon as possible. The specific order or sequence
is not as important as rapidly completing the task (1):
• Stop the procedure to evaluate situation
• Stop the flow of gases
• Remove endotracheal tube (ETT)
• Remove drapes
• Pour saline or water in airway
FOLLOW-UP
• In the non-intubated patients, assess for smoke inhalation injury.

• In intubated patients:
– Examine the removed ETT for fragments that could still be present in the airway
– Re-establish ventilation but avoid the use of oxidizers to avoid re-kindling of embers
which may be present in the airway
– Perform rigid bronchoscopy if lower airway injury is suspected (1)
• Use fire extinguisher if initial attempts to extinguish the fire are not successful. Plan to
evacuate the OR if necessary.
• If fire or smoke is present, activate the facility fire alarm system, notify the local fire
department, and file a report with the fire marshal’s office according to local protocols
• Transfer to appropriate burn facility
CLOSED CLAIMS DATA
• Claims approaching $1.5 million per case have been paid for MAC cases resulting in fatal or
disfiguring burn injuries.
• Most cases involve head and neck surgeries.
• 74% of burn cases involve oxygen supplementation.
REFERENCES
1. merican Society of Anesthesiologists (ASA) Task Force on Operating Room Fires, Caplan
RA, Barker SJ, et al. Practice advisory for the prevention and management of operating
room fires. Anesthesiology. 2008;108(5):786–801.
2. Rinder CS. Fire safety in the operating room. Curr Opin Anaesthesiol. 2008;21(6):790–795.
3. ECRI New Clinical Guide to Surgical Fire Prevention [guidance article]. Health Dev.
2009;38(10):319.
4. ennsylvania Patient Safety Authority. Three “never complications of surgery” are hardly
that. Pa Patient Saf Advis. 2007;4(3):82.
5. oy S, Smith LP. What does it take to start an oropharyngeal fire? Oxygen requirements to
start fires in the operating room. Int J Pediatr Otorhinolaryngol. 2001;75(2):227–230.
ADDITIONAL READING
• Anesthesia Patient Safety Foundation (APSF). Prevention and management of surgical fires
[video]. APSF, 2009.
• Barker SJ, Polson JS. Fire in the operating room: A case report and laboratory study. Anesth
Analg. 2001;93:960–965.
• Department of the Army. Headquarters, United States Army Medical Command. Fires
associated with the performance of surgical procedures [online]. MEDCOM Regulation No.
40-48, August 2003.
• Smoke inhalation injury
• Burns
• Operating room fires
CLINICAL PEARLS
• Open delivery of oxygen should only be used as clinically necessary; oxygen concentrations
>30% pose a fire risk.
• Special precautions should be observed for high-risk procedures where use of an ignition
source is in close proximity to an oxidizer.
• Nitrous oxide supports combustion to the same extent as oxygen.
• Investigate sounds, smells, and noises that could be associated with OR fires.
• In MAC/sedation cases, replace supplemental oxygen with an ETT or supraglottic device if
the patient condition requires >30% oxygen when an ignition source is used.
ALCOHOL ABUSE
BASICS
DESCRIPTION
• Alcohol abuse is a chronic disease with profound societal implications. More than 19% of
cases resulting in deaths of young automobile drivers were related to alcohol. Additionally,
the annual total cost of alcohol-related problems reaches a staggering $180 billion.
• Both acute alcohol intoxication and chronic alcohol abuse can increase anesthetic
complications.
EPIDEMIOLOGY
Prevalence
In the US, the rate of alcohol use disorders, including abuse and dependence, is ~8.26%; this
correlates to ~15 million people.
Morbidity
• In the perioperative period, patients with alcohol abuse have been shown to have an
increased risk of infections, bleeding disorders, need for ventilator support, and cognitive
dysfunction.
• Maternal alcohol consumption during pregnancy can lead to fetal alcohol disorders; 1%
incidence.
Mortality
• Alcohol withdrawal during surgery may be associated with a mortality rate as high as 50%.
• Alcohol use is the third leading cause of preventable death in the US, and accounts for
∼85,000 deaths annually.
• Gender: Men are 5 times more likely than women to develop alcohol abuse.
• Family history: The rate of alcohol abuse is about 30% in men with one alcoholic parent.
• Genetic factors: May affect the process and response to alcohol in the human body
• Cultural factors: The high rate of alcohol abuse in the US and Europe may relate to the
common use and social acceptance of alcohol use.
• Psychiatric disorders: Higher in persons with depression, anxiety, antisocial behaviors, post-
traumatic stress disorder, high self-expectations, or low frustration tolerance
PATHOPHYSIOLOGY
• Alcohol has been shown to affect the following receptors in the human brain:
– GABA: Alcohol binds to the GABA receptor and increases chloride ion movement into the
cell with resultant hyperpolarization (decreases neural activity, by making the cell
membrane potential more negative). Responsible for the sedative and anxiolytic effects
(similar to hypnotic drugs and benzodiazepines).
– Glycine: Alcohol binds to the glycine receptor and potentiates its role as the major
inhibitory neurotransmitter in the spinal cord and brain stem.
– Serotonin: Alcohol increases levels either via increased release and/or decreased
breakdown, as well as potentiates its effects on receptor function. Serotonin may enhance
the release of other neurotransmitters that play a key role in tolerance and contribute to
alcohol withdrawal syndrome (AWS).
– Glutamate: Alcohol decreases glutamate’s excitatory effect on NMDA receptors. Chronic
consumption, however, makes NMDA receptors hypersensitive to glutamate while
desensitizing the GABAergic receptors; believed to play a role in AWS.
– Opiates: Alcohol induces the release of endogenous opioid peptides (can cause euphoria
and blunt the sensation of pain). The body’s endogenous opioid system (enkephalins,
endorphins) is linked with the brain’s reward pathway; may play a role in addiction.
– Dopamine: The increased levels/effects that are seen with alcohol abuse is a poorly
understood mechanism. It has been postulated to result from disinhibition of
dopaminergic neurons, decreased breakdown, and increased release. Dopamine pathways
play a role in reward and reinforcement and may play a role in addiction.
• Alcohol is absorbed directly through the stomach wall (∼20%) and small intestines
(∼80%). The liver functions to break down alcohol.
• Effects on other organs may result from direct inflammation or possibly from “blood
sludging.” Blood sludging describes the clumping of red blood cells with resultant plugging
of small vessels, ischemia, and cell/tissue death distally. The increased pressure can result in
capillaries breaking (red eyes, blotchy skin, “drinker’s nose”).
• Preoperative evaluation should determine concomitant organ dysfunction. A high index of
suspicion for alcohol cardiomyopathy should be present, as this is often underdiagnosed.
• Prevent aspiration in patients with cirrhosis and ascites
• Anticipate prophylaxis and treatment of alcohol withdrawal and delirium tremens
SYMPTOMS
• A high index of suspicion is required to diagnose alcohol abuse.
• Nonspecific, but suggestive, symptoms include gastritis, tremor, and history of falling.
History
• Despite the brief preoperative encounter, a social history including alcohol use should be
elicited. If suspected, consider further focused questioning.
• Alcohol Use Disorders Identification Test (AUDIT) is 92% effective in detecting hazardous or
harmful drinking. A total score of ≥8 indicates harmful drinking behavior. It is also helpful
in identifying those at greatest risk for postoperative complications.
• Inquire about other substances of abuse
Signs/Physical Exam
• Usually nonspecific; abnormalities are usually related to the systemic diseases associated
with chronic use.
• “Drinker’s nose”: A purple nose that results from tiny broken capillaries
MEDICATIONS
No specific medications, unless being treated for abuse.
Labs/Studies
• Glucose: May be low, particularly in diabetics
• CBC with platelets: Anemia
• Liver function tests, PT and aPTT: May be abnormal due to alcoholic hepatitis or cirrhosis.
• EKG: May show left ventricular hypertrophy and arrhythmias.
• CXR: May show aspiration, pleural effusions and cardiomegaly.
• Nervous system: Cerebellar degeneration, tremors, delirium tremens, dementia, depression,
memory loss, Wernicke–Korsakoff syndrome, peripheral neuropathy (burning, numbness,
weakness)
• Cardiovascular: Alcoholic cardiomyopathy, hypertension
• Pulmonary: Aspiration, pleural effusion, and pulmonary hypertension (may occur in end
stage liver disease).
• Hepatic: Alcoholic hepatitis, cirrhosis
• Gastrointestinal: Absorption of B vitamins and other nutrients may be impaired. Gastritis,
ulcers, and increased risk of stomach cancer. Acute and chronic pancreatitis; may eventually
result in diabetes.
• Metabolic: Impairs fat and glucose metabolism in the liver and pancreas. Acute alcohol
ingestion can result in a steep rise in blood sugar that is met by an increased release of
insulin, with resultant hypoglycemia.
• Hematologic: Anemia can result from malnutrition or direct suppression of bone marrow.
• Malnutrition is very common and can lead to anemia (folic acid, vitamin B12 deficiency), or
hypoalbuminemia (low protein intake) and Wernicke–Korsakoff syndrome (vitamin B1
deficiency).
• Other: Sexual dysfunction (decreased testosterone), birth defects, osteoporosis
• Elective surgery should be postponed in patients with acute alcohol toxicity, alcoholic
hepatitis, or decompensated systemic diseases.
• Treatment of alcohol abuse or dependence should be considered before elective surgery in
order to decrease perioperative morbidity and mortality.
• Severe dehydration or electrolyte imbalance should be corrected prior to surgery.
CLASSIFICATIONS
• Alcohol abuse is defined by the following characteristics: Drinking even when it is
dangerous; excessive drinking; legal problems related to drinking; and interpersonal
problems with family, coworkers, and friends because of alcohol use.
• Alcohol dependence (alcoholism) is characterized by: Drinking excessive amount frequently;
the inability to stop drinking despite social, psychiatric, or medical complications; increased
tolerance of alcohol; and the occurrence of alcohol withdrawal symptoms when drinking is
discontinued.
TREATMENT
Premedications
Benzodiazepines are helpful in reducing anxiety and preventing withdrawal.
INTRAOPERATIVE CARE
Regional anesthesia (spinal, epidural, or peripheral nerve blocks) may decrease systemic
effects and CNS disturbance with general anesthesia. It is also easier to monitor mental status
changes in awake patients, especially in those at risk of alcohol withdrawal. In patients with
liver disease, however, coagulopathy may preclude neuraxial techniques.
Monitors
• Invasive monitoring may be considered when alcoholic cardiomyopathy is suspected or
present, and depending upon the surgical procedure.
• Acute alcohol intoxication may reduce anesthetic dose requirement.
• Chronic alcohol abuse may require higher anesthetic doses due to cross-tolerance (e.g.,
increased propofol induction doses). Cirrhotics have an increased volume of distribution
which may necessitate increased doses (but may have increased sensitivity to drugs and
decreased clearance). In alcoholic cardiomyopathy, intravenous induction should be
accomplished by careful titration to avoid hypotension.
• Rapid-sequence induction with cricoid pressure should be considered in patients with
delayed gastric emptying due to ascites. Intoxicated trauma patients are at an increased risk
for aspiration.
Maintenance
• In cirrhotic patients, maintenance doses may need to be decreased due to impaired liver
metabolic function.
• Non-depolarizing muscle relaxants should be cautiously titrated due to impaired hepatic
function.
• “Banana bag” infusion may be considered.
Normal extubation criteria apply; however, alcoholics may have impaired clearance of muscle
relaxants and gastric motility. Ensure full recovery from NMBDs and a protective gag reflex.
FOLLOW-UP
BED ACUITY
• ICU admission may be required if alcohol withdrawal or delirium tremens is suspected.
• Supplemental oxygen should be provided, especially when the patient is receiving narcotics.
COMPLICATIONS
• AWS may be seen in patients who abuse or are dependent on alcohol when they stop
drinking abruptly because of injury, surgery, or acute illness. Typically develops 6–24 hours
after their last drink. Symptoms are related to autonomic hyperactivity and include
sweating, nausea, vomiting, anxiety, agitation, tachycardia, and hand tremor. Neuronal
excitation, including grand mal seizures, usually occurs within 24–48 hours of abstinence.
Delirium tremens is the most intense and serious form of AWS. It is characterized by visual
or auditory hallucinations, confusion, clouding of consciousness, impaired attention, and
pronounced autonomic hyperactivity. It usually appears 2–4 days after the patient’s last use
of alcohol. Death from cardiovascular and respiratory collapse may occur, if untreated.
Prophylaxis is with benzodiazepines. Treatment of AWS involves establishing the diagnosis
and severity with the CIWA-Ar Score and transferring to the ICU. Medical treatment
involves a combination of benzodiazepines, haloperidol, clonidine, and beta-blockers; in
some instances, a drink with meals may be ordered. Supportive care includes the treatment
of nutritional deficiency, hypoglycemia, arrhythmias, congestive heart failure, alcoholic
hepatitis, alcoholic pancreatitis, GI bleeding, and nervous system impairment.
• Postoperative cognitive dysfunction is increased in patients aged 55 years and older after
noncardiac surgery with general anesthesia.
• Increased risk of infections may be due to alteration of T-cell mediated immunity as well as
altered immune response to surgical stress.
REFERENCES
1. Lian J, Cagetti E, Richard W, et al. Altered pharmacology of synaptic and extrasynaptic
GABAA receptors on CA1 hippocampal neurons is consistent with subunit changes in a
model of alcohol withdrawal and dependence. J Pham and Exp Therap. 2004;310(3):1234–
1245.
2. Lovinger DM. Serotonin’s role in alcohol’s effects on the brain. Alcohol Health Res World.
1997;21(2):114–120.
3. Publications from the Institute on Alcohol Abuse and Alcoholism, NIH. www.niaaa.nih.gov.
4. Spies CD, Rommelspacher H. Anesthestic alcohol withdraw in the surgical patients:
Prevention and treatment. Anesth Analg. 1999;88:946–954.
• Alcohol cardiomyopathy
• Pregnancy substance abuse
• Cirrhosis
• Alcohol withdrawal syndrome
CODES
ICD9
• 303.90 Other and unspecified alcohol dependence, unspecified
• 305.00 Alcohol abuse, unspecified
• 305.01 Alcohol abuse, continuous
ICD10
• F10.10 Alcohol abuse, uncomplicated
• F10.129 Alcohol abuse with intoxication, unspecified
• F10.20 Alcohol dependence, uncomplicated
CLINICAL PEARLS
AUDIT (Alcohol Use Disorders Identification Test) utilizes 10 questions; scoring is on a scale
of 0–4 per question. A total score of ≥8 indicates alcohol abuse or dependence. (Note: A unit
is equal to one small glass of wine, a single purchased measure of spirits or half a pint of
beer.) The questions include:
• How often do you have a drink containing alcohol?
• How many units of alcohol do you drink on a typical day when you are drinking?
• How often do you have 6 or more units of alcohol on one occasion?
• How often during the last year have you found that you were not able to stop drinking once
you had started?
• How often during the last year have you failed to do what was normally expected from you
because of drinking?
• How often during the last year have you needed a first drink in the morning to get yourself
going after a heavy drinking session?
• How often during the last year have you had a feeling of guilt or remorse after drinking?
• How often during the last year have you been unable to remember what happened the night
before because you had been drinking?
• Have you or someone else been injured as a result of your drinking?
• Has a relative or friend or doctor or another health worker been concerned about your
drinking or suggested you should cut down?
ALCOHOL WITHDRAWAL SYNDROME
Martin M. Stechert, MD
Christopher G. Choukalas, MD, MS
BASICS
DESCRIPTION
• Alcohol withdrawal syndrome (AWS) develops after the cessation of chronic alcohol
use/abuse, generally within 6–48 hours. Alcohol abuse is characterized by impaired control
over drinking, preoccupation with alcohol, use of alcohol despite adverse consequences, and
denial.
• AWS exists as a spectrum of presentations:
– Mild: Cravings and psychomotor agitation
– Severe: Hallucinations, autonomic instability (sweating, tachycardia, hypertension), fever,
and disorientation. This constellation of symptoms is known as delirium tremens (DT).
• If withdrawal symptoms are not present within a week after the last alcohol consumption,
future development is unlikely.
EPIDEMIOLOGY
Prevalence
In general, outpatient estimates are between 4% and 15%, whereas 15–40% of all inpatients
are thought to have abuse or withdrawal. Of those who experience withdrawal symptoms, 5%
have severe symptoms characterized as DT.
Morbidity
• AWS: Dysrhythmias, myocardial ischemia, delirium, and seizures
• Chronic alcohol abuse: Immunosuppression, wound infections, malnutrition, and the
complications of cirrhosis and liver failure
Mortality
• Has decreased over time; historical estimates from severe AWS or DT reached levels as high
as 40%, but the current rate is probably under 5%.
• Results from dysrhythmia, aspiration pneumonia, or underlying illness that may have been
the cause of alcohol cessation in the first place (e.g., infection, pancreatitis, etc.).
• Alcohol use and abuse are obvious risk factors for developing AWS. Use and abuse are
associated with a number of demographic characteristics, including:
– Male sex
– Lower socioeconomic status
– White or Native American ethnicity
– Certain psychiatric conditions (e.g., depression, anxiety disorders)
• Risk factors for the development of DT include:
– Previous history of DT
– Presence of AWS despite elevated level of blood alcohol
– History of sustained drinking
• The pathophysiology of AWS is probably related to the neurophysiologic changes thought to
be caused by chronic alcohol use. Although the functional consequence of receptor-
mediated effects of alcohol remain to be elucidated, ingested ethanol has a number of
receptor targets:
– NMDA-related transmission is reduced.
– GABA function is enhanced.
– Glycine transmission (complex and location specific) are enhanced
– Cholinergic and serotonergic activities are enhanced.
• In order to maintain a normal arousal state, an adaptive response to chronic alcohol
exposure yields decreased GABAA sensitivity and increased NMDA sensitivity. When ethanol
is acutely withdrawn, reduced central inhibition (via GABAA) and aberrant activation of
excitatory NMDA receptors appear to be responsible for the acute withdrawal symptoms,
including altered mental state and noradrenergic overdrive during AWS.
• Prevention of AWS is a crucial aspect of treatment in the clinical arena, whereas public
health efforts to curb alcohol abuse are necessary to prevent AWS on a societal level.
• Perioperatively, prevention of AWS starts with an early identification of patients at risk for
this condition.
– The duration of potential abstinence from alcohol should be discussed with the primary
care physician and the patient, and possible management solutions must be negotiated
with the patient.
– Nutrition including multivitamin administration should be optimized preoperatively.
– Optimal medical management can be organized according to the degree of risk going into
withdrawal, including additional invasive monitoring intraoperatively and appropriate
designation (ICU, TCU) postoperatively.
– Long-acting benzodiazepines (e.g., chlordiazepoxide) administered preoperatively may
reduce the severity of AWS.
• AWS is a clinical diagnosis and requires a detailed history and physical examination.
– Key elements of the history include chronic alcohol use, recent cessation, and determining
whether cessation was caused by some other illness.
– Screening tools like the PAT (Paddington Alcohol Test) and AUDIT (Alcohol Use Disorders
Identification Test) questionnaires can identify patients at risk for AWS.
• Clinical manifestations of alcohol withdrawal often follow a timely schedule after the last
consumption of alcohol:
– Early symptoms, including anxiety, tremulousness, palpitations, nausea, anorexia,
typically begin after 6–8 hours.
– Generalized seizures typically occur after 6–48 hours.
– Alcoholic hallucinations after 12–48 hours
– Delirium tremens after 48–96 hours
• The latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR)
provides more precise diagnostic criteria that can be summarized as 2 or more of the
following signs and symptoms occurring (1) in the context of cessation or reduction of
previously heavy alcohol use and (2) not due to some other medical or mental disorder:
– Sweating or tachycardia
– Hand tremor
– Insomnia
– Nausea or vomiting
– Hallucinations
– Agitation
– Anxiety
– Generalized tonic–clonic seizure
• It is important to note that in an anesthetized patient, symptoms may be obscured and
limited to sympathetic surge (i.e., tachycardia, hypertension).
• Other causes of agitation and tremor, including caffeine overdose, cocaine and other
stimulant use, as well as withdrawal from nicotine, illicit drugs, and medications (e.g.,
clonidine)
• Other causes of hallucinations such as psychotic disorders, acute intoxication, sleep
withdrawal, and drug side effects
• Other causes of seizures such as metabolic or electrolyte derangements, intracranial
pathology, meningitis, or underlying seizure disorder
• Other hyper-metabolic syndromes that can mimic DT, such as malignant hyperthermia,
thyroid storm, neuroleptic malignant syndrome, and serotonin syndrome
TREATMENT
• Essential elements of therapy include:

– Excluding alternate diagnoses (see above)
– Seizure prophylaxis
– Correcting metabolic and hemodynamic derangements
– Treating symptoms such as anxiety and hallucinations
– Managing complications (e.g., aspiration pneumonia and malnutrition)
– Appropriate monitoring
• Benzodiazepines bind to GABA receptors and are cross-tolerant with alcohol; they remain
the cornerstone of treatment for AWS. They are effective at reducing anxiety, agitation, and
the incidence of seizures; and they often reduce tachycardia and hypertension. They can
also be dosed prophylactically, in a scheduled fashion, or in response to symptom severity.
The latter has been associated with decreased complications and lower doses of
administered drug.
• Propofol in intubated, mechanically ventilated patients produces results similar to those of
benzodiazepines (e.g., anxiolysis, seizure prophylaxis, etc.). Patients receiving propofol
rarely need additional benzodiazepines to treat agitation or seizures associated with AWS.
• Other agents have been used, but none have completely replaced benzodiazepines:
– Antipsychotics, such as haloperidol or quetiapine, may reduce agitation and hallucinations
but may also reduce the seizure threshold.
– Antiepileptics, such as carbamazepine, may decrease the development of seizures but have
little effect on the other manifestations of AWS.
– Intravenous infusion of ethanol can precipitate a metabolic acidosis.
– Alternative sedatives, such as clonidine and dexmedetomidine, almost certainly reduce
benzodiazepine requirements but provide no seizure prophylaxis. Dexmedetomidine
reduces ICU delirium and may reduce delirium associated with AWS.
• The Clinical Institute for Withdrawal Assessment (CIWA) provides a symptom-driven dosing
scheme that calculates a score based upon signs and symptoms of withdrawal (e.g., tremor,
sweats, delirium). Higher scores signify more severe withdrawal and would trigger
administration of benzodiazepine.
• Bed acuity: The appropriate level of monitoring for patients with AWS has never been
defined. The frequent assessments required suggest that general ward care may be
inadequate. Additionally, managing hemodynamic abnormalities requires active monitoring
of hemodynamics, such as in a telemetry, step-down, or ICU unit. The presence of the
following may necessitate ICU care:
– Coexisting cardiac, pulmonary, or renal disease
– Having a history of or being at high risk for DTs
– Requiring propofol or a continuous infusion of sedatives to control symptoms during past
admissions
• Thiamine deficiency: Common in patients who abuse alcohol. Thiamine is critical in order to
avoid Wernicke’s encephalopathy, and must be administered prior to initiating glucose or
nutritional therapy. Further treatment should target specific nutritional deficiencies
identified by serology.
REFERENCES
1. Tetrault JM, O’Connor PG. Substance abuse and withdrawal in the critical care setting. Crit
Care Clin. 2008;24:767–788.
2. De Wit M, Jones DG, Sessler CN, et al. Alcohol-use disorders in the critically ill patient.
Chest. 2010;138(4):994–1003.
3. Kosten TR, O’Connor PG. Management of drug and alcohol withdrawal. N Engl J Med.
2003;348:1786–1795.
ADDITIONAL READING
• Spanagel R. Alcoholism: A systems approach from molecular physiology to addictive
behavior. Physiol Rev. 2009;89:649–705.
• Sullivan JT, Sykora K, Schneiderman J, et al. Assessment of alcohol withdrawal: The revised
clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Brit J Addict.
1989;84:1353–1357.
• Alcohol abuse
CODES
ICD9
291.81 Alcohol withdrawal
ICD10
F10.239 Alcohol dependence with withdrawal, unspecified
CLINICAL PEARLS
• Cessation of receptor-mediated activity during alcohol abstinence is likely at the root of
AWS. It may be that chronic exposure to ethanol decreases sensitivity of GABA receptors,
and that cessation reduces GABA output, leading to a state of generalized CNS arousal.
• Seizure may be an early symptom of AWS (“rum-fit”) which can occur as early as 2 hours
after the last consumption of ethanol.
• Alcohol-dependent, ambulatory patients may never exhibit AWS syndromes during the
hospital stay.
• Whenever AWS is suspected, thiamine should be given intravenously. The administration of
glucose in thiamine deficiency can precipitate Wernicke’s encephalopathy.
ALCOHOLIC CARDIOMYOPATHY
BASICS
DESCRIPTION
• Alcoholic cardiomyopathy (ACM) is classified as a non-ischemic, dilated cardiomyopathy
(CM) that results from exposure to a myocardial toxin.
• ACM shares common characteristics with all dilated CMs (depending on the clinical stage of
the disease progression):
– Dilated chambers
– Diastolic dysfunction (asymptomatic stage)
– Left ventricular dysfunction (symptomatic stage)
– Left ventricular hypertrophy (asymptomatic stage; followed by wall thinning in
symptomatic stage)
• Diagnosis is clinically based upon a history of significant chronic alcohol exposure in
conjunction with the exclusion of other causes of dilated CM.
• Epidemiology of ACM:
– Second most common cause of dilated CM (4% of all CMs)
– Prevalence in Western countries is variable, but ranges from 20% to 40% of all non-
ischemic dilated CMs.
– Significantly more prevalent in men (approximately 15% prevalence in women)
– The incidence of dilated CM is much higher in chronic alcoholics than in the total
population.
– The 5-year incidence ranges from 20% to 26% in chronic alcoholics.
• Amount and duration of alcohol exposure:
– Studies have demonstrated variability and a lack of a specific linear relationship between
the amount and duration of alcohol exposure and the development of asymptomatic and
symptomatic ACM (1,2,3).
– Studies have shown changes in cardiac structure and function consistent with ACM in
patients with a history of consuming >90 g/day of alcohol for >5 years (one drink
contains approximately 12 g of alcohol). Studies in patients with symptomatic ACM have
shown a history of longer durations of drinking (>10 years) (4,5).
– Despite the correlation between chronic heavy drinking and the development of ACM, not
all heavy drinkers will progress to ACM.
– Although there may be other variables responsible for the occurrence of heart failure in
alcoholics, the duration of heavy daily alcohol use is the most reliable predictor for the
development of ACM.
PHYSIOLOGY
• Myocardial wall tension is closely related to myocardial oxygen consumption.
– Left ventricle wall tension (T) is a function of the change in pressure (ΔP), left ventricle
radius (R), and left ventricle wall thickness (h). It can be described by the law of Laplace:
T = (ΔP × R)/2h.
– ΔP reflects the afterload that the left ventricle must pump against (directly related)
– Radius is a function of preload (left ventricular end-diastolic volume) (directly related).
– Wall thickness is a function of the number of myoctes (inversely related)
– Although not intrinsically contained within the equation, heart rate also is a determinant
of myocardial oxygen; it determines the number of times that tension needs to be
generated.
• The left ventricle is ellipsoid and facilitates low wall tension
• The pathophysiology is not completely understood, despite a large number of studies.
Animal studies have demonstrated characteristic histologic and cellular changes associated
with chronic alcohol exposure, including (1):
– Myocyte death
– Intracellular organelle dysfunction
– Interference of contractile protein function
– Abnormalities of calcium homeostasis
– Generation of reactive oxygen species (ROS)
– Changes in neurohormonal systems (sympathetic, renin-angiotensin, natriuretic peptide)
– Individual variations in the development of myocardial toxicity from alcohol suggest that
other variables including genetic or environmental factors may play a role.
• Clinical presentation: ACM presents in stages and can progress from asymptomatic to
symptomatic.
– Asymptomatic stage: Studies have demonstrated that in the early preclinical stage of ACM,
LV remodeling occurs in the form of LV dilation (increased end-diastolic and systolic
dimensions), increased LV mass, and LV hypertrophy (increased septal thickening).
Echocardiographic studies have demonstrated that diastolic dysfunction (impaired early
diastolic filling of the LV) appears to be an early feature of asymptomatic ACM, regardless
of LV mass and the presence of hypertension. Early ACM is often associated with a normal
LV ejection fraction (EF) (3,4,5,6).
– Symptomatic stage: Characterized by progressive increases in LV dilation and LV mass, as
well as the occurrence of systolic dysfunction with a decreased EF. Studies have
demonstrated significantly greater LV end-diastolic and systolic dimensions in
symptomatic ACM patients when compared to asymptomatic ACM patients (2,7).
• Tension: Dilated cardiomyopathy results in a more spherical left ventricle with subsequent
increases in wall stress (radius is increased). In the asymptomatic stage, the myocardial wall
hypertrophies and can decrease wall tension. However, in symptomatic stages, wall
thickness decreases with resultant increases in wall tension (and myocardial oxygen
demand).
• Diagnosis is clinically based upon having a history of significant alcohol consumption after
ruling out other causes of dilated CM.
– History: After excluding other causes of dilated CM, the most important factor for
diagnosis is a chronic history of heavy alcohol use.
– Symptoms/physical exam: Signs and symptoms of heart failure may be noted in patients
with symptomatic disease.
– EKG abnormalities are common and include nonspecific ST and T wave changes, QT
prolongation, and atrial arrhythmias including atrial fibrillation.
– Echocardiography allows for a noninvasive delineation of the LV chamber size, diastolic
function, and systolic function.
– There are no specific pathologic or immunologic tests for the diagnosis of ACM.
• Natural history and treatment
– Although the amount of alcohol required to cause progression of asymptomatic ACM to
overt heart failure appears variable, studies clearly show that decreases in systolic
function are significantly related to the amount and duration of alcohol consumption (1).
– Partial to complete regression of the pathologic cardiac changes associated with ACM may
occur in some patients with abstinence alone.
– LV function in ACM patients may improve with standard medical therapy for dilated CM
(diuretics, cardiac glycosides, ACE inhibitors, and beta blockade), although no therapies
specific for ACM have been studied or described. Despite improvements in the LV
function, survival is not improved in patients who continue to drink. The most important
factor impacting survival in symptomatic patients receiving medical therapy is abstinence
from further drinking.
• Chronic alcoholism results in a significantly higher incidence of postoperative cardiac
complications, hypoxemia, and infections.
• The anesthesia provider should maintain an appropriate index of suspicion for the presence
of ACM in patients with a history of chronic alcohol use. The presence of ACM can have
worsened and even deleterious effects during the perioperative period. Even asymptomatic
patients can have a limited cardiac reserve when exposed to severe perioperative stress that
occurs with major surgery, trauma, or shock. Preoperative cardiac evaluation, including
echocardiography, should be considered for risk-stratification and determination of the need
for medical therapy for prospective surgical patients with a history of chronic alcohol use.
• Alcoholics presenting for emergency surgery may be acutely intoxicated or at risk for
alcohol withdrawal syndrome, both of which can adversely affect a patient with ACM (8).
REFERENCES
1. Piano MR. Alcoholic cardiomyopathy: Incidence, clinical characteristics, and
pathophysiology. Chest. 2002;121:1638–1650.
2. Fernandez-Sola J. Diastolic function impairment in alcoholics. Alcohol Clin Exp Med.
2000;24:1830–1835.
3. Fauchier L. Comparison of long-term outcome of alcoholic and idiopathic dilated
cardiomyopathy. Eur Heart J. 2000;21:306–314.
4. Kupari M. Left ventricular filling impairment in asymptomatic chronic alcoholics. Am J
Cardiol. 1990;66:1473–1477.
5. Lazarevic AM. Early changes in left ventricular function in chronic asymptomatic
alcoholics: Relation to the duration of heavy drinking. J Am Coll Cardiol. 2000;35:1599–
1606.
6. McKenna CJ. Alcohol consumption idiopathic dilated cardiomyopathy: A case control
study. Am Heart J. 1998;135:833–837.
7. Mathews EC. Echocardiogrphic abnormalities in chronic alcoholics with and without overt
congestive heart failure. Am J Cardio. 1981;47:570–578.
8. Spies C. Perioperative morbidity and mortality in chronic alcoholic patients. Alcohol Clin
Exp Res. 2001;25:164S–170S.
ADDITIONAL READING
• Laonigro I. Alcohol abuse and heart failure. Eur J Heart Failure. 2009;11:453–462.
• Spies CD. Effects of alcohol on the heart. Curr Opin Crit Care. 2001;7:337–343.
• Congestive heart failure
• Alcohol abuse
CODES
ICD9
425.5 Alcoholic cardiomyopathy
ICD10
I42.6 Alcoholic cardiomyopathy
CLINICAL PEARLS
• ACM is a type of dilated CM that is diagnosed clinically, based on a history of significant
chronic alcohol exposure in conjunction with the exclusion of other causes of dilated CM.
• The duration of heavy daily alcohol use is the most reliable predictor for the development of
ACM.
• The most important factor impacting survival in ACM patients is abstinence from further
drinking; medical therapy does not improve survival in patients who continue to drink
alcohol.
• The presence of ACM in the surgical patient can have deleterious effects; the anesthesia
provider should maintain an appropriate index of suspicion for the presence of ACM in
patients with a history of chronic alcohol use.
ALDOSTERONE
Joe C. Hong, MD
BASICS
DESCRIPTION
• Aldosterone is a steroid hormone in the mineralocorticoid family that plays a vital role in
the maintenance of intravascular volume status and sodium balance.
• Aldosterone is synthesized and secreted by the zona glomerulosa of the adrenal cortex in
response to low intravascular volume, decreased renal perfusion, hyperkalemia, and
acidosis.
• Disease states include Addison disease (hypoaldosteronism) and Conn syndrome
(hyperaldosteronism).
• Aldosterone is synthesized from cholesterol within the adrenal cortex by a series of
steroidogenic reactions catalyzed by enzymes of the cytochrome p450 family. It is a steroid
hormone that exerts its action by binding to an intracellular cytoplasmic receptor. This
bound complex enters the cell nucleus and stimulates DNA transcription, resulting in
protein production that mediates the ultimate effects of aldosterone.
• Renin–angiotensin system (RAS) regulation: Aldosterone secretion is regulated primarily by
RAS via the following mechanism:
– Intravascular volume depletion triggers a decrease in renal perfusion pressure.
– Renin is secreted by the juxtaglomerular cells of the afferent arteriole in response to this
decrease in renal perfusion pressure.
– Renin catalyzes the conversion of angiotensinogen to angiotensin I in plasma.
– Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to
angiotensin II, primarily in the lungs.
– Angiotensin II stimulates the synthesis and secretion of aldosterone.
• Adrenocorticotropic hormone (ACTH): Aldosterone is also under tonic control by ACTH
(secreted by the anterior pituitary gland).
• Aldosterone hormone regulates volume and blood pressure via:
– Binding to mineralocorticoid receptors located in the principal cells of nephrons. This
upregulates sodium/potassium pumps with resultant sodium and water reabsorption and
potassium sercetion by the distal tubules and collecting ducts. The net effect is the
restoration of intravascular volume and blood pressure.
– Acting on alpha-intercalated cells of the late distal tubule and collecting duct, resulting in
increased renal hydrogen ion secretion.
ANATOMY
• Aldosterone is produced by cells within the zona glomerulosa of the adrenal cortex.
• The adrenal gland is composed of the inner medulla which produces catecholamines and the
outer cortex which is divided into 3 histologic zones. Going from outside and moving
inwards:
– The outermost zona glomerulosa is the source of aldosterone production.
– Just beneath is the zona fasciculata, the source of glucocorticoid production.
– The inner-most layer of the cortex is the zona reticularis, responsible for the production of
androgens.
• Primary adrenocortical insufficiency (Addison disease)—a hypoaldosterone state:
– Most common cause is autoimmune destruction of the adrenal cortex, resulting in acute
adrenal crisis (1). Other causes of adrenocortical insufficiency include metastatic disease
to the adrenal cortex, adrenal hemorrhage, infection of the adrenal gland (tuberculosis,
opportunistic infections with HIV, fungemia), and amyloid infiltration.
– Characterized by elevated ACTH levels but decreased levels of glucocorticoids and
mineralocorticoids
– Clinical features are related to the adrenocortical hormone deficiency. Hypoglycemia is
caused by cortisol deficiency. Hypotension, hyperkalemia, metabolic acidosis, and volume
contraction are caused by aldosterone deficiency. Hyperpigmentation is caused by
elevated ACTH secretion. Other signs and symptoms include weakness, fatigue, lethargy,
anorexia, nausea, abdominal pain, prerenal azotemia, hypercalcemia, convulsions, fever,
and syncope.
– Treatment: Replacement of glucocorticoids (hydrocortisone, prednisone,
methylprednisolone) and mineralocorticoids (fludrocortisone)
• Secondary adrenocortical insufficiency is caused by decreased ACTH secretion, resulting
primarily in a glucocorticoid deficiency. Mineralocorticoid deficiency is also seen but to a
lesser degree.
– Most common cause of secondary adrenocortical insufficiency is sudden withdrawal of
long-term corticosteroid therapy (2). Other causes include pituitary tumor, pituitary
surgery or radiation, postpartum hypopituitarism (Sheehan syndrome), and sarcoid
infiltration of the pituitary gland.
– Chronic corticosteroid therapy suppresses the hypothalamus and anterior pituitary,
resulting in decreased production of corticotropin-releasing hormone (CRH) and ACTH,
respectively. Decreased levels of CRH and ACTH cause atrophy of the zona fasciculata,
resulting in glucocorticoid deficiency. During times of physiologic stress, the patient is
unable to acutely increase cortisol production, resulting in acute secondary adrenocortical
deficiency.
• Primary hyperaldosteronism is caused by aldosterone-secreting tumors.
– Conn syndrome (aldosterone-secreting adrenocortical adenoma) is the most common
cause. Bilateral adrenal hyperplasia occurs less commonly.
– Characterized by hypertension, hypokalemia, metabolic alkalosis, and a low renin state.
Other signs and symptoms include tetany, polyuria, and an inability to concentrate urine.
– Primary hyperaldosteronism may be present in 0.5–1% of patients with hypertension (3).
– Treatment: Medically by spironolactone (aldosterone receptor antagonist), surgically with
adrenalectomy
• Hypoaldosterone states:
– Patients with adrenocortical insufficiency should continue their mineralocorticoid and
glucocorticoid replacement therapy up until their time of surgery. Clinical features of
overt hypoaldosteronism include hyperkalemia, hyponatremia, acidosis, and myocardial
conduction defects. Administration of mineralocorticoids (fludrocortisone 0.05–0.1 mg/d)
should occur preoperatively (1). Doses must be carefully titrated to avoid hypertension.
– Additional perioperative stress dose of glucocorticoids may be necessary since these
patients may not be able to mount an adequate stress response. The traditional
recommendation is 200 mg hydrocortisone per 70 kg body weight per day. However,
smaller doses of 100 mg per 70 kg body weight per day have been used with success (2).
– The amount of perioperative hydrocortisone is based on the anticipated stress of the
procedure. The relative degree of trauma and depth of anesthesia should be considered.
• Hyperaldosterone states:
– Patients presenting for elective surgery should be medically optimized in terms of their
adrenocortical disorder. Preoperative EKG, glucose, and serum electrolytes (particularly
sodium and potassium) should be checked. Volume status and blood pressure should be
optimized.
– Primary aldosteronism (Conn syndrome) should be suspected in patients who present with
concurrent hypertension and hypokalemia, severe refractory hypertension, adrenal
incidentaloma and hypertension, or onset of hypertension at a young age.
– Antihypertensive medications (e.g., spironolactone) should be maintained up to the time
of surgery. Careful cardiac assessment is necessary because these patients have increased
cardiac comorbidity. Serum sodium and especially serum potassium should be checked
prior to surgery. Hypokalemia is common. Severely hypokalemic patients should have
their potassium replaced preoperatively.
REFERENCES
1. Dorin RI, Qualis CR, Crapo LM. Diagnosis of adrenal insufficiency. Ann Intern Med.
2003;139:194–204.
2. Symreng T, Karlberg BE, Kagedal B, et al. Physiological cortisol substitution of long-term
steroid-treated patients undergoing major surgery. Br J Anaesth. 1981;53:949–954.
3. Young WF Jr. Adrenal causes of hypertension: Pheochromocytoma and primary
aldosteronism. Rev Endocr Metab Disord. 2007;8:309–320.
ADDITIONAL READING
disorders. Int Anesthesiol Clin. 2000;38:31–67.
• Lampe GH, Roizen MF. Anesthesia for patients with abnormal function of the adrenal cortex.
Anesthesiol Clin North Am. 1987;5:245–268.
• Udelsman R, Ramp J, Gallucci WT, et al. Adaptation during surgical stress: A reevaluation of
the role of glucocorticoids. J Clin Invest. 1986;77:1377–1381.
• Cortisol
• Acute adrenal insufficiency
CLINICAL PEARLS
• Patients with adrenocortical insufficiency have deficiencies in both mineralocorticoids and
glucocorticoids. Hydrocortisone has both glucocorticoid and mineralocorticoid activity.
Therefore, it is an ideal agent to use for the management of adrenocortical insufficiency.
• Patients with aldosterone deficiency should continue their fludrocortisone up until the time
of surgery. Hypokalemic acidosis or hypovolemia must be treated preoperatively.
Supplementation of mineralocorticoids (fludrocortisone 0.05–0.1 mg/d) should occur
preoperatively. Doses must be carefully titrated to avoid hypertension.
• Primary hyperaldosteronism (Conn syndrome) should be suspected in patients who present
with concurrent hypertension and hypokalemia, severe refractory hypertension, adrenal
incidentaloma and hypertension, or onset of hypertension at a young age.
ALVEOLAR ARTERIAL GRADIENT AND RATIO
Sharanya Nama, MD
Michael Mangione, MD
BASICS
DESCRIPTION
• The alveolar–arterial gradient and ratio provide a useful, objective means to determine how
effectively oxygen from the alveolus moves into the pulmonary circulation. It aids with:
– Identifying increases in venous admixtures, even in the presence of increased inspired
oxygen concentrations
– Monitoring improvement or worsening of the venous admixture
– Assessing effectiveness of treatment and interventions
– Differentiating between causes of hypoxia (impaired uptake vs. decreased alveolar oxygen
availability)
• Definitions:
– PAO2 = alveolar PO2. It is determined by the alveolar gas equation and is calculated as
follows: PAO2 = [FiO2 × (Patm – PH2O) – (PaCO2/0.8)]; measured in units of mm Hg.
– PaO2 = arterial PO2. It is determined by direct arterial blood gas values and is measured
in units of mm Hg. Small amounts of oxygen are dissolved in the plasma, which are in
equilibrium with the oxygen bound to hemoglobin. Thus, a decrease in arterial oxygen
content would reflect a decrease in hemoglobin binding and decreased oxygen saturation.
• A-a gradient: The difference between the alveolar and arterial partial pressure of oxygen
– Normal adult values in nonsmokers are <15 mm Hg on room air (FiO2 = 0.21) (1). For
example, a patient with a PAO2 = 100 mm Hg and a PaO2 = 93 mm Hg has an A-a
gradient of 7.
– Higher FIO2 values result in an increased A-a gradient. For every 10% increase in FiO2,
the A-a gradient increases by 5–7 mm Hg. This effect is caused by the loss of regional
hypoxic vasoconstriction in the lungs (2).
• Advancing age: Results in a steady rise in the A-a gradient (3); PaO2 predicted = 109 – (0.4
× age in years). For example, a 60-year-old breathing room air would have an average A-a
gradient of 14 mm Hg. In comparison, someone below the age of 40 would have a gradient
of 7 mm Hg (3).
• A-a gradient: The arterial oxygen concentration divided by the alveolar oxygen
concentration. This value is useful in predicting the change in PaO2 when the FIO2 also
changes since it is relatively unaffected by varying oxygen levels (4).
– The normal a/A PO2 ratio is 0.74–0.77 when breathing room air (FIO2 = 0.21). It only
increases to 0.80–0.82 when breathing 100% oxygen (5).
• Physiologic shunting and normal venous admixture
– The thebesian veins drain venous blood from all 4 walls of the myocardium (mostly right
atrium) and empty into the left atrium.
– Deep bronchial veins drain venous blood from the bronchi and roots of the lungs and
empty into the pulmonary veins (deoxygenated blood that returns to the left atrium).
– Venous blood from these areas does not enter the pulmonary circulation; instead, it
returns to the systemic circulation without becoming oxygenated. This accounts for a total
of 2–5% of cardiac output, and the mixing of oxygenated and deoxygenated blood is
known as venous admixture.
– This normal venous admixture accounts for the 10–15 mm Hg A-a gradient and the 0.74–
0.77 a/A ratio that is considered normal.
• Hypoxic pulmonary vasoconstriction describes a physiologic phenomenon in which the
pulmonary arterioles constrict in the presence of low oxygen tension in the alveoli (e.g.,
atelectasis).
– This vessel constriction results in re-directing blood flow to well-oxygenated lung units
and away from poorly oxygenated lung units to ultimately improve ventilation-perfusion
(V/Q) matching.
– When a patient is given supplemental oxygen, more alveoli become well-oxygenated;
however, it also, in turn, decreases hypoxic vasoconstriction.
– This increase in V/Q mismatch leads to more deoxygenated blood entering the systemic
circulatory system and in turn increases the A-a gradient.
ANATOMY
• Alveolus
– Air sac that is lined with a thin membrane consisting of epithelium with collagen and
elastin
– Gas exchange occurs across this membrane where gases move down a concentration
gradient between alveolus and pulmonary capillary.
• Pulmonary circulation
– Consists of blood vessels that carry deoxygenated blood to the site of gas exchange
• Pulmonary capillaries
– Consists of a single layer of squamous epithelium surrounded by a basement membrane
– Gases must diffuse across these layers to enter circulation.
• Hypoxia with increased A-a gradient and a/A ratio: Results from an increase in the venous
admixture secondary to blood passing through the lung without being properly oxygenated
(in addition to the physiologic admixture). Examples of this include:
– V/Q mismatch: Discrepancy between the alveolar ventilation and capillary perfusion
– Pulmonary shunt: Perfusion of the alveolar unit without ventilation, due to pathologic
processes. Atelectasis describes alveolar deflation or fluid collection of the alveolar unit.
Deflation can result from airway obstruction, mucus or blood plugging, inadequate tidal
volumes due to pain, or positioning changes; other causes include endobronchial
intubation, pneumothorax, collapse of emphysematous blebs, and one lung ventilation (6).
Fluid collection can result from pulmonary edema, pneumonia, or adult respiratory
distress syndrome (ARDS).
– Intracardiac shunt: Venous blood is diverted from the pulmonary circulation directly into
the systemic circulation. Examples include atrial or septal defects, pulmonary
atrioventricular (AV) malformations, and cyanotic congenital heart disease.
– Diffusion defects: Observed when the alveolar oxygen and carbon dioxide tensions are
normal, but oxygen uptake by the alveolar capillaries is abnormal or impaired. Examples
include pulmonary fibrosis, interstitial lung inflammation, and interstitial edema.
• Hypoxia with normal A-a gradient or a/A ratio: Can be seen in situations where the alveolar
oxygen (or carbon dioxide) is affected, but oxygen uptake by the capillaries is not impaired.
The decreased arterial oxygen concentration reflects the decreased alveolar concentration.
– Hypoxic delivery: Anesthesia machine or ventilator malfunction, or high altitude
– Hypoventilation: Respiratory depression from drugs, stroke in the pontine area,
respiratory muscle fatigue (such as myasthenia gravis), or obesity–hypoventilation
syndrome. The increase in carbon dioxide decreases the oxygen partial pressure
(concentration) within the alveoli.
• Assessing the A-a gradient or ratio can:
– Differentiate between hypoxia secondary to low alveolar oxygen tension or due to increase
in venous admixture from underlying pathology
– Provide an objective means to trend venous admixtures and, hence, assess pulmonary
processes
– Assess the effectiveness of treatment and interventions such as positive end expiratory
pressures (PEEP)
– The A-a gradient is directly proportional to shunt while being inversely proportional to the
mixed venous oxygen tension.
– Pulse oximetry only provides an assessment of hemoglobin binding. As oxygen saturation
reaches the high 90’s, it can no longer be a reliable marker for arterial oxygen content.
Therefore, pulse oximetry cannot aid with assessing the severity of the A-a gradient in a
given disease state. For example, patients A and B both have ARDS. Patient A is on 50%
FiO2; his PAO2 is 350 mm Hg and his PaO2 is 120 mm Hg resulting in an A-a gradient of
230 mm Hg and SpO2 of 99%. Patient B also has ARDS and is on 50% FiO2; his PAO2 is
350 mm Hg and his PaO2 is 320 mm Hg resulting in an A-a gradient of 30 and SpO2 of
99%. Therefore, it is not possible to assess the status of the underlying pathology with
higher supplemental oxygen based on oxygen saturation alone; one must obtain a blood
gas and calculate the A-a gradient.
– Assessing a/A ratio: In patients receiving higher or changing FiO2, the ratio can provide a
more consistent value that allows for comparison. Additionally, it has been shown to be
more reliable than the A-a gradient in hemodynamically stable patients (7).
– Perioperative conditions: The functional residual capacity (FRC) is decreased by several
factors that ultimately increase the venous admixture, A-a gradient, and a/A ratio.
General anesthesia
Positioning (supine, prone or steep Trendelenburg position)
Surgical procedure (laparoscopy, abdominal retractors)
Patient (obesity, pregnancy, ascites) (8)
• Maneuvers and techniques to improve lung oxygenation can be assessed objectively by
calculating the A-a gradient or a/A ratio.
– Pulmonary edema may be treated by optimizing preload (diuresis, venodilators) and
afterload (vasodilators) to increase inotropy.
– Ventilator adjustments such as PEEP, adjusting rate, volume, I:E ratios, and lung
recruitment maneuvers
– Surgical maneuvers such as decreasing the insufflation pressures during laparoscopy or
retractor tension
– Positioning changes: Elevating the head of the bed can shift the abdominal contents away
from the diaphragm and allow for increased lung expansion.
EQUATIONS
• A-a gradient = PAO2 – PaO2
• a/A ratio = PaO2/PAO2
• PAO2 = [FiO2 × (Patm – PH2O) – (PaCO2/0.8)]
• On room air (21%) at sea level, a simplified version: A-a gradient = [(150 – 5)/4(PCO2)] –
PaO2
• Normal A-a gradient ∼ (age +10)/4
REFERENCES
1. Mellemgaard K. The alveolar–arterial oxygen difference: Its size and components in normal
man. Acta Physiol Scand. 1966;67(1):10–20.
2. Williams AJ. ABC of oxygen: Assessing and interpreting arterial blood gases and acid-base
balance. BMJ. 1998;317(7167):1213–1216.
3. Kanber GJ, King FW, Eshchar YR, et al. The alveolar–arterial oxygen gradient in young and
elderly men during air and oxygen breathing. Am Rev Respir Dis. 1968;97(3):376–381.
4. Peris LV, Boix JH, Salom JV, et al. Clinical use of the arterial/alveolar oxygen tension
ratio. Crit Care Med. 1983;11(11):888–891.
5. Gilbert R, Kreighley JF. The arterial/alveolar oxygen tension ratio: An index of gas
exchange applicable to varying inspired oxygen concentrations. Am Rev Respir Dis.
1974;109:142–145.
6. Thurlbeck WM, Müller NL. Emphysema: Definition, imaging, and quantification. Am J
Roentgenol. 1994;163:1017–1025.
7. Gilbert R, Auchincloss JH Jr, Kuppinger M, et al. Stability of the arterial/alveolar oxygen
partial pressure ratio: Effects of low ventilation/perfusion regions. Crit Care Med.
1979;7(6):267–272.
8. Woodring JH, Reed JC. Types and mechanisms of pulmonary atelectasis. J Thorac Imaging.
1996;11:92–108.
ADDITIONAL READING
• Rodríguez-Roisin R, Roca J. Mechanisms of hypoxemia. Intensive Care Med.
2005;31(8):1017–1019.
• Functional residual capacity
• Mixed venous oxygen saturation
• Oxygen carrying capacity
• Pulmonary ventilation perfusion matching
• One lung ventilation
• Hypoxia, intraoperatively
• PaO2
CLINICAL PEARLS
• Pulse oximetry in the presence of a high FIO2 may not be an adequate marker of pulmonary
pathology as reflected by the A-a gradient.
• Hypoxemia caused by physiologic shunt may not be responsive to increased FiO2.
ALVEOLI
Megan Freestone-Bernd, MD
Mary E. McAlevy, MD
BASICS
DESCRIPTION
Alveoli are the thin-walled, sac-like, terminal dilations of the respiratory bronchioles, alveolar
ducts, and alveolar sacs. They serve as the functional unit for gas exchange with pulmonary
capillaries.
• The adult lung contains approximately 300 million alveoli.
• The combined maximal volume is approximately 5–6 L.
• Each alveoli is surrounded by capillaries.
• The combined surface area ranges from 50 to 100 m2.
• Alveolar walls: Comprised of a thin epithelial layer that consists of alveolar type I and
alveolar type II cells.
– Alveolar type I cells are squamous epithelial cells and cover approximately 80% of the
alveolar surface. They are highly differentiated and very susceptible to injury. If the type I
cell is damaged, the type II cells replicate and modify to form new type I cells.
– Alveolar type II cells are cuboidal epithelial cells that synthesize and secrete the fluid
layer (surfactant) that lines the alveoli. The type II alveolar cells also control local
electrolyte balance and lymphatic cell functions.
– Alveolar type III cells are alveolar macrophages and are an important element of lung
defense. They are part of the lung inflammatory response and ingest foreign materials
within the alveoli.
• Alveoli size:
– Individual alveoli range from about 75 to 300 μm.
– Surface tension: Describes the force exhibited by water molecules in the alveoli towards
one another. Water has a greater attraction to each other than to air, causing the alveoli
to tend towards collapse. For example, as alveoli become smaller, water molecules come
closer together, and surface tension is increased. As alveoli increase in size, water
molecules are further apart, and surface tension is decreased.
– Law of Laplace: The pressure required to keep an alveolus open is directly proportional to
the surface tension within the alveolus and indirectly proportional to the alveolar radius.
P = 2T/r, where P = pressure, T = surface tension, and r = radius.
– Surfactant: A phospholipoprotein that contains both a hydrophilic and hydrophobic region
that lines the alveoli. It adsorbs to the alveolar air–water interface and decreases surface
tension by decreasing the interaction between water molecules. Thus, surfactants function
to stabilize the alveoli; the tendency for small alveoli to collapse would result in emptying
into larger alveoli.
– Pleural pressure: Varies throughout the lung. At the apices, the pleural pressure is the
most negative; therefore, the alveoli are more expanded than at the bases of the lungs.
• Gas exchange across the alveoli is determined by the partial pressure difference across the
membrane and the solubility of the gas. The alveoli epithelium and basement membrane
provide minimal hindrance and are optimal for this function. Carbon dioxide diffuses 20
times as rapidly as oxygen; oxygen diffuses twice as rapidly as nitrogen.
ANATOMY
• Alveoli are the terminal branches in the pulmonary tree.
• The pulmonary tree begins with the trachea which then branches into the right and left
mainstem bronchi. These bronchi then further divide into bronchioles, alveolar ducts, and
alveolar sacs.
• The lungs receive blood from the pulmonary and bronchial circulation.
– Pulmonary circulation: Deoxygenated blood flows from the right ventricles into the
pulmonary arteries which branch along with the bronchial tree until they reach the
respiratory bronchioles. At this point, they form a dense capillary network that provides a
very large area for gas exchange. Oxygenated blood returns to the left atrium via the
pulmonary veins.
– Bronchial circulation: The blood is supplied from the aortic arch, the thoracic aorta, and
the intercostals arteries. It feeds the trachea, bronchi, and bronchioles as well as the
intrapulmonary nerves, ganglia, and interstitial lung tissue. It drains into the right atrium
as deoxygenated blood.
• Zones: Blood flow through the lungs is dependent upon gravity as well as the relative
pressures in each area. These pressures include the pulmonary artery pressure (Ppa), the
pulmonary venous pressure (Ppv), and the alveolar pressure (PA). Three zones have been
described:
– Zone 1: Located at the lung apex, the perfusion pressure is about equal to the alveolar
pressure so blood flow is low (PA > Ppa > Ppv). Zone 1 therefore has ventilation without
perfusion and is essentially dead space.
– Zone 2: The middle zone where the perfusion pressure is greater than the alveolar
pressure so blood flows easily (Ppa > PA > Ppv). Zone 2 is the area of “best matched”
ventilation and perfusion; it also contains the most number of alveoli.
– Zone 3: Located at the lung base, where the perfusion pressure is much greater than the
alveolar pressure so blood flow is high (Ppa > Ppv > PA). Zone 3 has very good
perfusion, but less ventilation which results in shunting.
• Atelectasis is the term used to describe “collapsed” alveoli; the term can be applied to a
single unit, lobe, or the entire right or left lung. Blood that perfuses the collapsed cannot
pick up oxygen or offload carbon dioxide, resulting in pulmonary shunting. As the number
of atelectatic units increases, it is less likely that the blood will be oxygenated by a proximal
or distal unit before returning to the left atrium.
• Neonatal respiratory distress syndrome (RDS) can be present in premature infants due to a
lack of surfactant. The increase in surface tension results in alveolar collapse (atelectasis),
with resultant hypoxemia, decreased compliance, and problems re-inflating the lungs.
Surfactant may be present by week 24 and is almost always present by gestational week 35.
If there are mature levels of surfactant, the amniotic fluid will have a
lecithin:sphingomyelin ratio >2:1. Corticosteroids may be given to encourage formation of
surfactant in cases of pre-term labor.
• Emphysema is a disease where alveoli undergo destruction and elastic recoil is decreased;
this results in increased alveolar size. It is most commonly caused by smoking, but can also
result from alpha-1 antitrypsin deficiency. Bronchoalveolar lavage will demonstrate the
presence of neutrophils; these cells cause damage to the lung parenchyma by secretion of
proteolytic enzymes. Alveolar damage decreases gas exchange area, leading to hypoxemia,
hypercarbia, and chronic dyspnea.
• Pulmonary fibrosis describes thickening of the alveolar wall; this impairs the diffusing
capacity of gas through the alveoli.
• Cystic fibrosis is a genetic disease of the epithelial chloride channel to open normally in
response to cyclic AMP. This defect decreases water passage across the epithelial membrane,
leading to abnormally thick mucous in the airways. Mucus can obstruct small airways
(plugs) and result in frequent pulmonary infections.
• Aspiration pneumonitis of acidic solutions may lead to destruction of surfactant-producing
type II pneumocytes and the capillary endothelium. Damage to these cells may lead to
atelectasis and leakage of fluid into the lungs. Arterial hypoxia may ensue, which leads to
pulmonary vasoconstriction with associated pulmonary hypertension, as well as tachypnea
and bronchospasm.
• Congestive heart failure describes cardiac dysfunction with “back-up” into the pulmonary
vasculature (increased capillary pressure). This initially causes dilation and recruitment of
pulmonary capillaries making it more difficult for alveoli to expand (results in decreased
lung compliance, and increased work of breathing). As capillary pressures increase, fluid
will eventually extravasate into the interstitial space around the alveoli. With further
increases in pressure, fluid will eventually enter into the alveoli.
• Acute respiratory distress syndrome (ARDS) is defined as severe hypoxemia, diffuse shadows
on CXR, low pulmonary compliance, and pulmonary edema not from left-sided heart failure.
The lung parenchyma is severely damaged due to chemical mediators and fibroblasts. There
is an inflow of protein-rich fluid into the alveoli due to increased permeability of the
alveolar capillary membranes. Diseases that may precipitate ARDS include: septic shock,
aspiration of gastric contents, pneumonia, pulmonary contusions, near drowning, severe
trauma with associated shock, and inhalation of toxic gases or smoke.
Positive end-expiratory pressure (PEEP) is effective in improving arterial oxygenation and
should be used when indicated. PEEP helps prevent alveolar collapse at the end of expiration
and in doing so may decrease the shear stress associated with the opening and closing of
alveoli with mechanical ventilation. PEEP also helps ventilation-to-perfusion matching as well
as decreasing right-to-left intrapulmonary shunt. Because PEEP recruits alveoli that were
previously collapsed, it helps to increase lung volumes and functional residual capacity (FRC).
However, by increasing the intrathoracic pressure, it can decrease preload to the right atrium
and decrease cardiac output.
EQUATIONS
Law of Laplace: P = 2T/r, where P = pressure, T = surface tension, and r = radius
REFERENCES
1. Daniels CB, Orgeig S. Pulmonary surfactant: The key to the evolution of air breathing.
News Physiol Sci. 2003;18:151–157.
2. Smetana GW. Preoperative pulmonary evaluation. N Engl J Med. 1999;340:937–944.
3. Staton GW, Ingram RH. Pulmonary edema. Sci Am Med. 1997:1–10.
4. Tobin MJ. Culmination of an era in research on the acute respiratory distress syndrome. N
Engl J Med. 2000;342:1360–1361.
• Atelectasis
• Surfactant
• Pulmonary ventilation and perfusion matching
• Acute respiratory distress syndrome
• Cardiogenic pulmonary edema
CLINICAL PEARLS
• During normal spontaneous ventilation, the alveolar-to-dead space ventilation ratio is 1:1.
During mechanical ventilation under anesthesia, dependent lung regions will have alveolar
collapse, and ventilation is preferably distributed to the nondependent areas (ratio changes
to 1:2). These alveoli may become over-aerated if high levels of PEEP are used.
AMNIOTIC FLUID EMBOLISM
Kanishka Monis, MD
BASICS
DESCRIPTION
• Amniotic fluid embolism (AFE) is a rare, but often fatal, obstetric emergency. It was first
described by Dr. Meyer in 1926.
• Entry of amniotic fluid into the maternal circulation via the placenta can occur during
pregnancy or in the immediate postpartum period.
• Amniotic fluid contains:
– Epithelial squamous cells from the fetal skin
– Mucin which originates from meconium
– Lanugo
– Fat from vernix caseosa
EPIDEMIOLOGY
Prevalence
Hard to assess due to a lack of sensitive and specific diagnostic studies; however, estimated to
be 7.7 in 100,000 births in the US.
Morbidity
Neurologic impairment is seen in 61% of women and 50% of infants who survive AFE
Mortality
• AFE is the fifth most common cause of maternal mortality in the world.
• Maternal mortality approaches 60%.
• Fetal mortality rate is around 21%.
• Advanced maternal age
• Tumultuous labor
• Placental abnormalities (placenta previa, abruptio placentae)
• Operative deliveries (Cesarean section, assisted vacuum deliveries, forceps-assisted
deliveries)
• Eclampsia
• Polyhydramnios
• Cervical lacerations
• Uterine rupture
• Medical induction of labor
• 4 main physiologic alterations in AFE:
– Maternal cardiovascular collapse
– Coagulopathy
– Respiratory distress
• Amniotic fluid entry. It is hypothesized that the combination of breaches to the maternal
circulation along with increased intrauterine pressures can facilitate entry of amniotic fluid
into the circulation.
– Breaches in the physical barrier can occur at the level of endocervical veins, the placental
attachement site, or at uterine trauma sites.
– Increased intrauterine pressure (and incidence of AFE) is seen in conditions such as
polyhydramnios, placenta previa, placenta abruption, operative deliveries, uterine
rupture, and cervical lacerations.
• Maternal cardio-respiratory collapse may result from the following mechanisms
– Mechanical obstruction of the pulmonary arteries (dead space; ventilation, but no
perfusion)
Amniotic debris obstructs the pulmonary artery leading to pulmonary hypertension and
acute right ventricular failure. The increased right ventricular afterload results in a
dilated right ventricle and deviation of the inter-ventricular septum. This can impair left
ventricular filling with resultant left ventricular failure. Transesophageal
echocardiography supports these findings.
– Immunologic responses. Generalized constriction of the pulmonary vasculature results in
relative shifting of blood flow to areas of lower ventilation from higher ventilation (shunt;
perfusion, but inadequate ventilation).
The complement cascade is activated and the subsequent immunologic reactions can
result in pulmonary vasoconstriction. Of note, low levels of complement (C3 and C4)
have been observed in some parturients with AFE
Endothelin has also been found in amniotic fluid and can lead to pulmonary
vasoconstriction
Other humoral mediators, such as histamine, serotonin, prostaglandins, and leukotrienes
have been linked to the onset of shock, myocardial depression, and disseminated
intravascular coagulopathy
• Coagulopathy associated with AFE is mainly related to consumption.
– Amniotic fluid contains tissue factors that activate the extrinsic pathway by binding to
factor VII.
– Amniotic fluid is also found to have a thromboplastin-like effect and factor X activating
property.
• Avoid trauma to the uterus during insertion of a pressure catheter or during artificial
rupture of the membrane.
• During a Cesarean section, incision on the placenta should be avoided.
• Excessively strong and frequent uterine contractions, as may be seen with oxytocin
administration, should be minimized.
• A diagnosis of exclusion, based on clinical presentation, or postmortem findings
• AFE usually occurs during the intrapartum period or immediately postpartum.
• Symptoms:
– Sudden breathlessness
– Nausea/vomiting
– Dizziness
– Chest pain
– Panic attack
– Pin and needle sensation in fingers
– Bleeding
• Signs:
– Hypotension
– Respiratory distress
– Cyanosis
– Fetal distress
• Diagnostic tests and imaging:
– Nonspecific tests include CBC, coagulation profile, ABG, BUN, and cardiac enzymes.
– EKG may shown an acute right ventricular strain pattern.
– Chest radiograph may indicate a dilated right heart, prominent pulmonary arteries, and
pulmonary edema.
– Transesophageal echocardiography may reveal pulmonary hypertension, acute right
ventricular failure with leftward deviation of the inter-ventricular and inter-atrial septum
and severe tricuspid regurgitation.
– Serum markers for AFE:
Specific markers include zinc coproporphyrin (a component of meconium) and sialyl Tn
antigen (a component of meconium and amniotic fluid).
Nonspecific serum markers include serum tryptase (marker of mast cell degranulation)
and complement factors.
The presence of fetal squamous cells in the maternal circulation is suggestive but not
diagnostic of AFE.
• Pulmonary thromboembolism
• Air embolism
• Myocardial infarction/cardiac arrhythmia
• Aortic dissection
• Anesthetic-related complication (total or high spinal block)
• Allergic anaphylaxis
• Abruptio placentae
• Uterine rupture
• Sepsis
TREATMENT
• Treatment is mainly supportive care aimed at the:

– Correction of hypoxia and maintenance of oxygenation:
Administer oxygen immediately with a goal of SpO2 >90%
Ventilate by face mask, Ambu bag, or endotracheal intubation
– Correction of hypotension and maintenance of cardiac output:
Initiate cardiopulmonary resuscitation (CPR) immediately
Rapid restoration of preload using crystalloid solution
Inotropic support in cases where hypotension is refractory to fluid therapy
Maintain a systolic blood pressure >90 mm Hg
– Correction of coagulopathy:
Transfuse packed red blood cells to maintain adequate blood oxygen-carrying capacity
and oxygen delivery to tissues.
Fresh frozen plasma, platelet, and cryoprecipitate can be transfused to correct specific
laboratory coagulation derangements.
Recombinant activated factor VIIa has been used to manage severe DIC not responding to
blood products transfusion
• Pulmonary hypertension may be treated with inhaled nitric oxide, prostacyclin, and
sildenafil.
FOLLOW-UP
• Risk of recurrence in the subsequent pregnancy is unknown.

• Neurologic disability in the mother and infant remains a common complication following
AFE.
REFERENCES
1. Abenhaim HA, Azoulay L, Kramer MS, et al. Incidence and risk factors of amniotic fluid
embolisms: A population-based study on 3 million births in the United States. Am J Obstet
Gynecol. 2008;199(1):49.e1–49.e8. Conde-Agudelo A, Romero R. Amniotic fluid embolism:
An evidence-based review. Am J Obstet Gynecol. 2009;201(5):445.e1–445.e13. Erratum in:
Am J Obstet Gynecol. 2010;202(1):92.
2. Harboe T, Benson MD, Oi H, et al. Cardiopulmonary distress during obstetrical anaesthesia:
Attempts to diagnose amniotic fluid embolism in a case series of suspected allergic
anaphylaxis. Acta Anaesthesiol Scand. 2006;50(3):324–330.
3. Kane SK. Historical perspective of amniotic fluid embolism. Int Anesthesiol Clin.
2005;43(4):99–108.
4. Moore J, Baldisseri MR. Amniotic fluid embolism. Crit Care Med. 2005;33(Suppl 10):S279–
S285.
• Venous air embolism
• Dead space
CODES
ICD9
• 673.10 Amniotic fluid embolism, unspecified as to episode of care or not applicable
• 673.11 Amniotic fluid embolism, delivered, with or without mention of antepartum
condition
• 673.12 Amniotic fluid embolism, delivered, with mention of postpartum complication
ICD10
• O88.111 Amniotic fluid embolism in pregnancy, first trimester
• O88.112 Amniotic fluid embolism in pregnancy, second trimester
• O88.119 Amniotic fluid embolism in pregnancy, unspecified trimester
CLINICAL PEARLS
• Due to significant morbidity and mortality, a high index of suspicion is warranted.
• Suspect AFE when the laboring patient complains of sudden breathlessness, or incurs
hypotension or cardiac arrest.
• Rule out pulmonary thromboembolism and anesthetic complications (e.g., high spinal) in
the parturient suspected of AFE.
• The mainstay of therapy is to support oxygenation and circulation to prevent end-organ
damage with severe debilitating neurologic sequelae.
• Parturients have improved prognosis when AFE is diagnosed early and aggressive treatment
is administered.
AMYLOIDOSIS
Ahmed Fikry Attaallah, MD, PhD
BASICS
DESCRIPTION
• Amyloidosis is a progressive connective tissue disease caused by the deposition of amyloid
proteins.
• It can involve various body systems but sometimes only one organ may be affected. Factors
leading to the specific pattern of organ involvement are not understood.
EPIDEMIOLOGY
Incidence
New cases: 8 persons per million annually
Prevalence
• 95% of cases are seen in people >40 years of age.
• 66% of cases are men.
• 15–20% of primary amyloidosis patients have associated multiple myeloma.
Morbidity
Varies between patients reflecting the extent of spread and the degree of organ dysfunction
Mortality
• The average survival with primary amyloidosis is 12 months.
• Amyloidosis associated with multiple myeloma is rapidly progressive and the life expectancy
is usually <6 months.
• In secondary amyloidosis, medical or surgical treatment of the underlying cause may slow or
stop the disease progression.
• In familial amyloidosis, survival is 7–15 years.
• Family history of amyloidosis
• Advanced age
• Chronic infectious or inflammatory diseases
• Kidney disease requiring hemodialysis
PATHOPHYSIOLOGY
• The term “amyloid” describes an alteration in the secondary structure of a protein that
results in an aggregated and insoluble form. Amyloidosis can result from inherited
mutations in precursor genes or from plasma cell dyscrasia; amyloid deposits in the
extracellular spaces lead to organ failure and eventually death.
• Plasma cells are located in the bone marrow and function as part of the immune system by
producing antibodies. Monoclonal plasma cells produce small lambda (λ) or kappa (κ)
fragments that are processed in an abnormal manner by macrophage enzymes producing the
insoluble amyloid fibrils.
• Assess for multiorgan involvement and the severity of disease progression in each system.
• The anesthetic plan should focus on monitoring and preventing hemodynamic instability.
• Maintain a high index of suspicion for a possible difficult intubation in order to prevent
perioperative airway compromise.
• Calcium channel blockers are contraindicated in cardiac amyloidosis and may produce or
worsen bradyarrhythmias. Atropine may be useless or even worsen bradycardia in patients
with familial amyloidosis.
• Consider stress dose steroids for patients on chronic therapy.
SYMPTOMS
• Nervous system: Hand and foot numbness, visual changes, dementia
• Cardiac: Decreased exercise tolerance, irregular heartbeat, syncope (strong predictor of
sudden death)
• Respiratory: Hoarseness of voice, shortness of breath, hemoptysis
• Renal: Turbid urine, polyuria (early), or oliguria (late)
• Digestive: Dysphagia, swollen tongue, dry mouth, constipation or diarrhea, hematemesis,
melena, fresh bleeding, acid reflux
History
• Family history of amyloidosis
• Onset of initial diagnosis
• Coexisting chronic illness
• Kidney failure/hemodialysis
Signs/Physical Exam
• Nervous system: Peripheral neuropathy, autonomic neuropathy (postural hypotension),
visual field defects
• Cardiac: Signs of restrictive cardiomyopathy and congestive heart failure, cardiomegaly,
arrhythmias
• Respiratory: Stridor, wheezing
• Renal: Nephrotic syndrome, signs of renal failure
• Digestive: Macroglossia, hemorrhage, hepatic enlargement and splenomegaly, signs of
intestinal obstruction, malnutrition, and dehydration
• Skin: Raised waxy papules or plaques
TREATMENT HISTORY
• Localized radiation therapy aimed at destroying the local collection of plasma cells
• Stem cell transplant
• Surgical care:
– Organ transplant surgery (liver, kidney, heart, or lung)
– Carpal tunnel release
– Percutaneous cementoplasty of bone lesions
– Resection of bleeding friable amyloidomas in the respiratory, GI, or urinary tracts
• Supportive care:
– Renal: Hemodialysis and peritoneal dialysis
– Cardiac: Pacemaker
MEDICATIONS
• Melphalan and prednisone regimen is considered standard therapy.
• An anthracycline analogue of doxorubicin, 4’-iodo-4’-deoxydoxorubicin, has been shown to
solubilize amyloid fibrils.
• Lenalidomide, a derivative of thalidomide, is an immunomodulator that has shown some
success in patients.
• In patients with coexisting multiple myeloma, vincristine, carmustine, dexamethasone, and
cyclophosphamide can be used.
• Proteasome inhibitor: Bortezomib may be used with relapsed/refractory myeloma.
Labs/Studies
• Blood and urine tests are not diagnostic of amyloidosis, but can aid with monitoring organ
dysfunction and disease progression:
– Serum and urine protein analysis and immunoelectrophoresis
– Impaired renal function tests
– Impaired liver function tests
• Hematologic indices and coagulation profile: Anemia, increased fibrinolysis, and clotting
factors deficiency
• Pathologic diagnosis:
– Subcutaneous fat aspiration: Usually sufficient for diagnosis by immunostaining or fibril
amino acid sequence analysis
– Organ-specific biopsies: A needle biopsy of an involved organ ensures a cause-and-effect
relationship between the organ dysfunction and amyloid deposition.
– Bone marrow examination
• Extent of disease spread:
– Chest radiography
– Bone imaging (skeletal survey) of the skull, pelvis, and entire spine
– CT scan
– MRI
– Radioimmunodetection of amyloid deposits (SAP component scintigraphy or iodine-
labeled pentagonal component scanning): A noninvasive method of quantitative imaging
by iodine I123-labeled protein localizer that binds to amyloid deposits
– Cardiac involvement: EKG can show a low-voltage QRS complex, conduction arrhythmias,
and bradycardia. Echocardiography can demonstrate concentric biventricular wall
thickening, increased myocardial echodensity, restrictive filling pattern and diastolic
dysfunction, thickened valves, and decreased myocardial contractility.
• Varies depending on the nature of the chronic infectious or inflammatory diseases in
secondary amyloidosis
• Amyloid deposition can commonly affect the:
– Cardiovascular system: myocardium, conduction system, and cardiac valves
– Respiratory system: Upper and lower airways (the larynx is most common site) and the
lungs (diffuse infiltration or tumorous masses)
– Renal system: Kidneys, bladder
– Digestive system: GI tract, liver, and spleen
– Central and peripheral nervous systems
• Correction of electrolyte abnormalities
• Correction of anemia and coagulopathy
• Management of cardiac arrhythmias, including temporary or permanent pacemaker
placement
CLASSIFICATIONS
• Primary amyloidosis (AL type): Most common, without pre-existing or coexisting disease
• Secondary amyloidosis (AA type): Associated with a chronic infectious or inflammatory
process
• Amyloidosis with multiple myeloma (AL type)
• Familial amyloidosis (AF type)
• Local amyloidosis (AE type): Limited to a single organ
• Senile (AS type): Aging—Alzheimer’s disease
• Hemodialysis-related amyloidosis (AH type)
TREATMENT
Premedications
• Titrate sedation very cautiously; patients are prone to airway obstruction, particularly when
macroglossia is present.
• Appropriate pacemaker management
Advanced amyloidosis with severe organ dysfunction poses a high risk, and code status
during the perioperative period should be clarified.
INTRAOPERATIVE CARE
• Consider regional or neuraxial blocks to avoid airway instrumentation in patients with
tongue, larynx, and tracheal involvement that may lead to obstruction, hemorrhage, or
difficult intubation.
• On the other hand, in patients with peripheral neuropathy or coagulopathy, regional
anesthesia is relatively contraindicated.
Monitors
• DC defibrillator and emergency medications should be readily available to treat cardiac
arrhythmias and possible hemodynamic instability.
• Invasive monitoring (arterial line, central venous access, and pulmonary artery catheter)
and transesophageal echocardiography (TEE) should be determined on a case-by-case basis.
• Dose adjustment of induction drugs to avoid significant hypotension due to potential
myocardial disease and reduced protein binding.
• Patients may have undiagnosed supraglottic amyloid deposits (tongue, pharynx, and larynx),
and blind placement of the endotracheal tube, nasal, or oral airways is not recommended
since it may result in massive airway hemorrhage.
• Perform a fiberoptic exam (before or after induction), or a careful direct laryngoscopy, to
assess the feasibility of intubation. If extensive lesions are noted, an awake tracheostomy
tube placement may be warranted.
• If excision of the supraglottic lesions is planned, a small reinforced or laser cuffed
endotracheal tube should be utilized.
• Rapid-sequence induction is recommended if GI obstruction or delayed gastric emptying is
present due to autonomic neuropathy.
• In patients without aspiration or airway bleeding risks, a laryngeal mask airway (LMA)
maybe used to avoid airway instrumentation.
Maintenance
• Impaired hepatic and renal functions may influence drug metabolism and clearance.
• Ensure proper hydration but avoid intravenous overloading (limited cardiac and renal
reserve).
• Careful positioning to prevent nerve damage and fragile skin breakdown
• Patients who underwent upper airway or tracheobronchial lesion excisions need to be
assessed for possible edema or bleeding and may be kept sedated and intubated
postoperatively.
• Avoid excessive coughing and straining to prevent skin eruptions and ecchymosis.
POSTOPERATIVE CARE
BED ACUITY
• Patients with airway risk or with advanced amyloidosis who underwent major surgical
procedures may require an ICU bed and remain intubated with postoperative ventilation.
• If an implantable defibrillator was programmed off, ensure that it is turned back on.
COMPLICATIONS
• Difficult, or impossible, ventilation due to subglottic amyloid deposits that may lead to
tracheobronchial tree stenosis or hemorrhage. Treatment can be attempted with helium–
oxygen mixture, jet ventilation, and emergency cardiopulmonary bypass through femoral
access (guide-wires may be placed preoperatively).
• Hypotension may be treated by inotropic agents and vasopressors.
• Excessive bleeding can be treated by blood transfusion and correction of coagulopathies.
• Bradycardia and conduction abnormalities can be treated by isoproterenol and cardiac
pacing.
REFERENCES
1. Noguchi T, Minami K, Iwagaki T, et al. Anesthetic management of a patient with laryngeal
amyloidosis. J Clin Anesth. 1999;11:339–341.
2. Minogue SC, Morrisson M, Ansermino M. Laryngo-tracheo-bronchial stenosis in a patient
with primary pulmonary amyloidosis. Can J Anaesth. 2004;51(8):842–845.
3. Hirabayashi Y, Yokosuka S, Miyashita K, et al. Anesthetic management for a patient with
amyloidosis. J Anesth. 1992;6(2):218–221.
ADDITIONAL READING
• Holmes RO, Baethge BA, Edison JD. Amyloidosis. July 2009. Available at:
http://emedicine.medscape.com/article/335414-overview
CODES
ICD9
• 277.30 Amyloidosis, unspecified
• 277.39 Other amyloidosis
ICD10
• E85.3 Secondary systemic amyloidosis
• E85.9 Amyloidosis, unspecified
CLINICAL PEARLS
• Anesthesia providers must be aware of the multisystem involvement of amyloidosis and
disease severity which varies between patients. The anesthetic plan must be tailored on a
case-by-case basis with regard to complications that can arise.
• Life-threatening events include unanticipated loss of the airway and hemodynamic
instability resistant to therapy.
AMYOTROPHIC LATERAL SCLEROSIS (ALS)/LOU GEHRIG’S
DISEASE
BASICS
DESCRIPTION
• Amyotrophic lateral sclerosis (ALS) is a motor neuron disease that involves select upper
motor neurons (UMN) and lower motor neurons (LMN), often with involvement of the
frontotemporal cortex, sensory cortex, and autonomic nervous system.
• ALS manifests as a progressive loss of speech, swallowing, and motor function of the
extremities as well as respiratory muscles.
EPIDEMIOLOGY
Incidence
• In the US: 1.89–2.16 per 100,000/year
• Men > women 1.5:1 in sporadic ALS
• Men = women in familial ALS
• Rapid decrease after 80 years of age
Prevalence
• In the US: 2–5.2 per 100,000
• Peak age at onset: Overall 60 years. This value is usually lower in familial disease.
Morbidity
High risk of postoperative pulmonary complications (PPCs) secondary to the inability to clear
secretions and carbon dioxide retention. The risk increases even further with a vital capacity
that is 50% of predicted levels.
Mortality
• Respiratory failure is the most common cause of death in over 84% of patients.
• Average lifespan after diagnosis: 3–5 years. However, multidisciplinary care can increase
survival.
• Poorer prognosis is associated with bulbar palsy, advanced age.
Multifactorial with complex interaction between genetic and molecular pathways
• Genetic susceptibility: To date, 13 genes and loci have been identified (SOD1, TARDBP, FUS,
ANG, OPTN). Familial ALS has a Mendelian pattern (5–10%).
• Sporadic (SALS): Overlap with neurodegenerative disorders
• Environmental factors: Extensive physical exertion (footballer), active service in US armed
forces, cigarette smoking, neurotoxins (beta-methyl-amino-L-alanine), statins (under
discussion)
PATHOPHYSIOLOGY
The disease process involves glutamate-induced excitotoxicity, oxidative stress, mitochondrial
dysfunction, impaired axonal transport, neurofilament aggregation, intra-cytoplasmic protein
aggregates, inflammatory dysfunction, deficits in neurotrophic factors, and dysfunction of
signaling pathways.
• There is an increased risk of PPCs, and perioperative efforts should aim at maintaining
respiratory muscle strength and avoiding pulmonary aspiration.
• Succinylcholine is absolutely contraindicated; the proliferation of extrajunctional receptors
can result in life-threatening hyperkalemia.
SYMPTOMS
Clinical hallmark is the presence of UMN and LMN features, involving brainstem and spinal
cord regions:
• Spinal onset in 75% (limbs, most common)
• Bulbar onset in 25%
• Initial trunk or respiratory involvement in 5%
• Atypical onset: Weight loss, cramps without muscle weakness, cognitive dysfunction
History
Duration and progression: The median time to diagnosis is ∼14 months due to the insidious
onset.
Signs/Physical Exam
• Pulmonary: Observation of breathing, respiratory rate; auscultation; swallowing; coughing;
salivation
• Neurologic exam
TREATMENT HISTORY
• Supportive, palliative, and multidisciplinary management has been demonstrated to
decrease the risk of death by 45% at 5 years. Symptomatic treatment is the cornerstone and
involves:
– Noninvasive ventilation: Prolongs survival and improves quality of life
– Diaphragmatic pacing (DPS)
– Invasive ventilation via tracheostomy (avoided in most patients)
– Gastrostomy tube
– Nutrition (50–60% of patients are hypermetabolic)
MEDICATIONS
• Riluzole (glutamate antagonist): Only drug shown to extend survival by ~2–3 months
– Most common side effects: Fatigue, nausea
– ALT/SGPT levels rise in about 50% of patients.
– Decreased lung function
– Less common: Neutropenia, pain, dizziness, anorexia
– Overdose: Encephalopathy with stupor/coma, methemoglobinemia
• Common medications for symptomatic care:
– Glycopyrronium, atropine, hyoscyamine
– N-acetylcysteine
– Benzodiazepines such as lorazepam
– Dextromethorphan and quinidine
– Baclofen and tizanidine
– Anticonvulsants, e.g., carbamazepine
– Opioids, e.g., morphine, in late state
– Antidepressants, e.g., amitriptyline or SSRI
– Modafinil
Labs/Studies
• CBC to assess for neutropenia from riluzole
• Liver enzymes, especially ALT (affected by riluzole)
• ABG to assess for hypercarbia
• Pulmonary function tests
– Spirometry: FVC
– Maximum inspiratory pressure, sniff nasal inspiratory pressure of <40 cm H2O
• Polysomnography/nocturnal pulse oximetry: Desaturation, increased partial pressure of
carbon dioxide
• Electrophysiology: Nerve conduction, EMG, TMS, SEP
• Muscle ultrasound
• PET, MRI to exclude ALS mimics
• Motor system:
– Respiratory muscles:
Caudal cranial nerve (bulbar) palsy: Dysphagia, loss of tongue mobility, impaired cough,
swallow, gag reflex, dysarthria, or slurred/nasal speech
Weakness of respiratory muscles: Dyspnea, orthopnea, desaturation, or cyanosis
– Limbs:
Muscle weakness (“lateral sclerosis”, refers to anterior and lateral corticospinal tracts
replaced by gliosis) and atrophy (“amyotrophy") that starts distally and occurs more
frequently in the upper extremities
Fasciculations and cramps
Hyperreflexia and spasticity
• Sensory system, often subclinical:
– Dysesthesia, pain and temperature, vibration and position
– Autonomic impairment (in 20%), often sympathetic hyperactivity
• Neuropsychiatric symptoms:
– Executive dysfunctions (frontal lobe) in 30–50%: Attention, disinhibition, decision making
– Frontotemporal dementia in 5–15% with profound personality changes
– Pseudobulbar affect: Emotional lability, pathologic laughter, and crying
– Memory disturbance (temporal lobe)
• Critically reassess indication for surgery
• Contemplate exclusion from surgery if the FVC is below 45% predicted; predicts the
possibility of failure to extubate
CLASSIFICATIONS
• El Escorial Diagnostic Criteria: Physical examination, electromyography; neuroimaging to
exclude other diseases
• Awaji Criteria: More sensitive for early diagnosis
• ALS Functional Rating Scale (ALSFRS): Activities of daily living
TREATMENT
Premedications
• Review concomitant medication and potential interactions with anesthetics
• Caution with benzodiazepines is warranted (additive effect on respiratory depression).
Alternatively, consider use of alpha 2-agonists such as clonidine, dexmedetomidine.
• Consider starting NPPV if the FVC is <50% to accustom the patient prior to surgery.
• Executive function may be impaired in up to 50% of patients; consent may be necessary
from a power of attorney/family member.
• Discuss potential postoperative respiratory failure: ICU stay, weaning failure, and/or
tracheostomy. There is a considerable increase in respiratory complications with repeated
general anesthesia/surgery.
• Patient autonomy and the right of the patient to refuse or withdraw any treatment,
including mechanical ventilation, should be respected.
INTRAOPERATIVE CARE
• Regional techniques, including epidural anesthesia, may be considered in individual cases
after careful assessment of risks and benefits (“double-crush” phenomenon vs. respiratory
problems).
• General anesthesia
– May exacerbate respiratory insufficiency significantly
– Choose short-acting drugs, if possible
Monitors
• Advanced monitoring should be guided by concomitant diseases and surgery.
• Opioids and sedatives of choice; avoid excessive sedation
• Succinylcholine is absolutely contraindicated due to denervated muscles and the
proliferation of extrajunctional receptors. Can cause hyperkalemia.
• Risk of arterial hypotension due to suppression of sympathetic stimulation; have
vasopressors available.
Maintenance
• Any hypnotic agent may be utilized.
• Opioids: Any opioid may be administered; however, remifentanil is specifically
advantageous:
– Metabolism is independent of liver function (riluzole).
– Very short half-life
– High dosages can provide deep levels of anesthesia that preclude the need for muscle
relaxants.
• Muscle relaxants:
– Caution with all non-depolarizing muscle relaxants since they may cause prolonged and
pronounced neuromuscular blockade; consider low-dose cisatracurium.
– Contemplate alternatives, if feasible, such as use of topical lidocaine, deep intubation, or
use of an LMA
– If used, neuromuscular monitoring is mandatory.
– Anticholinesterases should be used and properly dosed to ensure adequate reversal.
• Adequate hydration
• Patient may not meet extubation criteria.
• Laryngospasm
POSTOPERATIVE CARE
BED ACUITY
• Routinely monitored overnight due to the risk of apnea; the outpatient setting is not
recommended even for minor procedures.
• ICU bed if necessary; patient may require prolonged postoperative ventilation.
MEDICATIONS/LAB STUDIES/CONSULTS
• Respirometer, vital capacity
• ABG to assess for hypercarbia (may present as confusion or sedation)
• The routine use of oxygen is not recommended due to the instability of the respiratory drive.
• Continue NPPV if the patient was on NPPV before
• Communication is often difficult (dysarthria, dementia): Organize a primary caregiver who
is often better able to communicate.
• Pulmonology consult recommended
COMPLICATIONS
• Arterial hypotension
• No risk for malignant hyperthermia with common triggering agents
• Respiratory complications:
– Hypercarbia
– Increased risk for pneumonia due to aspiration and immobility
REFERENCES
1. Onders RP, Carlin AM, Elmo M, et al. Amyotrophic lateral sclerosis: The Midwestern
surgical experience with the diaphragm pacing stimulation system shows that general
anesthesia can be safely performed. Am J Surg. 2009;197(3):386–390.
2. Paek CM, Yi JW, Lee BJ, et al. No supplemental muscle relaxants are required during
propofol and remifentanil total intravenous anesthesia for laparoscopic pelvic surgery. J
Laparoendosc Adv Surg Tech A. 2009;19(1):33–37.
3. Bedlack RS. Amyotrohic lateral sclerosis: Current practice and future treatment. Curr Opin
Neurol. 2010;23:524–529.
4. Cavallucci V, D’Amelio M. Matter of life and death: The pharmacological approaches
targeting apoptosis in brain diseases. Curr Pharm Des. 2011;17(3):215–229.
5. Kieman MC, Vucic S, Cheah BC, et al. Amyotrophic lateral sclerosis. Lancet. 2011;377:942–
955.
6. Wijesekera LC, Leigh PN. Amyotrophic lateral sclerosis. Orphanet J Rare Dis. 2009;4:3.
• Postoperative pulmonary complications
• Tracheostomy
CODES
ICD9
335.20 Amyotrophic lateral sclerosis
ICD10
G12.21 Amyotrophic lateral sclerosis
CLINICAL PEARLS
• Despite significant recent advances in knowledge about ALS, treatment is still focused on
improvement of quality of life.
• Respiratory failure is by far the most common cause for death in ALS patients and is
exacerbated by surgery and anesthesia.
• General anesthesia is usually preferred.
• Succinylcholine is absolutely contraindicated, and nondepolarizing neuromuscular blockade
needs to be monitored very closely.
ANAEROBIC METABOLISM
Amar M. Bhatt, MD
BASICS
DESCRIPTION
• Anaerobic metabolism is the body’s mechanism of continually responding to stress and
sustaining life-preserving measures during malperfusion, until favorable conditions are
resumed.
• The human body’s major source of energy comes from the consumption of glucose via
aerobic methods:
– Aerobic metabolism: Occurs when there is an adequate delivery of oxygen. The O2
molecule functions as an electron acceptor to produce a maximal amount of energy in the
form of ATP (adenosine triphosphate).
– Anaerobic metabolism: Occurs during times of malperfusion and oxygen supply–demand
mismatch. The body generates ATP via a rapid, oxygen-free variation of glycolysis with
lactate as a byproduct (the Pasteur Effect).
• ATP is a nucleotide that provides chemical energy for all cells in the body; it is produced via
carbohydrate (primarily) and non-carbohydrate metabolism.
• Aerobic metabolism (oxygen-dependent) occurs via metabolism of glucose within the
cytoplasm and mitochondria; each molecule of glucose is capable of producing 36 ATP.
– Glycolysis: Glucose is a 6-carbon structure that is first broken down into pyruvate, a 3-
carbon structure. This process takes place in the cytoplasm and results in the net
production of 2 ATP.
– Citric acid cycle (Krebs’ cycle): Using the pyruvate molecules and available oxygen, the
citric acid cycle generates 2 additional ATP per original glucose molecule via an 8-step
process and 18 different enzymes. In addition, this also generates NADH, FADH2, and
other byproducts (e.g., GTP) that can be converted to ATP.
– Oxidative phosphorylation: NADH and FADH2 are metabolized in the mitochondria to
create an additional 24 molecules of ATP per original glucose molecule. This occurs via
oxidative phosphorylation (the electron transport chain), driven by a proton gradient.
• Gluconeogenesis: In the absence of readily available supplies of glucose, the body is able to
use non-carbohydrates (e.g., lactate, glycerol, and certain amino acids or fatty acids) to
generate glucose. Gluconeogenesis takes places via enzymes found in the cytoplasm and
mitochondria of hepatic cells; liver dysfunction or failure can, thus, result in hypoglycemia
and require supplemental dextrose solutions.
• Glycogenolysis: The body can also convert complex carbohydrates, such as glycogen, to
glucose. This pathway occurs in the liver and muscle; it also requires a functioning liver.
• Anaerobic metabolism (oxygen-independent) occurs when the demand for oxygen is greater
than its supply. For each glucose molecule, only 2 ATP are produced.
– In states where oxygen is reduced/absent, pyruvate is metabolized to lactate via lactate
dehydrogenase as an end-product of anaerobic metabolism (pyruvate lactate
dehydrogenase)
– Physiologic states (exercise): The anaerobic threshold is a theoretical point during
dynamic exercise when muscle tissue switches over to anaerobic metabolism as an
additional energy source.
– Pathologic states: Stress, hypoxia, or hypotension/shock
• Central nervous system: The CNS consumes large amounts of energy to maintain normal
electrical function and cellular metabolism.
– Because it cannot store ATP, it requires a constant supply of both glucose and oxygen
(∼3–3.5 mLO2/100 g/min).
– Anaerobic metabolism can result in a 95% decrease in energy production per available
glucose. This can further worsen ischemic damage.
– It is not capable of utilizing amino acids or fatty acids as alternative sources of energy.
Thus, hypoxia, hypoglycemia, or impaired perfusion can rapidly lead to inadequate energy
levels.
• Myocardium: Due to its demand for a constant source of energy, cardiac muscle is highly
dependent on the aerobic metabolism of fats, carbohydrates, and amino acids. Under
ischemic or hypoxic conditions, the energy liberated by lactate production or anaerobic
metabolism (as compared to aerobic metabolism) is not sufficient for myocardial function
and ventricular contraction.
• Pulmonary: Lactic acidosis stimulates peripheral and central chemoreceptors to augment the
medullary respiratory center. This leads to a compensatory increase in oxygen intake and
excretion of carbon dioxide. As with any change in acid–base homeostasis, the ventilatory
response to acidosis is driven primarily by central chemoreceptors; whereas peripheral
chemoreceptors are primarily affected by hypoxemia.
• Hemoglobin: Acidosis decreases the affinity of hemoglobin for oxygen; it improves oxygen
uploading/delivery to acidotic tissue. This is expressed as a right shift in the oxygen–
hemoglobin dissociation curve.
ANATOMY
Erythrocytes do not possess mitochondria.
• Lactate accumulation occurs during anaerobic metabolism and results in an anion gap
metabolic acidosis.
– An anion gap is a term used to describe "unmeasured anions” (e.g., lactate, ethanol,
uremia, certain toxins, ketones) during states of metabolic acidosis.
– Normal lactate concentrations range from 0.5 to 1.0 mmol/L in healthy individuals and up
to 2.0 mmol/L in the critically ill.
– Base excess is more commonly measured in the perioperative period.
• Perioperative lactic acidosis indicates tissue hypoxia from any combination of the following:
– Hypovolemia (e.g., hemorrhagic shock in a trauma patient)
– Hypoperfusion (e.g., cardiogenic shock following cardiac surgery or myocardial ischemic
events)
– Hypotension (e.g., vasodilatory shock in a septic patient)
– Multifactorial from a combination of the above. For example, a trauma patient suffering
myocardial contusions and a perforated viscus could have a combination of hypovolemia,
hypoperfusion, and hypotension.
• Lactic acidosis leads to several cellular and microvascular changes in tissues (1).
– May aggravate structural damage of neurons and glia in the cerebral cortex
– In an attempt to maintain a normal acid–base environment, cells utilize protein
transporters and enzymes via an active process to maintain a homeostatic concentration of
carbon dioxide, bicarbonate, and protons.
• Hyperlactatemia can result from:
– Increased lactate production (Type A): Due to anaerobic metabolism
– Decreased lactate clearance (Type B): Due to liver disease, hypermetabolic states, and
inhibition of pyruvate dehydrogenase
– Some patients may develop lactic acidosis from both mechanisms (e.g., liver failure and
shock).
– Measuring pyruvate can assist in the differentiation of Type A and Type B lactic acidosis.
A lactate-to-pyruvate ratio >25:1 supports the underlying mechanism of tissue hypoxia
or Type A lactic acidosis.
A normal lactate-to-pyruvate ratio (10:1) supports Type B lactic acidosis.
• Anaerobic metabolism is not an uncommon physiologic derangement seen in the
perioperative arena; it can result when there is a mismatch of oxygen delivery and demand:
– Hypoxia/hypoxemia: Esophageal or mainstem intubation, hypoxic mixture,
hypoventilation, V/Q mismatch, shunt
– Hypoperfusion: Hypotension, hypovolemia, hemorrhage, myocardial impairment, shock
– Vasodilation: Anesthetic medications, neuraxial blocks; anaphylactic or septic shock
• Cardiopulmonary bypass: Lactate is associated with malperfusion (2). It not only allows for
prognostication, but also serves as an indicator of the efficacy of therapies used to restore
tissue perfusion.
– Hyperlactatemia is associated with longer intensive care stays and increased postoperative
ventilatory support, renal dysfunction, infectious complications, and circulatory disorders.
– Titrating therapies to traditional endpoints may not ensure that the microvascular bed is
perfused. For example, a normal or high blood pressure may be a vasoconstrictive
response to a low cardiac output state.
• Septic shock: Hyperlactatemia is typically present in patients with sepsis or septic shock and
the etiology is multifactorial (3).
– Hypovolemia: Septic shock is associated with fluid-responsive physiology. Thus, an
elevated lactate level could indicate a “dry” patient.
– Hypoperfusion: Sepsis is also accompanied by a hypermetabolic state with enhanced
glycolysis. Patients with “normal” filling pressures (e.g., central venous pressure) and
cardiac indices (e.g., cardiac index) may not have adequate oxygen delivery.
– Cytopathic hypoxia: Despite adequate volume status and perfusion, tissue dysfunction at
the cellular level may persist in sepsis and represents impaired cellular function.
– Lactate is a well-established prognostic indicator in sepsis and septic shock. Obtaining
serial serum lactate levels aids in identifying tissue hypoperfusion in patients who are not
hypotensive but are at risk for septic shock; an elevated lactate (>4 mmol/L or 36
mg/dL) likely indicates inadequate oxygen delivery. Early goal-directed therapy should be
considered in patients with sepsis and/or an elevated lactate level.
– As part of the Surviving Sepsis Guidelines, a resuscitation bundle for patients with sepsis
includes, but it is not limited to:
A minimal initial crystalloid bolus of 20 mL/kg or equivalent
Vasopressor therapy to maintain a mean arterial pressure >65 mm Hg
Obtaining blood cultures and administering appropriate antibiotic therapy
Maintaining adequate central venous pressure and central venous oxygen saturation
EQUATIONS
• Glucose + 2 ADP + 2 Pi → 2 Lactate + 2 ATP + 2 H2O
• Pyruvate + NADH + H+ ←→Lactate + NAD+
REFERENCES
1. Cassavaugh J, Lounsbury KM. Hypoxia mediated biological control. J Cellular Biochem.
2010;112(3):735–744.
2. Javidi L. Pathophysiology of lactic acidosis and its clinical importance after cardiac
surgery. Iran J Cardiac Surg. 2008;2:18–24.
3. Dellinger RP, Levy MM, Carlet JM, et al. Surviving sepsis campaign: International
guidelines for management of severe sepsis and septic shock. Crit Care Med.
2008;36:1394–1396.
ADDITIONAL READING
• Chaitman BR. Exercise stress testing. In: Bonow RO, Mann DL, Zipes DP, et al, eds.
Braunwald’s heart disease—a textbook of cardiovascular medicine, 9th ed. Philadelphia, PA:
Saunders/Elsevier, 2011, chap. 14.
• Levy B. Lactate and shock state: The metabolic view. Curr Opin Crit Care. 2006;12(4):315–
321.
• Surviving Sepsis Campaign. www.survivingsepsis.org
• Base excess
• Metabolic acidosis
• Septic shock
• Cardiopulmonary bypass (CPB)
CLINICAL PEARLS
• Lactate production can serve as a marker of anaerobic metabolism and tissue hypoxia.
• When there is concern for adequate oxygen delivery, lactate and base deficit measurements
can serve as markers of adequate tissue perfusion.
ANAPHYLAXIS
Lori Gilbert, MD
BASICS
DESCRIPTION
• An acute, life-threatening reaction with an onset of minutes to hours. It is usually, but not
always, the result of an immunologic mechanism that involves IgE-mast cell or basophil
mediator release; such mediators can include histamine, leukotrienes, and prostaglandins.
• The newest definition of anaphylaxis encompasses 1 of 3 scenarios:
– Acute onset (minutes to hours) of skin and mucosal manifestations, as well as respiratory
compromise, hypotension, or shock
– Signs as above, after exposure to a likely antigen, in addition to GI symptoms
– Hypotension after exposure to a known antigen
EPIDEMIOLOGY
Prevalence
• During anesthesia: Ranges from 1:4,000 to 1:25,000 anesthetics
• Hospital inpatients in the US: 1:3,000; in Europe, the incidence is reported to be much
lower.
• In the US, it is estimated that between 1.25% and 16% of the general population is at risk
for possibly experiencing an episode of anaphylaxis.
Prevalence
• Lifetime prevalence from all triggers: 0.05–2%
• Food triggers: 90% of anaphylaxis cases are caused by milk, soy, eggs, wheat, peanuts, tree
nuts, fish, and shellfish.
Morbidity
• Food allergies account for 30,000 ER visits a year; it is more common among children than
adults.
• Latex anaphylaxis is responsible for >200 cases/year.
Mortality
• In the US: ∼2 in 100,000 anaphylaxis cases
• In the UK: 0.65–2% of anaphylaxis cases
• Risk factors age 10–35 years old: Active asthma, peanut allergy, and delayed administration
of epinephrine
• Risk factors age 55–85 years old: Cardiovascular or respiratory illness, use of antibiotics or
anesthetic agents.
• History of a prior anaphylactic episode remains the most important factor in establishing
cause and risk factors.
• Outpatient setting:
– Drug-induced: Penicillin and other antibiotics, aspirin, and NSAIDs
– IV contrast dye
– Food: Peanuts, tree nuts, fish, shellfish, soy, egg, cow’s milk
– Other: Exercise-induced, idiopathic, insect stings, seminal fluid
• Perioperative setting:
– Neuromuscular blockers (most common)
– Natural rubber latex
– Antibiotics
– Hypnotics (propofol, thiopental)
– Aprotinin
– Bupivacaine
– Radiographic contrast material
– Opioids
– Protamine
– Blood transfusions
– Methylmethacrylate (bone cement; associated with hypotension but no IgE mechanism has
been found)
– Rare causes include etomidate, ketamine, midazolam, and amide local anesthetics.
• Anaphylactic and anaphylactoid reactions stem from the systemic release of mediators from
mast cells and basophils. The pathogenesis of anaphylactic reactions involves an
immunologic mechanism in which IgE is created in response to allergen exposure. Receptors
on the surface of mast cells and basophils bind with IgE.
• Re-exposure of the allergen results in activation of IgE-bound mast cells and basophils with
the resultant release of pre-formed mediators that are stored in cellular granules (histamine,
tryptase, heparin, chymase, cytokines). In addition, arachidonic acid is metabolized to
prostaglandins and leukotrienes and also released.
• Anaphylaxis often produces signs and symptoms within minutes of exposure but there are
also biphasic reactions that can occur 1–72 hours after the initial attack.
• Increased vascular permeability is a hallmark of anaphylaxis that allows the transfer of large
amounts of intravascular fluid into the extravascular space within 10 minutes. As a result,
cardiovascular collapse may be the first sign of anaphylaxis with little or no cutaneous or
respiratory signs.
• Primary prevention is based on allergen desensitization through immunotherapy.
• Venom immunotherapy is highly successful in preventing anaphylaxis.
• Pharmacologic prophylaxis (steroids, antihistamines) can be used to help prevent
occurrences to radiographic contrast material, fluorescein, and other dyes.
• For idiopathic anaphylaxis, prophylaxis with daily oral prednisone, combined with H1
antagonists, has resulted in decreased incidence.
• Most importantly, patient education and avoidance of known triggering substances is key in
prevention.
• A “TIME OUT" should be performed prior to any procedure and identify the presence of any
known drug allergies.
• Acute onset of reaction (minutes to hours)
• Cutaneous: Skin, mucosa, or both can present with hives, urticaria, angioedema, pruritus,
flushing, swollen lips and tongue.
• Respiratory: Bronchospasm, wheezing, dyspnea, stridor, reduced peak expiratory flow,
hypoxemia, respiratory arrest
• Cardiovascular: Hypotension or symptoms of end-organ dysfunction (cardiovascular
collapse), tachycardia
• Gastrointestinal: Persistent vomiting, diarrhea
• RAST testing (radioallergosorbent test) detects specific IgE antibodies to suspected or known
allergens. The suspected antigen is bound to an insoluble material and the patient’s serum is
added. If the serum contains antibodies to the allergen, those antibodies bind to the
allergen. Radiolabeled anti-human IgE antibody is added where it binds to those IgE
antibodies already bound to the insoluble material.
• Skin manifestations may be masked by surgical drapes and are not as common in the setting
of general anesthesia as in other settings.
• Bradycardia is, surprisingly, more common with anaphylaxis in the setting of general
anesthesia (not tachycardia).
• Cardiovascular collapse may be the only sign of anaphylaxis.
• Acute asthma exacerbation
• Syncope
• Panic attack/anxiety disorders
• Acute generalized hives
• Vocal cord/paradoxical vocal cord dysfunction
• Vasovagal reactions
• Nonimmunologic reactions that involve mechanisms outside of IgE mediation (transfusion
reactions, IgG or IgM antibody-mediated, antigen–antibody complexes and complement)
• Anaphylactoid reactions: The World Allergy Organization has suggested that the term be
eliminated in favor of calling all similar reactions “anaphylaxis.” Generally, the term is used
to describe non-IgE-mediated reactions; the initial treatment is the same, regardless of the
mechanism.
• Cardiovascular disorders: Pulmonary embolism, cardiogenic shock, etc.
• Flushing disorders: Carcinoid, “red-man” syndrome from vancomycin, medullary carcinoma
of the thyroid
• Other: Mastocytosis (systemic mast cell disease [SCMD]) is a clonal disorder characterized
by overproduction of mast cells in different tissues.
• Postprandial syndromes
• Diagnostic tests and interpretation:
– Serum tryptase peaks 60–90 minutes after the onset of anaphylaxis and persists for 6
hours; obtain between 1 and 2 hours after the first symptoms appear.
– Plasma histamine levels begin to rise within 5–10 minutes and remain elevated for 30–60
minutes.
– 24-hour urinary histamine metabolite
– Urinary vanillylmandelic acid to rule out pheochromocytoma and carcinoid syndrome
– Skin tests (or in vitro tests) determine the presence of specific IgE antibodies to foods,
medications (e.g., penicillin).
TREATMENT
• Discontinuation of the inciting factor (e.g., anesthetic agent or drug)

• Place the patient in the recumbent position (pertinent if antibiotics or medication is being
given on the floor or preoperative holding area)
• ABC’s: Manage airway, delivery 100% oxygen, and intubate (if appropriate)
• Rapid IV fluid replacement
• Epinephrine is the most important aspect of treatment for anaphylaxis and should be
administered immediately:
– IV: 5–10 mcg boluses
– IV drip: 1 mcg/min
– SQ: 200–500 mcg q5 minutes (aqueous 1:1,000 dilution which is equivalent to 1 mg/mL
or 0.2–0.5 mL)
– IM: 200–500 mcg into the vastus lateralis, or lateral aspect of the thigh (aqueous 1:1,000
dilution which is equivalent to 1 mg/mL or 0.2–0.5 mL)
– Cardiopulmonary arrest during anaphylaxis: 1–3 mg IV over 3 minutes, followed by 4–10
mcg/min infusion
– Severe or refractory anaphylaxis that is unresponsive to epinephrine has been reported
with patients on beta-blockers; it has been characterized by bradycardia, profound
hypotension, and severe bronchospasm; consider treating with glucagon 1–5 mg IV over 4
minutes, followed by an infusion of 5–15 mcg/min.
• Histamine 1 blocker. Diphenhydramine 1–2 mg/kg or 25–50 mg IV dose.
• Histamine 2 blockers. Ranitidine 50 mg IV diluted in 5% dextrose (total volume of 20 mL)
can be administered over 5 minutes. Alternatively, cimetidine 4 mg/kg IV may be given.
• Inhaled beta-2 agonists if bronchospasm is present
• Glucocorticoids are not helpful acutely but potentially can help prevent recurrences and
shorten the duration of attack.
• Monitors: Large-bore IV access, if not already in place, should be placed. Arterial line
placement can aid with monitoring blood pressure (particularly if chest compressions);
however, it should not interfere with immediate resuscitation with IV fluids and
epinephrine.
FOLLOW-UP
• Biphasic anaphylaxis can occur in up to one-fourth of episodes, and symptoms may recur
within hours after apparent resolution of initial presentation.
• Following resolution of the initial episode, patients should be provided with an epinephrine
pen and instructions for administration as well as instructions to go to the nearest
emergency room at the first hint of recurrence of symptoms.
• Patients should also be referred to an allergist/immunologist for further workup, possibly
including skin testing and desensitization, if appropriate.
REFERENCES
1. ieberman P, Nicklas R, Oppenheimer J, et al. The diagnosis and management of
anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol. 2010;126:477–480.
2. Hepner D, Castells M. Anaphylaxis during the perioperative period. Anesth Analg.
2003;97:1381–1395.
3. Estelle F, Simons R. Anaphylaxis. J Clin Immunol. 2010;S161–S180.
4. Kemp S, Lockey R. Anaphylaxis: A review of causes and mechanisms. J Allergy Clin
Immunol. 2002;110(3):341–348.
5. Leiberman P. Anaphylactic reactions during surgical and medical procedures. J Allergy
Clin Immunol. 2002;110(2):s64–s69.
6. Matasar M, Neugut A. Epidemiology of anaphylaxis in the United States. Curr Allergy
Asthma Rep. 2003;3:30–35.
ADDITIONAL READING
• www.aaaai.org
• www.acaai.org
• www.aafa.org
• Latex allergy
CODES
ICD9
• 995.0 Other anaphylactic reaction
• 995.60 Anaphylactic reaction due to unspecified food
ICD10
• T78.00XA Anaphylactic reaction due to unspecified food, init encntr
• T78.2XXA Anaphylactic shock, unspecified, initial encounter
• T78.2XXD Anaphylactic shock, unspecified, subsequent encounter
CLINICAL PEARLS
• Epinephrine, patient position, and oxygen are the most important therapeutic modalities in
treating anaphylaxis. Treatment (in order of importance) includes:
– Epinephrine
– Patient position (recumbent)
– Oxygen
– IV fluids
– Nebulized beta-2 agonists
– Vasopressors
– Antihistamines
– Corticosteroids
• Propofol and egg allergy: This topic has been a source of some controversy among
anesthesia providers. Propofol is formulated in a lipid emulsion containing soybean oil,
glycerol, egg lecithin, and disodium edetate with sodium hydroxide to adjust for pH.
– The egg lecithin component is a highly purified egg yolk component. The principal protein
of eggs is ovalbumin which is present in the egg white. Most egg allergies are related to
the egg white (albumin) and not the egg yolk (lecithin).
– Most allergic-type reactions to propofol are nonimmunologic because propofol can cause
direct stimulation of histamine release.
– Skin testing of egg-allergic patients is not consistent with allergies to propofol.
– However, there are case reports in the literature of anaphylaxis associated with propofol
in egg-allergic individuals.
– Furthermore, the propofol package insert monograph clearly states under
contraindications: “Propofol Injectable Emulsion is contraindicated in patients with
allergies to eggs, egg products, soybeans or soy products.”
• It is the author’s opinion that if propofol can be avoided in egg-allergic individuals, then an
appropriate substitute should be used. If propofol cannot be avoided, epinephrine, large-
bore IV access, and resuscitation equipment should be readily available.
ANEMIA
Gregory M. T. Hare, MD, PhD
Katerina Pavenski, MD, FRCPC
BASICS
DESCRIPTION
• Anemia is defined as a hemoglobin concentration <12 g/dL in females and <13 g/dL in
males.
• Red blood cells (RBCs) with normal functioning hemoglobin (Hg) are essential for delivering
oxygen to tissues. They also contribute to blood viscosity and may aid in hemostasis.
EPIDEMIOLOGY
Prevalence
• Highly variable and dependent on the etiology and patient demographics (1)
• 11–76% of patients may present with preoperative anemia. Postoperative anemia may be
present in up to 90% of patients undergoing major surgery (2,3).
Prevalence
An estimated 25% of the world’s population is anemic from nutritional, infectious,
malignancy, and genetic causes. Iron deficiency is the most common type of anemia
worldwide, and accounts for ∼50% of all cases (4).
Morbidity
Acute and chronic anemia is associated with an increased risk of stroke, myocardial
infarction, and renal injury in specific patient populations (2,5). Anemia is associated with
increased perioperative morbidity and higher likelihood of requiring an allogeneic transfusion
which is in turn associated with prolonged hospital stay and postoperative infections (6), and
increased risk of mortality (2).
Mortality
Preoperative anemia is an independent risk factor for mortality and is associated with a
greater likelihood of requiring allogeneic blood transfusion which has also been linked to
increased mortality in surgical and critical care patients (2).
• Decreased or impaired production
– Nutritional deficiencies (iron, folate, vitamin B12)
– Reduced erythropoietin (EPO) production due to renal failure
– Bone marrow causes: Aplastic anemia, dysplasia/cancer, or fibrosis
– Chronic inflammation (also known as anemia of chronic disease [ACD])
• Increased destruction (hemolysis)
– Intrinsic to RBCs
Membrane disorders
Hemoglobinopathies: Sickle cell disease, thalassemia
Enzyme deficiencies
– Extrinsic to RBCs
Immune (allo or autoantibody mediated)
Microangiopathy (disseminated intravascular coagulation, thrombotic thrombocytopenic
purpura)
Macroangiopathy (leaky valve)
– Infections (malaria)
Other (burns)
• RBC loss
– Bleeding (GI bleeding, menorrhagia, surgery, etc.)
– Blood donation
• RBC sequestration (related to splenomegaly)
• Dilution
– Iatrogenic (e.g., resuscitation with crystalloid)
– Pregnancy
• The mechanisms of anemia-induced morbidity and mortality have not been clearly
established. However, inadequate blood oxygen content and tissue oxygen delivery likely
contribute (2,7).
• Iron deficiency can result from poor nutritional intake, increased requirements (childhood,
pregnancy, breastfeeding), chronic blood loss, and impaired absorption (1).
• Vitamin deficiency can result from poor oral intake, impaired absorption or increased
requirements (e.g., folate deficiency in hemolysis).
• Renal failure leads to impaired EPO production which in turn results in anemia.
• ACD is a result of chronic inflammation. Pro-inflammatory mediators and RES cells induce
changes in iron homeostasis, proliferation of erythroid progenitor cells, production of EPO,
as well as affect the life span of red cells leading to anemia.
• Hemolytic anemia is a result of impaired red cell survival due to a variety of factors, and
can be either hereditary or acquired.
• Malignancy, both hematological and solid, may lead to anemia due to tumor occupying the
bone marrow, or bone marrow suppression resulting from the treatment of malignancy
(irradiation, chemotherapy) or from ACD.
• In addition to iron deficiency, pregnancy leads to increased plasma volume and dilutional
anemia. Dilutional anemia may also result from aggressive crystalloid resuscitation of
patients who present with bleeding.
• Each unit of transfused RBCs increases the Hg level by ∼1 g/dL and Hct by 3%.
• The decision to transfuse should not be based solely on Hg level; the clinical situation must
be taken into account. Most guidelines recommend transfusion for a euvolemic Hg <6.5
g/dL. Transfusion is almost never indicated for a euvolemic Hg level >10 g/dL. The area
between 6.5 and 10 dg/L is a gray zone, and the decision to transfuse should depend upon
clinical circumstances including ongoing blood loss, presence of relevant comorbidities,
symptoms of anemia, and signs indicative of inadequate oxygen delivery or hemodynamic
instability.
SYMPTOMS
• Fatigue, lightheadedness, syncope, impaired mentation
• Palpitations
• Shortness of breath and/or chest pain on exertion
• Jaundice, dark urine, gallstones (suggestive of hemolytic anemia)
History
• History of anemia, investigations, and treatments to date
• History of chronic inflammatory conditions (lupus, arthritis)
• History of major organ dysfunction: Kidney, heart, liver, lungs
• Illicit drugs and alcohol intake
• History of cancer and its treatment
• History of chronic blood loss
• History of GI disorders and surgery
• Known diagnosis of hereditary RBC disorder
Signs/Physical Exam
• Pale conjunctivae
• Tachypnea, tachycardia, systolic murmur, signs of CHF
• Masses, lymphadenopathy, organomegaly
TREATMENT HISTORY
Iron, erythropoiesis-stimulating agents (ESA), Vitamin B12, folate, transfusions
MEDICATIONS
Medications with myelotoxic potential: Immunosuppressive agents (e.g., Imuran),
chemotherapy (e.g., cyclophosphamide), anticonvulsants, etc.
Labs/Studies
• Hg, RDW, MCV (mean corpuscular volume). A low MCV (microcytic anemia) may indicate
iron deficiency anemia (IDA) or thalassemia. A high MCV may be suggestive of vitamin B12
or folate deficiency, liver disease, and excessive alcohol intake.
• Reticulocyte count reflects the adequacy of bone marrow compensation for anemia. A low
reticulocyte count in the face of significant anemia suggests either a lack of hematinics or a
bone marrow problem.
• Blood film
• Ferritin, serum iron, TIBC, iron saturation. A low ferritin and iron saturation point to iron
deficiency anemia (IDA). Note: Ferritin is an acute phase reactant, and may not be an
accurate marker of iron stores in a patient with chronic inflammation.
• Soluble transferrin receptor may help differentiate between IDA and ACD. A low-soluble
transferrin receptor is indicative of ACD.
• Folate, vitamin B12
• CRP is a marker of inflammation, and may be helpful in assessing patients with suspected
ACD.
• Standard biochemistry tests, such as creatinine, transaminases, and bilirubin, are useful to
determine the presence or extent of either renal or liver disease.
Concomitant lung or heart disease may lower the body’s ability to compensate for anemia.
These patients may have symptoms of anemia at higher Hg levels than their healthy peers.
• Symptoms of impaired oxygen delivery to the cerebral or myocardial system
• If significant anemia (Hg <10 g/L) is present and surgery could be safely postponed, a
patient should undergo evaluation by an internist or hematologist and treated for anemia
prior to surgery. This is especially true for patients who will be undergoing high blood loss
procedures, have a rare blood type, or significant alloimmunization against RBC antigens, or
those who object to blood transfusion for religious reasons.
CLASSIFICATIONS
• Morphological: Microcytic, macrocytic, normocytic
• Kinetic: Decreased RBC production, increased RBC destruction, increased RBC loss,
sequestration and dilution
TREATMENT
Premedications
• Attempt to correct anemia with hematinics (vitamins or minerals) and ESA as necessary (8)
• If there is significant anemia and surgery is urgent (e.g., there is no time to institute blood
conservation measures or see their benefit), an allogeneic RBC transfusion may be
necessary.
• Consider administration of antifibrinolytic agents (e.g., tranexamic acid) and topical
hemostatic agents to reduce blood loss
• Discuss the possibility of blood product transfusion and describe associated risks
• Describe risks and benefits of the proposed blood conservation measures (e.g.,
thromboembolic risk with ESA)
INTRAOPERATIVE CARE
Depends on the surgical procedure. The sympatholysis from neuraxial techniques may be
profound.
Monitors
Standard ASA monitors
Prepare for hypotension
Maintenance
• Blood loss intraoperatively is whole blood loss. Laboratory values may not reflect this
initially until volume replacement has occurred.
• Assess blood loss on laps, sponges, drapes, floor, as well as the suction canister
• Consider cell salvage
• Avoid hypothermia
• Use point of care testing (if available and appropriate) to guide hemotherapy
Postoperative intubation and ventilator support may be considered when large volume shifts
and transfusion have taken place.
FOLLOW-UP
BED ACUITY
Not applicable
• Follow Hg levels closely, as well as symptoms and bleeding; consider transfusion as
appropriate. Over-transfusion should be avoided; in stable patients, transfuse 1 unit at a
time followed by reassessment.
• Eliminate unnecessary blood draws; collect samples into pediatric tubes.
• Consider consulting hematology or the blood conservation service to assist with iron
supplementation and other medical therapy for optimization of Hg.
• Do not forget about appropriate thromboprophylaxis especially for those patients who have
received ESA and tranexamic acid (TXA) perioperatively.
REFERENCES
1. de Benoist B, McLean E, Egli I, et al., eds. Worldwide prevalence of anaemia 1993–2005.
2. Geneva, Switzerland: World Health Organization, 2008.
3. Shander A, Javidroozi M, Ozawa S, et al. What is really dangerous—anemia or transfusion.
Br J Anaesth. 2011;107(Suppl 1):i41–i59.
4. Beris P, Munoz M, Garcia-Erce JA, et al. Perioperative anaemia management: Consensus
statement on the role of intravenous Iron. Br J Anaesth. 2008;100:599–604.
5. Stoltzfus RJ. Iron deficiency: Global prevalence and consequences. Food Nutr Bull.
2003;24:S99–S103.
6. Hare GMT, Baker JE, Pavenski K. Assessment and treatment of preoperative anemia. Can J
Anaesth. 2011;58:569–581.
7. Freedman J, Luke K, Escobar M, et al. Experience of a network of transfusion coordinators
for blood conservation (ONTraC). Transfusion. 2008;48:237–250.
8. Tsui AK, Dattani ND, Marsden PA, et al. Reassessing the risk of hemodilutional anemia:
Some new pieces to an old puzzle. Can J Anaesth. 2010;57:779–791.
9. Pasricha SR, Flecknoe-Brown SC, Allen KJ, et al. Diagnosis and management of iron
deficiency anaemia: A clinical update. Med J Aust. 2010;193:525–532.
• Blood oxygen carrying capacity
• Transfusion related lung injury (TRALI)
• Transfusion infections
CODES
ICD9
• 280.9 Iron deficiency anemia, unspecified
• 284.9 Aplastic anemia, unspecified
• 285.9 Anemia, unspecified
ICD10
• D50.9 Iron deficiency anemia, unspecified
• D61.9 Aplastic anemia, unspecified
• D64.9 Anemia, unspecified
CLINICAL PEARLS
• Transfuse actively bleeding patients more aggressively than non-bleeding patients
• Use all aspects of clinical analysis to support your decision to transfuse
• Treat and diagnose anemia prior to elective surgery to avoid risk of anemia and transfusion
ANEMIA OF PREMATURITY
Alberto J. De Armendi, MD, AM, MBA
BASICS
DESCRIPTION
• The physiologic nadir of hemoglobin in newborns occurs at 8–12 weeks. It is the result of a
decrease in erythropoietin in response to the transition from a relatively hypoxic state in
utero to a hyperoxic state in room air. It is usually asymptomatic and gradually increases to
adult values within the first 2 years of birth.
• Anemia of prematurity (AOP), however, is a pathologic and exaggerated response to
decreased erythropoietin seen in premature infants (<37 weeks).
– Reduced hemoglobin, with lowest hemoglobin levels 6–7 g/dL in extremely low birth
weight (ELBW) infants
– Signs and symptoms of anemia manifest
– Independent risk factor related to apnea
– Spontaneous resolution by 6 months of age
– Starts earlier and lasts longer than in normal newborns
– Normocytic and normochromic red blood cells (RBCs)
• This patient population is at-risk for several other causes of anemia, including shortened
RBC life span and enhanced blood loss. Thus, the premature infant’s impaired ability to
increase erythropoietin levels further compounds the levels of anemia.
EPIDEMIOLOGY
Incidence
• Inversely proportional to:
– Gestational age
– Birth weight
• Advancements in technology have resulted in a new group of preterm infants that previously
could not survive; thus increasing the incidence of AOP.
Prevalence
• No sex prevalence
• No race prevalence
Morbidity
• Secondary to transfusions: Immune-related and infectious
• Apnea
• Poor feeding/decreased weight gain
Mortality
In general, mortality is increased in premature infants 42 per 1,000 (compared to term infants
1.8 per 1,000)
• Decreased RBC production that can be associated with prematurity (1,3,4).
– Inadequate synthesis of erythropoietin in response to hypoxia that results in suboptimal
erythropoiesis.
– Nutritional deficiencies: Iron, folate, protein, B12
• Decreased RBC life span that can be associated with prematurity (increased destruction):
– Immune hemolytic anemia: Rh or ABO incompatibility, maternal autoimmune disorders,
drug-induced
– Enzyme abnormalities: Glucose-6-phosphate dehydrogenase deficiency, pyruvate kinase
deficiency
– RBC membrane defects: Spherocytosis, stomatocytosis
– Hemoglobinopathies: Thalassemia
• Increased blood loss that can be associated with prematurity
– Frequent laboratory testing in critically ill infants (iatrogenic) can exacerbate AOP and
increase the need for transfusions.
– Fetomaternal or fetoplacental hemorrhage
– Placenta previa, placental abruption
– Internal bleeding: Intracranial, intra-abdominal, pulmonary
PATHOPHYSIOLOGY
• The fetal environment has several adaptations to accommodate the degree of hypoxia and
maximize oxygen delivery to the brain and heart (3,5).
– Hypoxic pulmonary vasoconstriction is maintained through decreased production of nitric
oxide (minimal pulmonary blood flow with oxygenation and ventilation occurring at the
placenta).
– High pulmonary artery pressures lead to high right heart pressures. This maintains the
right-to-left shunt through the foramen ovale (FO).
– Increased circulating prostaglandins that maintain the patency of the ductus arteriosus
(DA) and the ductus venosus (DV).
– Fetal hemoglobin has a strong affinity for oxygen to facilitate efficient extraction across
the placenta. The P50 is ∼19 mm Hg, compared to adult hemoglobin (∼27 mm Hg).
• Transition to the extrauterine environment involves decreased shunting secondary to
increased oxygen tensions and rapid right and left heart pressure changes. With the
neonate’s first several breaths, circulating oxygen tensions rise rapidly with resultant
increases in bradykinin and nitric oxide and decreased pulmonary vascular resistance; blood
flow increases through the pulmonary vasculature. Additionally, circulating prostaglandins
decrease rapidly and result in closure of the ductus arteriosus. The relatively hyperoxic
environment suppresses erythropoietin production (3).
• Erythropoietin: In utero, it is produced by the liver and kidneys in response to transcription
factor hypoxia inducible factor-1 (HIF-1). In the premature infant, it is believed that there is
a relative insensitivity by the hepatic oxygen sensor to hypoxia and anemia, resulting in
inadequate synthesis of HIF-1.
• Delay surgery, if possible. When surgery must proceed, consider blood transfusion prior to
arrival to the operating room or during the case. Type and cross matched, leukocyte-
reduced, and CMV-negative blood should be administered.
• Minimize laboratory blood draws to those absolutely needed; additionally, decrease the
volume drawn
• Maintain a thermoneutral environment. The combination of cold and hypoxia can result in
patent ductus arteriosus (PDA) shunting.
SYMPTOMS
• Apnea
• Poor weight gain
• Difficulty feeding
• Decreased activity
History
• Apnea history
• Feeding history
• Weight gain history
• Retinopathy of prematurity (ROP)
Signs/Physical Exam
• Tachypnea
• Tachycardia
• Pallor
• Decreased activity
• Flow murmurs
• Distended abdomen
TREATMENT HISTORY
• Transfusions: Indications and guidelines are nonspecific, including hemoglobin levels,
apnea, bradycardia, poor weight gain, ventilator needs. Packed RBCs should be CMV-
negative and leukocyte-reduced.
• Placental RBC transfusion: Umbilical cord blood may decrease the need for non-autologous
blood transfusion. However, studies cite limitations to this method, such as insufficient
volumes collected, clotting, hemolysis, contamination, and cost.
• Reduced RBC drawing and utilization of tubes with fill-lines (allow close approximation of
the volumes needed for testing)
• Observation
MEDICATIONS
• Supplemental vitamins
– Iron
– Vitamin E
– Vitamin B12
– Folic acid
• Recombinant erythropoietin: The primary pathophysiology of AOP is an impaired ability to
increase erythropoietin production; thus, exogenous administration can be an effective
therapeutic modality. Studies have suggested that when administered early, it can reduce
the use of RBC transfusion. However, concerns have been raised that there is an increased
incidence of ROP.
Labs/Studies
Hemoglobin/hematocrit levels
Issues with prematurity, including
• Neurologic: Intraventricular hemorrhage, hydrocephalus
• Retinopathy of prematurity
• Cardiac: PDA
• Respiratory: Bronchopulmonary dysplasia, respiratory distress requiring ventilatory support,
apnea of prematurity
• Gastrointestinal: Necrotizing enterocolitis, perforation, inguinal hernia (incarceration),
history of re-anastomosis or fundoplication
• Sepsis
Need optimization of hemoglobin/hematocrit prior to arrival in the operating room.
CLASSIFICATIONS
Gestational age and birth weight are indirectly related to occurrence of AOP.
• Low birth weight (LBW): <2,500 g, 36–37 weeks gestational age
• Very low birth weight (VLBW): <1,500 g, 31–36 weeks gestational age
• ELBW: <1,000 g, 24–30 weeks gestational age
TREATMENT
Premedications
• Blood transfusion, as appropriate
• May give atropine (20 mcg/kg) to prophylax against bradycardia
• Parental consultation for postoperative ventilatory support
• Risk of hypothermia, ROP, blood transfusions
INTRAOPERATIVE CARE
Dependent on surgical procedure
Monitors
• Standard ASA monitors, with 2 pulse oximeters for preductal and postductal measurements
• Precordial stethoscope
• Urinary Foley catheter may be considered when blood transfusion is expected.
Majority of cases will arrive intubated to the OR.
Maintenance
• Avoid hypoxia, hypothermia, and increased airway pressures that can increase pulmonary
vascular pressures and favor right-to-left shunting.
• Avoid administering high FIO2 (retinopathy of prematurity)
Patients who were intubated on arrival will usually return to the neonatal intensive care unit
(NICU) intubated.
POSTOPERATIVE CARE
BED ACUITY
NICU
• Iron
• Caffeine 10 mg/kg (2)
• Minimal laboratory requirements except monitoring of hemoglobin levels
COMPLICATIONS
• Transfusion related:
– Fluid overload
– Electrolyte imbalance
– Hypothermia
– Infectious
– Immune-related
REFERENCES
1. Peiris K, Fell D. The prematurely born infant and anesthesia: Continuing education in
anaesthesia. Crit Care Pain. 2009;9(3):73–77.
2. Welborn LG, Greenspan JC. Anesthesia and apnea: Perioperative considerations in the
former preterm infant. Pediatr Clin North Am. 1994;41(1):181–198.
3. Aher S, Malwatkar K, Kadam S. Neonatal anemia. Semin Fetal Neonatal Med.
2008;13(4):239–247.
4. Salsbury DC. Anemia of prematurity. Neonatal Netw. 2001;20(5):13–20.
5. Widness JA. Pathophysiology of anemia during the neonatal period, including anemia of
prematurity. Neoreviews. 2008;9(11):e520.
ADDITIONAL READING
• Ohisson A, Aher SM. Early erythropoietin for preventing red blood cell transfusion in
preterm and/or low birth weight infants. Cochrane Database Syst Rev. 2006;3:CD004863.
• Hemoglobin
CODES
ICD9
776.6 Anemia of prematurity
ICD10
P61.2 Anemia of prematurity
CLINICAL PEARLS
• Anemia of prematurity is the result of impaired erythropoietin production in response to
anemia and tissue hypoxia. Additionally, in premature infants, the concomitant increase in
RBC destruction and shortened lifespan can further exacerbate the anemia.
ANESTHESIA FOR NEURORADIOLOGY
Eman Nada, MD, PhD
BASICS
DESCRIPTION
General
• Advancement in imaging technology and the growing field of interventional neuroradiology
have increased the need for anesthesia services in the “out-of-OR” setting. However, several
challenges exist:
– Radiation exposure hazards: Early effects of ionizing radiation are dose-dependent and
risk increases with increased radiation dose (may occur many years after exposure).
– Special OR setup: Suites are often crowded by large radiology equipments that are difficult
to move; the anesthesia space is usually small; large radiation protective shields and heavy
aprons can make movement and access to the patient difficult; the airway can be distant
from the machine and anaesthetist; the room is dark; and paramedical personnel are not
familiar with anesthesia support (experienced help is often remote).
– MRI hazards: Ferrometallic materials can be projectile and may cause accidents; electric
noise can distort monitored waveforms; acoustic noise may present a distraction;
electromagnetic waves can cause patient burns in areas of contact with monitor cords or
in the presence of metallic implants; and in an emergency situation it takes 90 seconds to
retract the magnet tube and have a crash cart in the room (patient may need to be
removed from the room).
• Angiographic interventions can be broadly classified as those that:
– Obliterate the lumen. Embolization of cerebral and dural arteriovenous malformation
(AVM), vessel-feeding tumors, cerebral aneurysms, and fistulae.
– Open the lumen and revascularize. Angioplasty of atherosclerotic lesions and thrombolysis
or thrombectomy of acute thromboembolic stroke.
• Intraoperative magnetic resonance imaging system (IMRIS) is used for the:
– Resection of brain tumors
– Implantation of deep brain stimulators (DBS) and electroencephalographic (EEG)
electrodes
• Anesthesia is usually requested for diagnostic procedures in:
– Pediatric patients
– Uncooperative or claustrophobic patients
– Patients with complex medical problems when strict hemodynamic monitoring is needed
Position
• Diagnostic and interventional angiographic procedures: Supine with arms tucked
• Intraoperative MRI: Supine, prone, lateral, and semi-sitting position have been reported.
Incision
• Diagnostic and interventional procedures: Typically via femoral catheterization; however,
carotid or brachial arteries may be utilized.
• Intraoperative MRI: Craniotomy incision
Approximate Time
• Diagnostic: ∼30–60 minutes
• Angiographic interventional procedures: ∼4–6 hours
• Intraoperative MRI: ∼4–6 hours
EBL Expected
• Diagnostic and interventional angiographic procedures: None to minimal
• Intraoperative MRI: ∼50–500 mL, depending on the location and size of the lesion, and
complexity of the procedure
Hospital Stay
Diagnostic procedures: Out-patient or in-patient
• Contrast material
• Endovascular catheters to deliver coils, detachable balloons, and embolizing agents
• MRI suite specially equipped to provide surgery with compatible anesthesia machines,
monitors, and other equipments
EPIDEMIOLOGY
Incidence
• In 2009, an estimated 40,663 cerebral angiograms, 109,000 angioplastic carotid
endarterectomies, and 700,000 endovascular aneurysmal repairs were performed.
• In 2010, ∼1,047 neuro interventional MRI procedures were performed; this is a 300%
increase over 5 years since its start.
Morbidity
See “Complications”
Mortality
IV contrast: 1 out of 170,000 reactions
• A full preoperative evaluation should be performed even in patients receiving deep
sedation/analgesia for diagnostic procedures.
• Out-of-OR standards are necessary for the safe delivery of anesthesia. They include:
– A reliable source of oxygen with a back-up
– Airway equipment (e.g., Ambu bag)
– Standard ASA monitors
– Suction
– Waste gas scavenger if volatile agents are administered
– Anesthetic drugs and emergency drugs
– Sufficient space
– Means to provide cardiopulmonary resuscitation
– Sufficient safe electrical outlets
– Adequate illumination with battery-powered backup
• Maintain a still field as well as a patent airway and hemodynamic stability
SYMPTOMS
Depends on diagnosis or indication
History
• NPO status
• Shellfish, iodine, IV contrast, or protamine reactions
• Ability to lie flat, snoring, sleep apnea
• Acquired or implanted metallic devices, extensive tattoos, permanent eye make-up
Signs/Physical Exam
• Depends on diagnosis or indication and can include a baseline-focused neurologic exam,
Glasgow Coma Scale, disease-specific scoring system (Hunt Hess for subarachnoid
hemorrhage and NIHSS for stroke)
• General medical and airway exam
MEDICATIONS
• Interventional procedures: Antiplatelets, anticoagulants; calcium channel blockers for
cerebral protection or reducing vasospasm; triple H therapy for prophylaxis or treatment of
vasospasm (induced hypertension, hemodilution, hypervolemia)
• Intraoperative MRI: Steroids, diuretics, anticonvulsants
• Pain medications: For headache, surgical pain in iMRI procedures
• Medications specific to the patient’s co-morbidities
Labs/Studies
• BUN/Cr is often attained prior to IV contrast.
• Depends on comorbidities
Depends on procedure indication
TREATMENT
Premedications
• Anxiolysis as needed; caution or avoidance in elderly or altered patients as well as epileptic
patients for EEG electrode implantation
• Stroked patients may present with a full stomach; gastric acid and volume-reducing
medications should be considered.
• Parkinsonian patients scheduled for DBS should have their morning dopaminergic and
anticholinergic medications held.
• Tumor patients may require re-dosing of steroids or antiepileptics.
• Corticosteroids and possibly an antihistamine may decrease the incidence of contrast
reactions in “at-risk” patients.
• Radiation safety: Lead aprons, thyroid shields, and protective eye goggles should be
considered, as appropriate, for the patient (as well as the anesthesia provider!)
• Setup should be meticulous due to the difficulties encountered with patient manipulation
once the procedure has begun.
• Pediatric patients require parent consent.
• Uncooperative or altered patients require a family member or power of attorney consent.
• Diagnostic and interventional angiographic procedures: Usually considered clean
procedures; antibiotics are given only in high-risk procedures.
• Intraoperative MRI: Skin organisms, third-generation cephalosporins are usually given.
INTRAOPERATIVE CARE
• Diagnostic procedures may need minimal or conscious sedation and can be performed by
non-anaesthetists certified in administering sedation. Anesthesia care providers are often
called upon to provide deep sedation/analgesia or general anesthesia; the choice is based
upon the procedure, positioning, comorbidities, access/nearness to the patient, and ease of
ventilation or intubation in the event that the patient obstructs or becomes apneic.
• Interventional: Typically general anesthesia; deep sedation/analgesia is used in some
revascularization procedures.
• Intraoperative MRI: GA. Awake craniotomy is sometimes needed to resect a tumor under
MRI near eloquent area.
Monitors
• Intra-arterial pressure monitoring for interventional procedures and intraoperative MRIs
• Neurophysiologic-evoked potential monitoring in some spinal cord pathology embolization
procedures
• Intracranial pressure (ICP) monitoring
• Activated clotting time (ACT)
• Neuromuscular twitch monitor
• Neurologic exam in patients under MAC
• Foley catheter to measure urine output
• Oropharyngeal temperature probes will interfere with the angiography pictures; axillary or
skin probes are better options. In IMRIS a fiberoptic probe can be used in the groin.
• Be prepared to induce anesthesia and manage the airway in a less than optimal position.
• Extra-long breathing tubes and infusion lines are needed because anesthetic equipments are
often relocated after induction to allow for imaging equipment to move freely or to move to
safer magnetic fields in MRI scanners.
• Some iMRI suites have an induction room outside the scanner. This provides free access to
all anesthesia equipments at induction; the patient is then transported with
assisted/controlled ventilation (Ambu bag, Bain circuit) to the scanner.
• An ETT with muscle relaxation can provide a more secure and controllable airway, along
with extreme immobilization compared to an LMA.
Maintenance
• Pressure points are secured meticulously since the patient is going to be covered and arms
tucked with limited access.
• Renal protection for contrast: No proven strategy is agreed upon; preoperative hydration for
impaired renal function is usually used. Approximately 2/3rd of the severe and fatal contrast
reactions occur within the first several minutes.
• Heparinization is required whenever catheters are introduced into blood vessels. ACT
monitoring is utilized to guide therapy. Protamine should be standby whenever heparin is
used.
• Antiplatelets are used by the neurointerventionalist after the procedure.
• Avoid patient coughing, bucking, or straining which can cause hypertension and increased
ICP.
• Patient should be awake enough to have a neurologic exam.
POSTOPERATIVE CARE
• May require transport over long distances to the postanesthesia care unit (PACU); monitors,
supplemental oxygenation, airway equipment, and emergency drugs should be considered
as appropriate.
• Standard PACU evaluation, care, and discharge criteria
• No flexion at the groin for a few hours after femoral groin access is removed; consider
reverse Trendelenburg positioning if “head up" is needed.
BED ACUITY
Variable
ANALGESIA
• Interventional radiologic procedures are usually not painful, and local anesthetics are
injected at the access site.
• Short-acting narcotics are often preferable to longer-acting narcotics.
COMPLICATIONS
• Vascular perforation of the access site
• Obliteration of the wrong vessel
• Contrast dye reactions can range from mild symptoms such as scattered urticaria and
pruritus to laryngeal edema, life-threatening arrhythmias, hypotension, bronchospasm,
pulmonary edema, seizures, syncope, and even death. Nonionic contrast media has been
shown to decrease the incidence significantly.
• Contrast nephropathy: Usually occurs at 1–3 days after contrast injection. Patients at
increased risk include pre-existing renal disease, volume depletion, high or repeat doses of
contrast, and administration of other nephrotoxic drugs. Use of oral or IV theophylline,
acetylcysteine, fenoldapam, statins, or bosentan (an endothelin antagonist) have not shown
consistent efficacy against renal insult.
PROGNOSIS
Variable depending on the preoperative morbidity, the underlying pathology, site and extent
of procedure
REFERENCES
1. Bergese SD, Puente EG. Anesthesia in the intraoperative MRI environment. Neurosurg Clin
N Am. 2009;20:155–162.
2. Cloft HJ, Rubenstein A, Lanzino G, et al. Intra-arterial stroke therapy: An assessment of
demand and available work force. AJNR Am J Neuroradiol. 2009;30:453–458.
3. Gasser T, Senft C, Rathert J, et al. The combination of semi-sitting position and
intraoperative MRI—first report on feasibility. Acta Neurochir (Wien). 2010;152:947–951.
4. Qureshi AI. Ten years of advances in neuroendovascular procedures. J Endovasc Ther.
2004;11(Suppl 2):II1–II4.
5. Siddiqi N. Contrast medium reactions. Available at:
http://emedicine.medscape.com/article/422855-overview
6. US Department of Health and Human Services. Agency of Human Health care and Quality.
http://hcupnet.ahrq.gov/
• Cerebral embolization
• Craniotomy, awake
• Radiation safety
• Perioperative statins
CLINICAL PEARLS
• The anesthesia provider should not forget to wear radiation protective lead before they
engage in work with challenging cases.
• Anticipate potential complications and ensure appropriate anesthetic equipment setup.
• Continuous infusion of muscle relaxant under GA will help provide a motionless patient for
embolization or revascularization.
• For resection of tumors near eloquent areas, sedation or an “asleep-awake-asleep" technique
may be utilized.
ANGIOTENSIN
BASICS
DESCRIPTION
• Angiotensin is:
– A natural hormone that is part of the renin-angiotensin-aldosterone system (RAAS)
– Stimulated in response to acute, sustained decreases in arterial pressure and enhanced
sympathetic outflow
– A direct, potent arteriolar vasoconstrictor (angiotensin II)
– Responsible for stimulating the adrenal cortex to release aldosterone
• Medications targeting either angiotensin receptors or angiotensin-converting enzymes (ACE)
have been developed for the treatment of hypertension (HTN) and have major implications
for anesthetic management.
• The body has 3 control systems to regulate arterial blood pressure:
– “Immediate control:” The autonomic nervous system reflexes are capable of minute-to-
minute control of blood pressure.
– “Intermediate control:” Renin and angiotensin
– “Long-term control:” Occurs hours after the decrease in blood pressure by altering the
sodium and water balance. This process is mediated by aldosterone with the aim of
restoring blood pressure to a normal level.
• Renin
– Synthesized and stored in the juxtaglomerular cells in the wall of the renal afferent
arterioles
– Stimulated by a decrease in renal perfusion pressure associated with dehydration, acute
hemorrhage, renal artery stenosis, or chronic hyponatremia
– Converts circulating angiotensinogen to form angiotensin I
• Angiotensinogen is synthesized in the liver and released into the plasma.
• Angiotensin I
– Decapeptide prohormone
– Not all angiotensin I comes from conversion of angiotensinogen by renin; it is also
generated by the vascular endothelium.
• Angiotensin II
– Octapeptide
– Not all angiotensin II comes from conversion of angiotensin I by ACE; it is also generated
by the vascular endothelium.
– Plasma half-life is about 50 seconds and is cleared rapidly by a variety of enzymes, namely
angiotensinases, in the circulation.
– Has significant physiological activity on the:
Cardiovascular system: Angiotensin II binds to angiotensin AT1 receptor (a G protein-
coupled receptor) on the vascular smooth muscle, leading to vasoconstriction of the
precapillary arterioles and postcapillary venules. It is 40 times more potent than
norepinephrine, which makes angiotensin II the most powerful endogenous
vasoconstrictor. This effect is most profound in the skin, splanchnic vasculature, and
kidneys, and can lead to significant decreases in blood flow to these organs. Coronary
artery and cerebral artery (to a lesser extent) are also decreased. These pressor responses
do not lead to a reflex bradycardia since angiotensin II acts centrally to reset the
baroreceptor reflex to a higher pressure. The direct mitogenic effect of angiotensin II on
cardiac cells affects cardiac remodeling, and may increase myocardial contractility and
lead to hypertrophy from chronic stimulation.
Central nervous system: Angiotensin II acts on the medullary vasomotor center leading to
sustained HTN. It can also enhance the release of vasopressin and adrenocorticotropic
hormone (ACTH) as well as regulate prolactin release in the pituitary gland.
Peripheral autonomic nervous system: Angiotensin can stimulate the chromaffin cells in
the adrenal medulla to release catecholamines, which is the underlying mechanism for
marked HTN associated with pheochromocytoma.
Adrenal cortex: Angiotensin can stimulate the synthesis and secretion of aldosterone
from the adrenal cortex, leading to the retention of sodium and excretion of potassium
and hydrogen in the kidneys.
– It regulates ovulation and hormone production in the ovary and hormone production in
the testes. It may be partially responsible for preeclamptic symptoms.
ANATOMY
• Kidneys: Produce renin
• Liver: Produces angiotensinogen.
• Vascular endothelium: Produces angiotensin (90% of angiotensin I and 64% of angiotensin
II are generated within endothelium).
• Lungs: Contain the highest concentration of ACE (peptidyl dipeptidase)
• Hypertension: Elevated levels of renin and angiotensin lead to increased vascular resistance;
this is considered as one of the mechanisms responsible for idiopathic HTN.
• Coronary artery disease: In patients with HTN, the incidence of myocardial infarction was
independently associated with the plasma renin activity. The growth effects of angiotensin
II may play an important role in the development of coronary artery atherosclerosis and
peripheral vascular disease.
• Cardiac hypertrophy: Is caused not only by the increased cardiac workload from HTN, but
also the mitogenic effect of angiotensin II on the cardiac muscle cells (plays a role in
myocardial remodeling).
• Renin-secreting tumors
• Angiotensinogen-secreting tumors
• ACE inhibitors (ACE-I) or angiotensin receptor antagonists/blockers (ARBs) are commonly
used drugs in the treatment of HTN, chronic heart failure, or diabetic nephropathy.
– Heart rate: Minimal effect
– Contractility: Reflexive increase
– Cardiac output: Indirect increase
– Blood pressure: Decrease
– Systemic and pulmonary vascular resistance: Direct decrease
– Preload: Decrease
– Renovascular resistance: Decrease
– Natriuresis: Increase
• Side effects and adverse events:
– Profound and prolonged hypotension: The RAAS is responsible for restoring normotension
during surgery, especially in a state of hypovolemia and decreased vascular resistance.
Patients taking ACE inhibitors or angiotensin receptor antagonists preoperatively may
develop profound and prolonged hypotension from the blockage of this physiologic
response during surgery. Whether patients on ACE inhibitors or angiotensin receptor
antagonists should discontinue the medication preoperatively remains controversial.
– Persistent, dry cough and angioedema from increased kinins; it appears that there is a
decreased incidence with ARBs.
– Hyperkalemia from decreased aldosterone
– Exacerbates renal failure in renal artery stenosis, and vasoconstricts the efferent arterioles
of the glomeruli resulting in an increased glomerular filtration rate (GFR)
– Angiotensin “escape:” Not all angiotensin arises from the RAAS system. ACE is contained
the heart and blood vessels where it can exert harmful local effects.
– Pregnancy: May cause congenital malformations and fetal abnormalities
• Benefits: May decrease the degree of vasoconstriction from increased sympathetic tone
caused by intraoperative surgical stress; therefore, it may potentially improve perfusion of
the vital organs and maintain their normal function.
REFERENCES
1. Colson P, Ryckwaert F, Coriat P. Review article: Renin angiotensin system antagonists and
2. Sarkar P, Nicholson G, Hall G. Brief review: Angiotensin converting enzyme inhibitors and
angioedema—anesthetic implications. Can J Anesth. 2006;53(10):994–1003.
• Hypertension
• ACE inhibitors and hypotension
• Hypotension
• Chronic angina
CLINICAL PEARLS
• Angiotensin is an endogenous hormone that is part of the renin–angiotensin–aldosterone
system. Its role has been exploited pharmacologically for the treatment of hypertension.
• Patients on ACE-I and ARBs may have an increased risk of refractory hypotension
perioperatively. However, this has been challenged, and there are currently no guidelines
based upon strong evidence for the preoperative management of these long-term
medications.
ANION GAP
J. Andrew Dziewit, MD
BASICS
DESCRIPTION
• Anion gap (AG) = [(Na+ + K+) – (Cl− + HCO3−)]; normal 7–14 mEq/L
• In metabolic acidosis, the concept of the AG is utilized to assist with the differential
diagnosis. It functions to distinguish acidosis as either an:
– Increase in total body acids (HCO3− anion is titrated by H+); or a
– Decrease in total body HCO3− (abnormal loss from the body).
– In both scenarios, HCO3− is reduced; a calculation of the AG aids in determining which of
these 2 mechanisms is responsible.
• The term “gap” does not imply that anions are missing, but only that they are not directly
measured. By applying the concept that the serum is electrically neutral, measurable values
for major cations and anions allow for unmeasured anions to be calculated.
• Unmeasured anions include phosphates (PO4−) and sulfates (SO4−) as well as lactates,
ketoacids, and toxins. Their corresponding cation (H+) dissociates and is titrated by HCO3−
or other buffering systems, or it increases the acid:base ratio (causing a metabolic acidosis).
• The anions of organic and inorganic acids are not easily or routinely measured. However, it
is possible to measure serum Na+ and K+ (cations) and Cl− and HCO3− (anions) and
“calculate” the AG: [(Na+ + K+) – (Cl− + HCO3−)]. Or, AG = measured cations –
measured anions; potassium may be excluded.
• Normally, the serum AG is determined by negative charges on serum proteins, particularly
albumin.
• Metabolism results in the production of volatile, organic, and inorganic acids.
– Volatile acids: Carbon dioxide (CO2) is a byproduct of sugar, fat, and amino acid
metabolism. Basal CO2 production is approximately 12,000 mmols/d and is
exhaled/excreted by the lungs, as well as buffered by the bicarbonate system.
– Inorganic acids: Sulfate and phosphates are byproducts of amino acid metabolism; basal
production is approximately 50–100 mEq/d. Excretion occurs renally.
– Organic acids: Lactate and ketones. Lactate is produced via anaerobic metabolism. Ketones
result from fatty acid breakdown when insulin is not present via a beta-oxidizing process.
Both are excreted by the liver and kidneys.
• HCO3− is ubiquitous in the body and exists in equilibrium between the intravascular and
extracellular compartments. It is present in the stool and carefully regulated by the renal
tubules.
• High AG metabolic acidosis:
– Results from an increase in an acid molecule’s corresponding anion; thus represents
increased total body acid.
– Acids are composed of a cation (H+) and an anion (A−).
– In solution, the acid compound (HA) dissociates into a H+ and its corresponding anion
(HA ←→ H+ + A−).
– The H+ is buffered by one of the body’s buffering systems, including bicarbonate (H+ +
HCO3− ←→ H2CO3 ←→ H2O + CO2) in order to “cushion” or decrease adverse effects of
the acid load.
– However, this “titration” results in a reduction in HCO3− values; when the acid load
exceeds the buffering capacity, acidosis manifests.
– Electroneutrality is maintained during this titration process (H+ cation plus a HCO3−
anion). There is no increase or decrease in positive- or negative-charged molecules.
– Increased acid production can result from anaerobic metabolism (lactic acidosis), ketone
production (diabetic ketoacidosis), toxins (methylene, ethanol, salicylates), and
hyperosmolar hyperglycemia.
– Reduced acid excretion can result from impaired renal function (uremia).
• Normal AG metabolic acidosis:
– Loss of HCO3− (or bicarbonate precursors) from the body results in an increase in the
acid:base ratio.
– There is no increase in total body acid, and hence no increase in anions.
– In order to maintain electroneutrality, a loss in HCO3− is balanced by a “gain” in Cl−; this
results in a hyperchloremic state.
– HCO3− can be lost by diarrhea, renal tubular acidosis, carbonic anhydrase inhibitors,
ureteral diversion, and intestinal losses; additionally, hyperchloremic crystalloid solutions
(normal saline, [Cl−] 154 mEq/L) serve to dilute the bicarbonate concentration as well as
increase the chloride concentration (resulting in renal excretion of bicarbonate).
• Low AG is a less commonly utilized term that describes low albumin states. Albumin is a
negatively charged protein and its loss from the serum results in the retention of other
negatively charged ions such as chloride and bicarbonate. Because they are utilized in the
calculations, there is a decrease in the gap. AG falls by 2.3–2.5 mEq/L for every 1 g/dL
reduction in serum albumin concentration.
• Base excess is more frequently utilized than the AG in the perioperative period. This is
because metabolic acidosis is often the result of lactic acidosis secondary to anaerobic
metabolism.
– Lactic acidosis indicates that there is tissue hypoxia either from hypovolemia,
hypoperfusion, hypovolemia, or hypotension.
– Perioperatively, this can result from surgical blood loss; evaporative/insensible losses;
episodes of hypoxia at induction, intraoperatively, or at emergence; anemia; or
hypotension.
– Base excess is useful in determining the extent of the increased acid load, as opposed to
aiding in the differential diagnosis.
• The AG can be implemented perioperatively to determine if the metabolic acidosis is
secondary to a hyperchloremic non-AG acidosis. This can manifest from as little as 2 L of
normal saline solution. Na+ 154 mEq/L is balanced by Cl− 154 mEq/L. The chloride
concentration is not physiologic and initially results in the dilution of HCO3−. Ultimately,
however, HCO3− anion is eliminated by the kidneys in order to maintain electroneutrality
(increased chloride anion load). Clinical consequences of the metabolic acidosis are unclear.
However, attempts at correcting the abnormality may actually cause more issues (iatrogenic
causes such as administering additional hyperchloremic crystalloids).
• In the ICU and at the bedside, the AG can provide a clinically useful tool to identify one of
the many causes of metabolic acidosis in the critically ill, especially when hypoalbuminemia
and lactate are considered. Additionally, it can be utilized to monitor, assess, and guide
therapy during sepsis.
• Ketoacidosis: The measured AG disturbance is often less than expected from the fall in
serum bicarbonate. This results from the renal loss of ketoacid anions (beta hydroxyl
butyrate) that accompany sodium and potassium salt excretion.
• Multiple myeloma results in a pathologic increase in cations that are not measured; IgG
paraproteinemia causes a reduced AG.
• Postcardiac surgery metabolic acidosis is typically the result of an increase in unmeasured
acids, and less commonly from lactic acidosis.
– Cardiopulmonary bypass (CPB) circuits are usually primed with 1.4–2 L of hyperchloremic
crystalloid.
– ABG taken immediately after “going on pump” demonstrates a non-AG metabolic acidosis.
– More frequent in children due to the ratio of CPB priming fluid to smaller blood volumes
(even with low-volume priming)
– This acidosis is transient and lasts <24 hours.
EQUATIONS
• AG = [(Na+ + K+) – (Cl− + HCO3−)]
• AG corrected (for albumin) = calculated AG + 2.5 (normal albumin g/dL – observed
albumin g/dL)
REFERENCES
1. Chawla LS, Shih S, Davidson D, et al. Anion gap, anion gap corrected for albumin, base
deficit and unmeasured anions in critically ill patients: Implications on the assessment of
metabolic acidosis and the diagnosis of hyperlactatemia. BMC Emerg Med. 2008;8(18).
2. ernon C, Letourneau JL. Lactic acidosis: Recognition, kinetics, and associated prognosis.
Crit Care Clin. 2010;26(2):255–282.
3. Liamis G, Milionis HJ, Elisaf M. Pharmacologically-induced metabolic acidosis: A review.
Drug Saf. 2010;33(5):371–391.
4. Filipescu D, Raileanu I, Luchian M, et al. Hyperchloremic metabolic acidosis after cardiac
surgery. Crit Care. 2006;10(Suppl1):P200.
5. Murray DM, Olhsson V, Fraser JI. Defining acidosis in postoperative cardiac patients using
Stewart’s method of strong ion difference. Pediatr Crit Care Med. 2004;5(3):240–245.
6. Liskaser FJ, Bellomo R, Hayhoe M, et al. Role of pump prime in etiology and pathogenesis
of cardiopulmonary bypass-associated acidosis. Anesthesiology. 2000;93(5):1170–1173.
ADDITIONAL READING
• Ishihara K, Szerlip HM. Anion gap acidosis. Semin Nephrol. 1998;18(1):83–97.
• Lim S. Metabolic acidosis. Acta Med Indonesia. 2007;39(3):145–150.
• Diabetic ketoacidosis
• Carbon dioxide transport
• Lactic acidosis
CLINICAL PEARLS
• Anion gap represents the difference in charge between measured cations and measured
anions.
• “Missing” negative charge is composed of weak acids (A−) like albumin and phosphate and
strong unmeasured anions such as lactate.
• Frequent causes of an elevated anion gap metabolic acidosis are represented by the
mnemonic MUDPILES:
– Methanol
– Uremia
– Diabetic ketoacidosis
– Paraldehyde
– Iron, isoniazid (INH)
– Lactic acid
– Ethanol, ethylene glycol
– Salicylates
• Frequent causes of a normal anion gap metabolic acidosis are represented by the mnemonic
USEDCARP:
– Ureterostomy
– Small bowel fistula
– Extra chloride
– Diarrhea
– Carbonic anhydrase inhibitors (acetazolamide)
– Adrenal insufficiency
– RTA
– Pancreatic fistula
ANTERIOR CERVICAL DISCECTOMY AND FUSION (ACDF)
Chris A. Steel, MD
BASICS
DESCRIPTION
General
• Removal of a herniated or degenerative disc that is compressing on the cervical spine
– A herniated disk refers to the gel-like material either bulging or rupturing through a weak
area in the surrounding wall (annulus). Irritation and swelling occurs when this material
squeezes out and presses on a nerve.
– Degenerative disc disease refers to the drying out of the disc, resulting in shrinkage and
loss of flexibility and cushioning properties (increases with age). Osteophytes (bone spurs)
result from wear, damage, and inflammation. These changes can result in spinal cord
compression, or myelopathy.
• After induction and intubation, the neck is prepped; the anterior approach allows access to
the disc without disturbing the spinal cord, spinal nerves, and strong neck muscles of the
back. If an autograft will be utilized for fusion, the hip area is also prepped.
• Surgical exposure involves creating an avascular dissection place or tunnel to the disc via
moving aside muscles in the neck, retracting the trachea, esophagus, and arteries.
• Preparation to remove the disc involves localizing the affected level and utilizing spreaders
above and below to facilitate removal of the damaged disc.
• Nerve decompression consists of removal of disc fragments and osteophytes (bone spurs).
The annulus (outer wall of the disc) is incised, followed by removal of the disc; bone spurs
are removed with a Burr (a small rotary cutting tool). A microscope is utilized to remove
disc material and bone spurs near the spinal cord. The posterior longitudinal ligament
(courses behind the vertebrae) is removed to reach the spinal canal and any material
pressing on the nerves is removed.
• A foraminotomy is then performed (the foramen through which the spinal nerve exits, is
enlarged with a drill) to allow more room to exit the spinal canal.
• Fusion: After the disc is removed, the space between the vertebrae is empty and a bone graft
may be inserted to prevent the vertebrae from collapsing and rubbing together; serves as a
bridge. To prepare the graft for fusion, the outer cortical layer of bone is roughened up until
punctuate bleeding is seen. This will allow blood vessels to grow into the grafted bone. The
bone graft is shaped to fit snugly into the space and is typically further immobilized and
held together with a metal plate and screws (reduced incidence of bone graft migration,
improved fusion).
Position
Supine; shoulder roll may be utilized to enhance neck extension and exposure; arms are
typically tucked to allow the surgical team to stand on both sides of the neck.
Incision
• 2–3 inches, depending upon the number of levels
• Left-sided approach is preferred by some in order to reduce injury to the recurrent laryngeal
nerve (RLN); the right side has a 2–3% anomalous course.
Approximate Time
1–1.5 hours per level
EBL Expected
Less than 50 mL
Hospital Stay
• Advocates for same-day discharge cite that the short operative time, minimal blood loss, and
low risk of postoperative hematoma make it ideal in patients without significant
comorbidities and good home help. May significantly reduce procedure costs.
• Advocates for hospital admission cite that the need for a drain and the catastrophic risk of a
postoperative neck hematoma preclude discharge home on POD 0.
• Fluoroscopy or portable x-ray
• Bone graft (autologous or cadaveric)
• Neuromonitoring: Computer and personnel for monitoring EMG, SSEPs, and MEPs
EPIDEMIOLOGY
Incidence
150,000 per year in the US
Prevalence
Increases with age, osteoporosis
Morbidity
• Isolated postoperative dysphagia: 60% initially, 5% at 1 year (1)
• Symptomatic RLN palsy: 3.1%
• Postoperative hematoma: 1–2%
• Bone graft migration: 1–2%
• Dural penetration/tear, worsening or pre-existing myelopathy, Horner’s syndrome,
instrumentation backout, superficial wound infection: Each less than 1%
Mortality
Rare. Esophageal perforation, retropharyngeal edema or hematoma, quadriplegia
• Patients have often failed a course of conservative treatment (epidural steroid injections,
physical therapy, acupuncture, oral pain medications).
• Airway management may be affected by a limited range of neck motion due to pain,
elicitation of myelopathy, or potential for injury. The sniffing position, or even
flexion/extension, to align the oropharynx, hypopharynx, and larynx may not be possible.
• Neuromonitoring. EMG, SSEPs, and MEPs require modification of anesthetic technique to
optimize quality of results.
• Controlled hypotension may be requested to reduce bone bleeding.
SYMPTOMS
• Weakness, pain, paresthesias, numbness in C2–7 distribution (neck, shoulder, arms, hand)
• Arm pain often worse than neck pain
History
• No improvement with conservative therapy
• Chronic pain medications: Patients may or may not have taken their scheduled doses on day
before or day of surgery.
• Comorbidities increase with age.
Signs/Physical Exam
• Sensory and motor deficits should be clarified and noted, including the ability to swallow
and if any baseline hoarseness.
• Ability to extend the neck without experiencing symptomatic spinal cord compression
(Lhermitte’s phenomenon)
MEDICATIONS
Pain patches, pain medications
Labs/Studies
• Laboratory exam depends upon comorbidities.
• PT/PTT/INR, if clinical history of bruising, bleeding, or drugs
• MRI, CT, and myelogram are often performed prior to surgery.
• Osteoporosis
• Chronic pain syndrome
TREATMENT
Premedications
• Anxiolysis and analgesia as needed; chronic pain patients may require increased dosing.
• Dexamethasone 10 mg IV may be requested by some surgeons.
• Smoking cessation: Nicotine reduces successful fusion.
• Hoarseness, swallowing difficulties postoperatively
• Postoperative hematoma
INTRAOPERATIVE CARE
• General anesthesia with ETT
• Partial or total intravenous anesthesia (TIVA) to optimize neuromonitoring
Monitors
• EMG: Supplements visual identification to avoid RLN injury. An ETT with special electrodes
that connect to a computer can measure the muscle electrical potential of the vocal cords.
Because RLN stimulation causes movement of the cords, it allows the surgeon to identify
and avoid inadvertent nerve injury. Must avoid NMBDs (2).
• SSEPs: Assess the integrity of the posterior spinal cord. Volatile agents at a MAC >0.5
decrease the amplitude and increase the latency of the waveforms (false positive).
• MEPs: Assess the integrity of the anterior spinal cord; must avoid NMBDs.
• Arterial line based on comorbidities
• A limited range of motion (pain, myelopathy, prior fusion, stiffness) may preclude sniffing
position or even flexion. Consider having a video laryngoscope, fiberoptic bronchoscopy
(awake or asleep depending on ability or ease of bag mask ventilation), or other special
management devices available in the event of difficulty (alternatively, may consider
utilizing for initial attempts).
• Consider having the patient self-position their neck while on the OR table and maintaining
this position after induction; document if this is performed.
• ETT cuff may increase pressure exerted on the tracheal wall and the submucosal portion of
the RLN; when this is combined with surgical tissue retractors transmitting pressure through
the soft tissues of the neck to the trachea, it can result in ischemic injury. Maintaining a cuff
pressure <25 cm H2O to ensure adequate blood flow to the capillary beds may prevent this.
Other studies have suggested the utilization of the “just seal” pressure (air is withdrawn
from the ETT cuff until a leak around the cuff is detected, and subsequently reinjected
slowly until an air seal is barely obtained).
• Secure the ETT to the contralateral side of the incision; tape should not be attached to
maxilla or mandible on the operative side.
• Neuromuscular blockade cannot be utilized if EMG or MEP is performed. Succinylcholine or
small intubating dose of nondepolarizing muscle relaxants may be utilized to optimize
intubating conditions (opening of mouth, vocal cord aperture to pass ETT), and will wear
off quickly.
Maintenance
• Confirm that the head is supported and not levitating.
• Fluoroscopy or single shots require appropriate radiation protection.
• EMG, MEPs, and SSEPs, may have improved conduction with the use of partial or total
intravenous drug administration. Propofol is often utilized as either the sole agent, or in
conjunction with volatile, nitrous, narcotic (remifentanil, sufentanil, fentanyl), or other
sedative/analgesic (dexmedetomidine, ketamine). Choice is based upon the preference or
experience of the anaesthetist, surgeon, neuromonitoring team, institution’s availability,
cost considerations, and patient factors. The goal is to maintain a steady state, particularly
during the period where injury may occur (dissection, discectomy), and avoid bolusing
(may create false positives) (3).
• Critical to maintain an adequate level of anesthesia since sudden movements can result in
danger to the patient (coughing, bucking, sitting up), especially since NMBDs cannot
provide a layer of safety against this.
• Avoid coughing and bucking
• Consider 30° reverse Trendelenburg position to avoid passive aspiration
• Neurologic exam soon after emergence
• RLN injury may increase risk of aspiration and stridor.
POSTOPERATIVE CARE
BED ACUITY
• Same-day discharge is practiced at some centers; however, the potential for postoperative
hematoma with resultant airway compromise makes it controversial. Proponents argue that
it can significantly reduce healthcare costs and there is only a minimal risk of postoperative
hematoma.
• Admission: Typically 1–2 days allowing for drain removal, neurologic assessment,
monitoring of swallowing/hoarseness, and hematoma. On POD 0, the patient should sit up
in a chair and begin supervised ambulation.
• Telemetry or ICU if significant comorbidities or frequent neurologic testing needs to be done
(new neurologic deficit, stridor)
• Cervical collar often utilized to allow time for the bone graft to fuse
ANALGESIA
• Typically mild at the incision site. Significant pain can occur at the bone grafting site.
• Persistent pain is often the result of permanent damage to the nerve making it unresponsive
to decompressive surgery; spinal cord stimulators may provide relief.
COMPLICATIONS
• Airway compromise: Hematoma formation may impinge on the trachea; RLN damage can
cause unopposed adduction of the cricothyroid muscle resulting in stridor; a traumatic
intubation or surgical trauma can cause airway edema.
• Anesthesia awareness
• Tongue laceration from MEPs
• Hoarseness and swallowing difficulties often resolve in a few months; they persist in
~1/250 cases and require an ENT consult.
• Failure to fuse: Increased in smokers (nicotine inhibits bone-growing cells), osteoporosis,
obesity, and malnutrition
• Hardware fracture: The metals, rods, and plates used to stabilize the spine may move or
break before the vertebrae are completely fused. Requires surgery to remediate.
• Bone graft migration: Movement from the correct position. Occurs soon after surgery and
more likely if hardware is not utilized to secure the graft or if multiple levels are fused.
Requires surgery to remediate.
• Transitional syndrome, also known as adjacent-segment disease: Occurs when the vertebrae
above or below a fusion take on extra stress. The added stress can eventually degenerate the
adjacent vertebrae and cause pain.
• Nerve damage: Numbness or paralysis is possible from direct injury during the procedure.
• Major vascular injury (rare): Internal and external jugular veins, vertebral, carotid and
thyroid arteries
• Dural tear, venous air embolism, and pneumothorax are rare but possible.
• Vocal cord paresis, epiglottis paralysis, and aphasia require feeding tube placement.
PROGNOSIS
• Relief of arm pain: 92–100% (3)
• Relief of neck pain: 73–83%
• Weakness and numbness may persist for weeks to months.
REFERENCES
1. Daniels AH, Riew KD. Adverse events associated with anterior cervical spine surgery. J Am
Acad Orthop Surg. 2008;16:729–738.
2. Padberg AM, Thuet ED. Intraoperative electrophysiologic monitoring: Consideration for
complex spinal surgery. Neurosurg Clin N Am. 2006;17:205–226.
3. Bohlman HH, Emery SE. Robinson anterior cervical diskectomy and arthrodesis for cervical
radiculopathy: A long-term follow-up of 122 pts. J Bone Joint Surg. 1993;75(9):1298–
1307.
• Somatosensory and motor evoked potentials
• Electromyelogram
CLINICAL PEARLS
• Careful airway evaluation and management (video laryngoscopy, awake or asleep FOB may
be considered)
• Keep neutral position of the neck and minimize airway manipulation during intubation.
• Neurophysiologic monitoring may be improved with TIVA.
• Postoperative airway compromise can result secondary to hematoma formation, RLN injury,
or soft-tissue swelling.
ANTERIOR MEDIASTINAL MASS
Shital Vachhani, MD
BASICS
DESCRIPTION
• Anterior mediastinal masses include teratomas, thyroid tumors, lymphomas, and thymomas.
They can result in dangerous and fatal cardiovascular or pulmonary structure compression
at the time of anesthesia induction, muscle relaxation, and positive pressure ventilation.
• Patients present to the operating room for biopsy or excision of the mass via a sternotomy,
thoracotomy, cervical mediastinoscopy, anterior parasternal mediastinoscopy, video-assisted
thoracoscopic biopsy, or awake CT-guided percutaneous biopsy.
• There are also case reports of patients with undiagnosed anterior mediastinal masses (AMM)
presenting emergently to the operating room for ascending aortic aneurysm and Cesarean
sections (1).
EPIDEMIOLOGY
Prevalence
• Half of all mediastinal masses are anterior (2).
• 60% of surgically resected lesions are neurogenic tumors, thymomas, and benign cysts (2).
Prevalence
In children, lymphoma is the most common AMM, followed by germ-cell tumors and thymic
masses.
Morbidity
• Masses in the anterior mediastinum are more likely to be malignant than those found in
other mediastinal compartments.
• Perioperative morbidity results from mass compression on vascular or pulmonary structures.
Mortality
Not available
• Depends on tissue diagnosis of mass, usually secondary to a mutation
• Often an incidental finding
• During spontaneous ventilation (SV), airways are held open by baseline negative
intrathoracic pressures and adherence of the pleura to the chest wall.
• Intrathoracic versus extrathoracic masses:
– Intrathoracic masses are found within the chest cavity. During SV, inspiration expands the
rib cage upward and outward and “lifts” the mass off vascular and respiratory structures.
In the standing position, exhalation does not typically result in symptoms. However, in the
recumbent and supine positions, exhalation can result in compression of structures.
– Extrathoracic masses are located outside the chest cavity and are further divided into
variable and fixed lesions.
Variable lesions: Redundant airway tissue (snoring), tracheomalacia, etc. During SV,
obstruction occurs during inspiration. The negative pressure that is generated in the
chest, distal to the mass, results in collapse of the airway. During exhalation, the
position pressure that is generated by the abdominal muscles, distal to the mass, stent
the airway open.
Fixed lesions: Goiter. Obstruction to airflow occurs during inspiration and exhalation.
• AMMs (intrathoracic masses) can result in extrinsic compression of structures:
– Respiratory: Trachea, major bronchus. The mass may prevent adequate ventilation by
compressing the trachea/bronchus while perfusion remains unchanged. This can result in
a V/Q mismatch called a pulmonary shunt.
– Cardiovascular: Great vessels, right ventricular outflow tract (posterior mediastinal masses
are more likely to affect the left atrium or ventricle). Encroachment does not produce
hemodynamic effects, whereas compression results in clinical manifestations similar to
pericardial tamponade. Right ventricular failure may be responsible for hypotension with
resultant dead space lung physiology (blood flow to the alveoli is decreased; hypoxemia
can result even in the absence of tracheal obstruction).
• Infants and children have more compressible airways and may be more susceptible than
adults to extrinsic airway obstruction (1).
• Superior vena cava (SVC) syndrome: The thin-walled venous system is easily compressible
by a large mediastinal mass. Thus, if there is obstruction to venous drainage from the upper
body, this can cause interstitial edema. Therefore, collateral veins with low resistance
become dilated.
• Management depends on the anatomy and pathology of the mass, as well as the surgical
procedure.
• Look for compression of the heart, great vessels, and airway structures during induction and
throughout the surgical procedure.
SYMPTOMS
• Respiratory symptoms: Nonproductive cough, stridor, wheezing, dyspnea, orthopnea that
worsens with recumbency or lying flat
• Syncope
• Patient may be asymptomatic and the mass incidentally found on CXR.
History
Shortness of breath or cough when lying flat (1)
Signs/Physical Exam
• Use of accessory muscles
• Plethora of the face (SVC syndrome)
TREATMENT HISTORY
If lymphoma, find out if pretreated with steroids or radiation to shrink the tumor. The
disadvantage of pretreatment is that it might affect tissue pathology (diagnosis).
MEDICATIONS
• Bronchodilators
• Steroids, if part of a chemotherapeutic regimen
Labs/Studies
• Flow volume loops to look for extrinsic or intrinsic compression in the supine and upright
positions (may see decrease in FEV1 and peak expiratory flow in supine position) (3). Their
predictive value has been questioned, particularly with the advent of newer and
sophisticated imaging modalities.
• CXR often incidentally identifies the mass; further imaging should be ordered.
• Arterial blood gas
• CT/MRI of the chest to display the location and extent of airway or cardiovascular
compromise; patients who are unable to lie flat may be done in the 30° angle, lateral, or
prone position.
• Echocardiogram to assess for cardiovascular effects (mass effect, cardiac compression, or
pericardial effusion). Anterior masses tend to compress the right heart.
• If thymoma, rule out myasthenia gravis by testing for acetylcholine receptor antibodies.
• Fine needle aspiration for biopsy
• Signs of SVC syndrome from compression
• Dynamic cardiac or airway compression with positional changes
• Parathyroid masses may be associated with hyperparathyroidism.
• Thymomas may have concurrent myasthenia gravis or immune deficiency.
• If the patient is a candidate to receive radiation or steroids to decrease the mass size
• If there is a potential for severe airway compromise, but a cardiopulmonary bypass (CPB)
machine and perfusionist are not available
CLASSIFICATIONS
• Mediastinal masses are described based on their location relative to the heart:
– Anterior: Teratomas, thyroid tumors, “terrible” lymphomas, thymomas (4Ts)
– Middle: Lymph nodes, vascular masses
– Posterior: Esophageal and neurogenic tumors, aneurysms
TREATMENT
Premedications
• If the patient is symptomatic, no benzodiazepines or opioids should be administered; they
can compound respiratory effects.
• If an awake, semi-sitting fiberoptic is planned (due to tracheal compression), glycopyrrolate
can be administered as an antisialagogue, and lidocaine to topicalize the airway.
• Thoracic epidural placement for tumor resection via a thoracotomy or sternotomy
• Postoperative intubation and ventilation may be necessary.
• CPB is a possibility.
INTRAOPERATIVE CARE
• Intubate while maintaining SV if possible
• A rigid bronchoscope and surgeon should be available for immediate assistance if airway
collapse occurs. The rigid bronchoscope can be inserted distal to the compression, and
“stent” the area open allowing adequate oxygenation/ventilation.
• Awake fiberoptic bronchoscopy may be appropriate if the mass appears to compress the
trachea. The endotracheal tube acts similar to the rigid bronchoscope to “stent” the area
open.
Monitors
• In patients with SVC syndrome, intravenous access should be placed in the lower extremity.
• Arterial line for blood pressure assessment and management; also if placed in the right
radial position, can serve as an indicator of mediastinal compression of the innominate
artery.
• Femoral cannulation under local anesthesia with CPB readily available, if there is a potential
for severe obstruction. If asymptomatic and there is no reason to believe that the mass will
compress the respiratory or cardiovascular structures, slow controlled induction may be
pursued.
• If unsure, try to maintain SV with inhalational agents, ketamine, or dexmedetomidine and
secure the airway.
• A surgeon should be available in the room during induction in the event that the mass
compresses the airway and SV is lost; or if a smaller endotracheal tube cannot be passed. A
rigid bronchoscope can be passed distal to the site of compression and stent the airway
open.
Maintenance
• While SV is ideal for large masses, positive pressure ventilation with a volatile agent is
usually used to optimize surgical conditions.
• Use of short-acting anesthetics is ideal.
• Avoid muscle relaxants, if possible. If they are necessary for the procedure, assisted manual
ventilation should be first attempted to assure that positive-pressure ventilation is possible
(1).
• Compression and cardiopulmonary collapse:
– Mainstem the endotracheal tube or insert a rigid bronchoscope
– Awaken the patient and return to SV
– Lateral position or prone position; positional changes can displace the mass and alleviate
compression. The history and physical is important to determine if the patient’s symptoms
are alleviated with certain positional changes.
– Chest compressions in the supine position
– Sternotomy and surgical elevation of the mass off the great vessels
– CPB
Extubation /Emergence
• Extubation should be performed only in a fully awake patient, with the rigid bronchoscope
in the room for backup in the event of airway collapse.
• Look for underlying tracheomalacia from tumor compression
FOLLOW-UP
BED ACUITY
• Floor bed may be appropriate.
• ICU care may be needed depending on the intraoperative course.
• CBC to check for anemia
• For thoracic epidurals, the acute pain service should be contacted.
COMPLICATIONS
• Damage to the surrounding structures from procedure (e.g., phrenic and recurrent laryngeal
nerve)
• Pneumothorax
REFERENCES
1. Slinger P, Karsli C. Management of the patient with a large anterior mediastinal mass:
Recurring myths. Curr Opin Anaesthesiol. 2007;20(1):1–3.
2. Strollo DC, Rosado de Christenson ML, Jett JR. Primary mediastinal tumors. Part 1: Tumors
of the anterior mediastinum. Chest. 1997;112(2):511–512.
3. Neuman GG, Weingarten AE, Abramowitz RM, et al. The anesthetic management of an
anterior mediastinal mass. Anesthesiology. 1984;60:144–147.
• Mediastinoscopy
• Flow-volume loops
• Superior vena cava syndrome
• Recurrent laryngeal nerve
CODES
ICD9
519.3 Other diseases of mediastinum, not elsewhere classified
ICD10
J98.5 Diseases of mediastinum, not elsewhere classified
CLINICAL PEARLS
• History, physical, and review of imaging studies are critical in determining the extent of
mediastinal mass involvement.
• Major airway complications are more commonly seen in the postoperative period, rather
than in the operating room.
ANTI-DIURETIC HORMONE (ADH)
BASICS
DESCRIPTION
Antidiuretic hormone (ADH), also known as vasopressin, regulates urinary volume and
osmolality by decreasing diuresis; it also functions as a potent vasoconstrictor at higher doses.
• ADH is a nonapeptide (consists of nine amino acids) with an arginine vasopressin attached
to the 8th amino acid location; thus also referred to as arginine vasopressin (AVP).
• AVP (V1) serves as an important backup system for blood pressure control and
cardiovascular sympathetic modulation in the hypotensive and hypovolemic states.
– Hypotension is sensed by baroreceptors in the left heart, aortic arch, and carotid sinus and
is a very potent trigger for AVP release. It can increase levels by 10–1000-fold.
– At these elevated concentrations, AVP acts as a vasoconstrictor of the mesentery, skin, and
skeletal tissues by stimulating the V1 receptor on vascular smooth muscle.
• ADH (V2) increases tubular conservation of water and urine osmolality, while decreasing
plasma osmolality in response to decreased (5–10%) plasma volume, increased plasma
osmolality, or pain, stress, hypoxia.
– When extracellular fluid osmolality increases, osmoreceptors in the hypothalamus shrink,
which stimulates ADH release from the posterior pituitary.
– In the thick ascending loop of Henle, it increases solute (NaCl) reabsorption; however,
water is impermeable, resulting in decreased osmolarity within the tubules.
– In the collecting ducts, it acts on V2 receptors to increase water permeability and hence
water movement along the osmotic gradient (increases water reabsorption/conservation,
no effect on solute).
• V3 receptor agonist stimulates ACTH and cortisol secretion by activating corticotropin-
releasing hormone.
• Signaling cascades:
– V1 and V3 activation stimulates phospholipase C, ultimately mobilizing intracellular
calcium stored in the endoplasmic reticulum.
– The V2 receptor responds to ADH through the activation of a G protein-coupled adenylyl
cyclase. ATP is converted to cAMP, which activates protein kinase. Protein kinase causes
water channels to fuse with the apical cell membrane and increases its permeability to
water.
• AVP promotes platelet aggregation and coagulation by increasing endothelial release of
factor VIII and von Willebrand factor (vWF).
ANATOMY
• Produced in the paraventricular and supraoptic nuclei of the hypothalamus and then
transported by way of neuronal axons to the posterior pituitary, where it is stored in
granules.
– When extracellular fluid osmolality increases, these nuclei shrink and release ADH from
the posterior pituitary. Conversely, a decrease in osmolality causes osmoreceptors to swell
and suppress ADH release.
• ADH is metabolized in the liver and kidneys and the half-life is between 5 and 20 minutes.
• Diabetes insipidus (DI) is characterized by impairment in renal concentrating ability due to
either decreased ADH secretion (central DI) or failure of the renal tubules to respond
normally to circulating ADH (nephrogenic DI).
– Central DI causes: Trauma and postsurgical state (neurosurgical), anatomic (tumors and
infiltrative diseases, e.g., histiocytosis X), infectious (meningitis and encephalitis),
hereditary, and vascular (pituitary apoplexy)
– Nephrogenic DI causes: Chronic renal disease, electrolyte disorders (hypokalemia and
hypercalcemia), sickle cell disease, hyperproteinemias, and drugs (most notably lithium).
Nephrogenic DI is due to either a decreased response to circulating ADH or interference
with the renal countercurrent mechanism.
– Signs and symptoms of DI are polyuria and polydipsia.
– Laboratory findings are increased plasma osmolarity and decreased urine osmolarity.
– In the water deprivation test, water is withheld from the patient to induce dehydration
and to assess urinary water retention. In DI, the plasma osmolarity increases without a
urinary response to retain water. In central DI (hypothalamic), treatment with ADH
concentrates the urine. In nephrogenic DI, the kidneys fail to produce hypertonic urine
following the administration of exogenous ADH.
– Treatment of central DI involves the administration of intranasal DDAVP (1-deamino-8-D-
arginine vasopressin). Nephrogenic DI therapy is directed toward the underlying disorder
and ensuring adequate fluid intake. Thiazides induce diuresis causing an ablation of the
medullary gradient, thus decreasing urine volume output.
• Syndrome of inappropriate antidiuretic hormone (SIADH) is characterized by fluid retention,
hypoosmolality, and hyponatremia due to excessive release of ADH.
– Causes include CNS disorders including skull fracture; subdural or subarachnoid
hemorrhage; acute encephalitis; TB meningitis; Guillain–Barré syndrome; malignant
neoplasm; drugs including antineoplastics, oxytocin, narcotics, phenothiazines, tricyclic
antidepressants, carbamazepine; positive pressure ventilation; and postoperative pain.
– Signs and symptoms: Confusion, seizures, and coma due to osmotic water shifts causing
brain edema
– Laboratory findings include a decreased [Na+] (<130 mEq/L), decreased plasma
osmolarity (<270 mOsm/kg), and hypertonic urine.
– Treatment includes correction of the underlying cause, water restriction to 800–1,000
mL/d, demeclocycline which interferes with renal action of ADH, and 3% saline given
over several hours. Central pontine myelinolysis may occur if serum Na+ is corrected too
quickly.
• Hyponatremia (plasma [Na+] <130 mEq/L) due to SIADH should be corrected prior to all
elective procedures, even in the absence of symptoms. Lower concentrations may result in
significant cerebral edema that can be manifested intraoperatively as a decrease in the MAC
for volatile agents, or postoperatively as agitation, confusion, or somnolence.
• Anesthetic agents have little direct effect on ADH secretion. Indirectly, the surgical stress
response increases ADH secretion and may last 2–3 days postoperatively.
• Vasopressin and synthetic agonists may be used to treat intraoperative hypotension,
vasodilatory shock including anaphylaxis and sepsis, and during CPR.
– Septic shock: Endogenous AVP depletion contributes to vasodilation. AVP, when combined
with norepinephrine, increases peripheral vascular resistance and arterial blood pressure
(1)[A]. Some markers of renal function are improved with short-term AVP infusion, and
mortality is reduced at 28 days when AVP is combined with corticosteroids. Alone, AVP
permits sparing of conventional vasopressors in septic patients with relative AVP
deficiency (2)[B]. Therefore, AVP (0.01–0.04 U/min) is commonly used in the
management of septic patients and is endorsed by international sepsis treatment
guidelines (3)[A].
– Refractory hypotension in patients taking ACE inhibitors or ARBs. The administration of
vasopressin 1–2 units may be helpful in refractory cases.
– Cardiac arrest: 40 U of vasopressin via either the intravenous or intraosseous route can
replace the first or second 1 mg dose of epinephrine in patients with pulseless arrest
(pulseless electrical activity, ventricular fibrillation, or tachycardia) according to the 2010
American Heart Association guidelines on CPR (4)[B].
• DDAVP: In perioperative patients with mild hemophilia A and type 1 von Willebrand
disease, desmopressin increases endothelial release of factor VIII and vWF.
Orally administered ADH is essentially biologically inactive due to rapid hydrolysis by trypsin
and therefore must be administered parenterally. DDAVP is the only clinically available ADH
agonist and is bio-available via the intravenous, intranasal, and subcutaneous routes.
EQUATIONS
The sodium deficit, or amount of NaCl necessary to raise plasma [Na+] to the desired level,
can be estimated by the following formula:
[Na+] deficit = TBW × (desired [Na+] – measured [Na+]), where TBW = total body
weight in kilograms
FIGURE 1. In the thick ascending loop of Henle, ADH increases NaCl reabsorption thereby decreasing osmolarity within
the tubules. In the collecting ductules, ADH induces water reabsorption along the osmotic gradient resulting in more
concentrated urine.
REFERENCES
1. Treschan TA, Peters J. The vasopressin system: Physiology and clinical strategies.
2. Patel BM, Chittock DR, Russell JA, et al. Beneficial effect of short-term vasopressin infusion
during severe septic shock. Anesthesiology. 2002;96:576–582.
3. Holt NF, Haspel KL. Vasopressin: A review of therapeutic applications. J Cardiothorac Vasc
Anesth. 2010;24:330–347.
4. Neumar RW, Otto CW, Link MS, et al. Part 8. Adult advanced cardiovascular life support:
2010 American Heart Association guidelines for cardiopulmonary resuscitation and
emergency cardiovascular care. Circulation. 2010;122:S729–S767.
• Diabetes insipidus
• Carotid sinus
• Syndrome of inappropriate diuretic hormone (SIADH)
• Von Willebrand disease
• Hyponatremia
• Urine osmolarity
CLINICAL PEARLS
• Antidiuretic hormone (ADH) increases NaCl reabsorption in the loop of Henle and water
permeability in the collecting duct resulting in increased water conservation, increased
urine osmolality, and decreased plasma osmolality.
• The management of nephrogenic DI is directed toward the underlying cause and also
includes fluids and thiazides. Central DI is treated with intranasal DDAVP.
• Treatment of SIADH includes correction of the underlying cause, water restriction,
demeclocycline and possibly 3% saline given over several hours. Central pontine
myelinolysis may occur if serum Na+ is corrected too quickly.
• Elevated AVP concentrations, triggered by hypotension, result in vasoconstriction.
• Vasopressin and synthetic agonists may be used to treat intraoperative hypotension,
anaphylactic and septic shock, and during CPR.
ANTIFIBRINOLYTICS
BASICS
DESCRIPTION
• The 2 antifibrinolytic agents in current clinical use – epsilon-aminocaproic acid (EACA) and
tranexamic acid (TA) – are synthetic lysine analogs that are similar in mechanism of action,
molecular weight, metabolism, and clinical effects.
• Clinical uses include prophylaxis and/or adjunctive therapy for the prevention of
perioperative bleeding in a variety of patients and surgeries:
– Cardiac surgery requiring cardiopulmonary bypass (CPB)
– Liver transplantation or resection
– Orthopedic procedures (e.g., revision joints, spinal surgery)
• Mechanism and regulation of fibrinolysis: The normal fibrinolytic response is a complex
physiologic reaction that prevents excessive intravascular hemostasis at the site of a
vascular injury.
– Vascular injury results in the activation of pro-coagulant pathways that culminate in the
formation of fibrin clot at the site of vascular injury.
– Intravascular fibrin and thrombin initiate the normal fibrinolytic response.
• Tissue plasminogen activator (tPA) and plasminogen are serine proteases in endothelial cells
that are released at the site of vascular injury. They bind to positively charged lysine
residues on the fibrin molecule.
– tPA and plasminogen bind to fibrin which then converts plasminogen to plasmin.
– Plasmin directly cleaves fibrin clot, resulting in fibrin degradation and clot breakdown.
– Regulation of fibrinolysis occurs via multiple local and systemic mechanisms. A delicate
balance between competing pro-coagulant and anti-coagulant systems occurs during
normal intravascular homeostasis.
• Mechanism of action of lysine analogs:
– EACA and TA share a common mechanism of action by reversibly inhibiting the binding of
plasminogen to charged lysine sites on the surface of fibrin molecules, thus preventing the
conversion of plasminogen to plasmin.
– Unlike the serine protease inhibitor aprotinin, lysine analogs do not directly inhibit the
actions of plasmin.
– The potency of TA is approximately 10 times higher than EACA.
– Plasma half-life of both drugs is approximately 2 hours, and excretion is primarily via
renal mechanisms. 95% of the drug is excreted unchanged in the urine.
• Excessive systemic fibrinolysis may be stimulated by:
– Disease states: Sepsis, massive trauma
– Major surgery: Cardiac surgery with CPB, liver transplantation, and major orthopedic
surgery
• Consumptive coagulopathy is defined by the presence of the simultaneous generation of
both thrombin and plasmin, which results in the potential for severe diffuse bleeding.
• Systemic fibrinolysis may be detected clinically by the observation of excessive bleeding at
sites of tissue injury:
– Surgical wounds
– Intravascular catheters
– Invasive devices such as Foley catheters
• Laboratory abnormalities reflecting the degradation of fibrin clot may assist in the diagnosis
of fibrinolysis. They include:
– Increased levels of fibrin split products
– Increased D-dimer
– Decreased levels of fibrinogen
– Increased levels and activity of tPA
– Characteristic abnormalities on thromboelastogram
• Side effects of antifibrinolytics:
– Renal:
EACA has been shown to exhibit a range of nephrotoxicity (acute tubular necrosis,
myoglobin-induced renal failure, glomerular capillary thrombosis) in patients following
prolonged use and/or receiving high doses. Cardiac surgical patients with normal renal
function who receive moderate dosing protocols do not demonstrate significant renal
effects.
Both drugs should be avoided in patients with severe renal dysfunction.
– Central nervous system:
Lysine analogs cross the blood–brain barrier and have the potential to cause neuronal
hyperexcitability.
TA has been associated with a higher level of seizure activity in cardiac surgical patients
compared to aprotinin.
– Immunologic:
Lysine analogs have low molecular weights, making them less antigenic than larger
molecules associated with anaphylaxis, such as aprotinin.
– Prothrombosis:
In non-heparinized surgical patients, co-administration of antifibrinolytics poses a
potential concern for prothrombotic complications.
Studies in cardiac and liver transplant surgery patients have not shown an increase in the
rate of thrombotic complications in patients receiving antifibrinolytics (myocardial
infarction, stroke, deep vein thrombosis, pulmonary embolism, or liver graft vascular
thrombosis) (1,2).
• Antifibrinolytic therapy has been mainly used to control the consumptive coagulopathy that
can occur during cardiac surgery with CPB, liver transplantation, and major orthopedic
surgery.
• Cardiac surgery with CPB: Application of all extracorporeal circulation devices, including
CPB, results in the continuous systemic generation of thrombin. Despite the use of heparin
to prevent massive intravascular coagulation, thrombin generation continues throughout
CPB. TPA release, stimulated by circulating thrombin, increases throughout the duration of
CPP and remains elevated for many hours after (accompanied by accelerated fibrinolysis).
Prophylactic antifibrinolytic therapy is regularly used to decrease CPB-associated
fibrinolysis.
– Multiple studies have demonstrated decreased postoperative transfusion, decreased risk of
re-exploration, and reduced plasma markers of fibrinolysis compared to placebo.
Additionally, no increase in acute coronary artery thrombosis has been shown to occur.
TA has been studied more intensively than EACA in cardiac surgery (1,3,4).
– TA may be administered in low- or high-dose regimens. Low-dose TA: 10 mg/kg loading
dose, 1 mg/kg/hr infusion. High-dose TA: 50–150 mg/kg loading dose, 1 mg/kg/hr
infusion.
– EACA dosages: 5–10 g loading dose prior to incision, 1 g/hr infusion. The maximum safe
total dosages of EACA have been described between 30 and 90 g.
– Abnormal renal function requires lower doses.
– Some experts recommend the continuation of antifibrinolytic therapy for up to 12 hours
following CPB, although common practice is to discontinue treatment upon completion of
surgery (5).
– Topical TA administered in the wound at surgical closure has been shown to reduce
postoperative blood drainage (5).
• Orthotopic liver transplantation (OLT): Enhanced fibrinolysis is common with OLT,
especially during the anhepatic and early post-anhepatic phases of the procedure. Increased
tPA activity and decreased fibrinolytic inhibitor activity regularly occur during OLT.
Fibrinolysis contributes to blood loss and transfusion requirements during OLT. Serial
laboratory coagulation testing (thromboelastography, fibrinogen, D-dimer, fibrin
degradation products) is routinely employed to assist in the diagnosis of excessive
fibrinolysis during OLT.
– Clinical use of antifibrinolytics in OLT varies by practice: Prophylactic infusion and
selective bolus rescue dosing have been described.
– Both TA and EACA have been used clinically in OLT for many years, although TA has been
studied more extensively (2).
– TA has not been shown to increase the incidence of postoperative deep vein thrombosis or
pulmonary embolism (3,6).
– EACA: A single 1 g dose has been shown to be effective in normalizing fibrinolytic
abnormalities on thromboelastography. However, it has not definitively been shown to
impact transfusion requirements during OLT (2).
– TA has been shown to decrease blood loss and reduce transfusion requirements in
prospective studies during OLT (2,3).
– Significant preoperative renal dysfunction poses an increased risk for the exacerbation of
acute kidney injury by antifibrinolytics.
– Thromboembolic complications are a rare but devastating intraoperative complication
during OLT; there are concerns regarding the pro-thrombotic potential of antifibrinolytics
in this setting. However, antifibrinolytic therapy has never been determined as a definitive
cause of thromboembolic complications in this patient population. Antifibrinolytic therapy
should be withheld in OLT patients with a known pre-existing hypercoagulable state (2).
• Orthopedic surgery: Antifibrinolytic therapy has been employed in a variety of major
orthopedic procedures with a risk of significant blood loss, including adult and pediatric
scoliosis spine surgery and revision joints. Major prolonged orthopedic surgery may result in
significant bone and tissue trauma that can stimulate fibrinolysis. The use of a lower
extremity tourniquet, as in total knee arthroplasty, may be associated with enhanced
fibrinolysis.
– Total knee arthroplasty: Studies have demonstrated that TA use decreases blood loss and
transfusion requirements (3,6).
– Pediatric scoliosis: TA has also been shown to decrease intraoperative blood loss.
– A variety of regimens, including preoperative and postoperative oral and IV dosing, have
been described.
• Future directions in antifibrinolytic therapy:
– Fibrinogen levels: Effective antifibrinolytic therapy requires maintenance of adequate
levels of fibrinogen. Low fibrinogen levels are associated with significant post-CPB
bleeding in cardiac surgery. Cryoprecipitate transfusion has been the standard treatment
for increasing fibrinogen levels. Newly developed factor concentrates, including virus-
inactivated purified fibrinogen, may be an alternative to cryoprecipitate and fresh frozen
plasma for the treatment of hypofibrinogenemia (7).
– Aprotinin: Following the withdrawal of aprotinin in 2007, antifibrinolytic therapy has
been limited to the use of the lysine analogs.
– CU-2010—a synthetic protease inhibitor with properties similar to aprotinin—has recently
been described as a new antifibrinolytic agent; however, further clinical studies are
required (8).
REFERENCES
1. evi M. Pharmacological strategies to decrease excessive blood loss in cardiac surgery: A
meta-analysis of clinically relevant endpoints. Lancet. 1999;354:1940–1947.
2. Xia VW, Steadman RH. Antifibrinolytics in orthotopic liver transplantation: Current status
and controversies. Liver Transplant. 2005;11(1):10–18.
3. Levi M. Pharmacologic methods to reduce perioperative bleeding. Transfusion.
2008;48:S31–S38. Laupacis A. Drugs to minimize perioperative blood loss in cardiac
surgery: Meta-analysis using perioperative blood transfusion as the outcome. The
International Study of Peri-operative Transfusion (ISPOT) Investigators. Anesth Analg.
1997;85:1258–1267.
4. Edmunds HL. Managing fibrinolysis without aprotinin. Ann Thorac Surg. 2010;89:324–331.
5. Eubanks JD. Antifibrinolytics in Major Orthopaedic Surgery. J Am Acad Orthop Surg
March 2010;18: 132–138.
6. evy JH. Prohemostatic Treatment in Cardiac Surgery. Seminars in Thrombosis and
Hemostasis 2012;38:237–243.
7. ietrich W. Anesthesiology. 2009;110(1):123–130.
ADDITIONAL READING
• Dalmau A. Hemostasis and coagulation monitoring and management during liver
transplantation. Curr Opin Organ Transplant. 2009;14;286–290.
• Ide M. Lessons from the aprotinin saga: Current perspective on antifibrinolytic therapy in
cardiac surgery. J Anesth. 2010;24:96–106.
• Pulmonary embolism
• Cardiopulmonary bypass
• D-dimer
• Fibrinogen
CLINICAL PEARLS
• Excessive intravascular activity of the fibrinolytic system that results in clinically significant
bleeding may be stimulated by disease states or major surgery.
• Following the withdrawal of aprotinin, current antifibrinolytic therapy is limited to the
lysine analogs—EACA and TA.
• TA has been better studied than EACA for perioperative antifibrinolytic therapy.
• TA has been shown to improve perioperative bleeding in cardiac surgery with CPB, OLT,
and major orthopedic surgery.
ANTITHROMBIN III
Fei Zheng, MD, MPH, MS
Nanhi Mitter, MD
BASICS
DESCRIPTION
• Antithrombin III (ATIII) is one of the most important coagulation inhibitors; it stops the
progression of clot formation by inhibiting serine proteases. It is also known as
antithrombin or heparin cofactor 1.
• ATIII is the fundamental enzyme for the therapeutic action of heparin.
• ATIII is a single-chain glycoprotein weighing 58 kD. It is produced by the liver and vascular
endothelial cells and is composed of 432 amino acids. ATIII circulates in the plasma with a
half-life of 2–3 days.
• ATIII inhibits serine proteases (IXa, XIa, XIIa and plasmin to a lesser degree); by blocking
their action, it prevents thrombin and factor Xa activity and ultimately clot formation.
• There are 2 functional sites on antithrombin:
– Site that binds serine proteases
– Site that binds glycosaminoglycans (i.e., heparin)
• ATIII concentrates have been developed. Currently, there are 2 types available for
intravenous administration:
– Human plasma-derived concentrate (i.e., Thrombate III®).
Prior to usage, it needs to be reconstituted with sterile water and used within 3 hours.
Must be administered intravenously; other medications should not be given through the
same line.
Classified as a pregnancy category B; safety has not been established in the pediatric
population.
Possible adverse reactions: Dizziness, chest tightness, nausea, unpleasant taste in the
mouth, chills, or cramps. Additionally, because it is derived from plasma, it has the
potential for infectious agent transmission (i.e., Creutzfeldt–Jakob, hepatitis).
– Recombinant human concentrate (i.e., ATryn®) is produced in transgenic goats with a
copy of the human antithrombin gene.
Prior to usage, it needs to be reconstituted with sterile water and should be used within
3 hours.
It is available for intravenous use only.
Classified as a pregnancy category C; safety has not been established in the pediatric
population.
Contraindications to use include a hypersensitivity to goat or goat milk.
The most common adverse reactions include hemorrhage and infusion site reaction.
ANATOMY
Produced by the liver and vascular endothelial cells
• ATIII can have decreased levels or impaired function from either acquired or familial causes.
• Acquired causes:
– Impaired function
Heparinized patients; can decrease to 1/3rd normal values
Estrogen-based contraceptives
– Decreased levels
Neonates/infants <6 months old possibly secondary to severe malnutrition
Pregnancy: Third trimester, preeclampsia, eclampsia, disseminated intravascular
coagulation (DIC)
Cirrhosis, nephrotic syndrome, estrogen, chemotherapy, malnutrition, inflammatory
bowel disease, small bowel resection, etc.
• Familial antithrombin deficiency is mostly an autosomal dominant trait and has a 1:2,000–
5,000 prevalence in the general population. Up to 5% of individuals can present with
thrombotic disease.
– Type I (quantitative): Various DNA mutations that reduce the quantity of antithrombin.
Diagnosed with immunoassays.
– Type II (qualitative): 1 amino acid change that reduces the quality of antithrombin at
either the heparin or the thrombin binding site. Diagnosed with functional assays.
– Type III: Insufficient heparin receptors (normal quantity and quality of antithrombin)
– Clinical presentations:
Recurrent thromboembolic events
Peak incidence between 15 and 40 years of age
Most common site of thrombosis is the legs.
Thrombosis or fetal loss during pregnancy
Resistance to heparin
Family history
• Management of patients with ATIII deficiency (qualitative or quantitative) is controversial.
Some potential treatment options that are currently available include:
– Asymptomatic patients: No prophylaxis is needed but patients should be informed of the
increased risk of thromboembolic events under prothrombotic conditions (i.e., prolonged
bed rest, major surgeries or trauma, pregnancy, carcinoma, oral contraceptives).
– Heparin is generally the first-line treatment but it may deplete the low concentration of
normal antithrombin already present. Heparin binds to and causes a conformational
change that results in a 4,000-fold increase in ATIII activity.
– Coumadin may be added as an oral maintenance after initiation of heparin.
– Fresh frozen plasma transfusion can provide a source of antithrombin. Drawbacks include
transfusion-related acute lung injury (TRALI) and the transmission of infections.
– Antithrombin concentrates may be considered for:
Thromboembolic prophylaxis or treatment of ATIII deficiency, predominately for surgical
and peripartum women
Homozygous antithrombin deficiency not responding to heparin. Shown to be as
effective as 2 units of FFP in heparin-resistant patients undergoing elective cardiac
surgery
Acute situations (i.e., ongoing thrombosis, DIC)
Critically ill individuals
Patients in whom anticoagulation is contraindicated
– Steroids may stimulate antithrombin synthesis; however, more research is needed.
EQUATIONS
• Human plasma-derived concentrate:
– Initial dose = [(desired – current antithrombin level expressed in% of normal level) ×
weight in kg] /1.4
– For example: 70 kg patient with baseline antithrombin level of 50% and desired level of
150%. Initial dose = [(150 – 50) × 70] / 1.4 = 5,000 IU
– Maintenance dose: 60% of initial dose, given once every 24 hours
• Recombinant human concentrate:
– Initial dose = [(100 – current antithrombin activity expressed in% of normal level) ×
weight in kg] / 2.3 (1.3 in parturients)
– For example: 70 kg patient with a baseline antithrombin level of 50%. Initial dose =
[(100 – 50) × 70] / 2.3 = 1,522 IU
– Maintenance dose = [(100 – current antithrombin activity expressed in% of normal level)
× weight in kg] / 10.2 (5.4 in parturients)
REFERENCES
1. Ambruso D, Jacobson LJ, Hathaway WE. Inherited antithrombin III deficiency and cerebral
thrombosis in a child. Pediatrics. 1980;65: 125–131.
2. Avidan MS. Recombinant human antithrombin III restores heparin responsiveness and
decreases activation of coagulation in heparin-resistant patients during cardiopulmonary
bypass. J Thorac Cardiovasc Surg. 2005;130(1):107–113.
3. Beresford CH. Antithrombin III deficiency. Blood Rev. 1988;2:239–250.
4. http://en.wikipedia.org/wiki/Alexander_Schmidt_%28physiologist%29
5.
http://www.fda.gov/downloads/BiologicsBloodVaccines/BloodBloodProducts/ApprovedProd
6. http://www.talecris-pi.info/inserts/thrombate.pdf
7. Patnaik MM. Inherited antithrombin deficiency: A review. Haemophilia. 2008;14:1229–
1239.
8. Perry DJ. Antithrombin and its inherited deficiencies. Blood Rev. 1994;8:37–55.
9. Sawamura A, Gando S, Hayakawa M. Effects of antithrombin III in patients with
disseminated intravascular coagulation diagnosed by newly developed diagnostic criteria
for critical illness. Clin Appl Thromb Hemost. 2009;15(5):561–566.
10. The Medical Letter Online. Recombinant human antithrombin (ATryn). Med Lett Drug
Therap. 2009;51(1323):83–84.
• End-stage liver disease
• Fresh frozen plasma
CLINICAL PEARLS
• If ACT levels remain unchanged following heparin administration:
– Flush the line through which heparin was given
– Verify that the heparin is entering the bloodstream (e.g., the intravenous line is within a
vessel)
– Verify that the correct heparin dose was administered
– Check the expiration date on the heparin vial
– Administer additional heparin (up to 600 U/kg)
– Consider administering ATIII concentrate
– Consider administering FFP (2–4 units in adults)
AORTIC DISSECTION
Michael L. Boisen, MD
David G. Metro, MD
BASICS
DESCRIPTION
• Aortic dissection is characterized by the development of a tear in the aortic intima that
allows blood to enter a false lumen and cause a separation in the layers of the vessel wall.
• It is the most common aortic catastrophe, occurring with a frequency exceeding that of
abdominal aortic aneurysm rupture.
• Most acute dissections (80%) develop in the absence of a pre-existing aneurysm; thus,
distinction should be made between the terms “dissection” and “aneurysm.”
• The diagnosis of aortic dissection is missed in up to 40% of patients at initial presentation as
physical findings may be absent or nonspecific or mimic conditions for which the
therapeutic strategy is dissimilar (e.g., myocardial ischemia).
EPIDEMIOLOGY
Incidence
• Peak incidence in the 6th and 7th decades with the mean age of diagnosis at 63 years
• Males account for 65% of cases
• Circadian and seasonal patterns have been described with peak frequency between 8:00 AM
and 9:00 AM and during winter months.
• 3.5 per 100,000 persons per year (US data)
Prevalence
Actual prevalence unknown since many patients (∼20%) die prior to hospital presentation.
Autopsy series report 1 acute aortic dissection for every 128 to 745 autopsies.
Morbidity
Neurologic complications are the main cause of disability among survivors.
Mortality
• Acute dissection of the ascending aorta has a 30-day mortality rate of 20% with surgical
repair and 50% with medical therapy alone.
• Death most often results from aortic rupture, cardiac tamponade, stroke, and visceral
ischemia.
• Hypertension (72%)
• Atherosclerosis (31%)
• Smoking
• Bicuspid aortic valve
• Coarctation
• Deceleration trauma
• Cocaine/crack
• Pregnancy
• Iatrogenic (percutaneous cardiac and aortic or valvular surgical procedures)
• Hereditary fibrillinopathies (Marfan, Ehlers–Danlos, annuloaortic ectasia, and familial aortic
dissection)
• Vascular inflammation (Behet’s disease, syphilitic aortitis, Takayasu arteritis, and giant cell
arteritis)
PATHOPHYSIOLOGY
• The development of a tear in the intimal layer of the aorta exposes the medial layer to the
force of intraluminal blood flow. Entry of blood cleaves the intima and media longitudinally
in an anterograde and/or retrograde direction; this serves to create a second or “false”
lumen, separated from the true lumen by an intimal flap.
• Propagation of aortic dissection is linked to mean, peak, and diastolic recoil arterial pressure
as well as the rate of rise of aortic pressure (aortic dP/dt).
• Malperfusion of branch vessels can occur due to occlusion by the intimal flap or by
compression of the true lumen by expansion of the false lumen.
• Most originate in the ascending aorta (65%), followed by the descending aorta (20%), aortic
arch (10%), and abdominal aorta (5%).
• Hemodynamic stabilization, pain control, and blood pressure optimization are priorities of
initial management. In general, systolic blood pressure should be maintained at 100–120
mm Hg or the lowest level that maintains effective end-organ perfusion.
• In the past, uncomplicated distal aortic dissection (Stanford B, DeBakey III) was managed
medically; however, endovascular techniques are increasingly being applied.
• Uncomplicated distal aortic dissection (Stanford B, DeBakey III) was historically managed
medically; however, endovascular techniques are increasingly being applied.
SYMPTOMS
• Sudden, severe chest, back, and abdominal pain are the most common symptoms (>90%).
• Syncope (up to 20%) with or without a history of pain
• Neurologic symptoms (stroke, spinal cord ischemia, peripheral nerve ischemia)
• Acute heart failure (7%) due to myocardial ischemia or acute aortic insufficiency
• Limb ischemia
• Hoarseness (due to recurrent laryngeal nerve compression)
History
• 96% of acute aortic dissections are identified with the following prediction model:
– Aortic pain with immediate onset, a tearing or ripping character, or both
– Mediastinal widening, aortic widening, or both on chest radiography
– Pulse differentials (absence of a proximal extremity or carotid pulse), blood pressure
differentials (systolic pressure difference >20 mm Hg between arms), or both
Signs/Physical Exam
• Hypertension (69% of distal and 36% of proximal dissections)
• Hypotension, shock, or tamponade (27% of proximal dissections)
• Pulse or blood pressure differentials (20%)
• Focal neurologic deficits (12%)
• Murmur of aortic insufficiency (32%)
• Pleural effusion (left > right)
• Horner syndrome
Labs/Studies
• Baseline and serial cardiac biomarkers, BUN/Cr, CBC with platelets, coagulation profile and
TEG, if available
• ECG may be normal (∼30%) or show nonspecific ST-T changes (40%), left ventricular
hypertrophy (26%), ischemia (15%), or infarction (10%).
• Chest radiograph findings include mediastinal widening (61%), abnormal aortic contour
(49%), pleural effusion (19%), displacement/calcification of aorta (14%). Normal findings
are present in 12% of patients.
• CT angiography is quick, highly sensitive, and specific; 64-slice multidetector CT with
cardiac gating may allow for simultaneous evaluation of pulmonary and coronary arteries.
• TEE is highly sensitive for ascending aortic dissection and allows rapid evaluation of
hemodynamic instability (tamponade, coronary dissection, valvular regurgitation, tension
hemothorax, etc.).
• MRI/MRA has high sensitivity and specificity, avoids radiation, and iodinated contrast; but
is more time-consuming and contraindicated with metallic implants.
• Aortography: Previously the reference standard, this is performed less often and rarely as
the initial study.
• Compromise of aortic branches and subsequent malperfusion can affect several systems:
– Cardiovascular: Acute aortic valvular insufficiency due to aortic root dilation or leaflet
disruption; ischemia/infarction (dissections often arise from right sinus of Valsalva
causing inferior wall myocardial infarction); limb ischemia from subclavian or iliac
arteries
– Neurologic: Syncope, stroke (innominate or common carotid arteries), spinal cord
ischemia (radicular arteries), peripheral ischemic neuropathy
– Pulmonary: Left pleural effusion/hemothorax
– Renal: Ischemia, infarction, acute renal failure
• Gastrointestinal: Abdominal organ ischemia (celiac, mesenteric arteries)
CIRCUMSTANCES TO DELAY/CONDITIONS
• Delays are associated with increased mortality; thus, evaluation should be limited to the
acquisition of appropriate diagnostic studies and evaluation of conditions that will alter
surgical candidacy or affect perioperative management.
• Pericardiocentesis as a temporizing measure for tamponade has been associated with
increased risk of PEA arrest and death compared to immediate sternotomy and surgical
control of the aorta.
CLASSIFICATIONS
• Acute (<2 weeks) or chronic (>2 weeks)
• Stanford:
– Type A: Ascending aorta involved
– Type B: Ascending aorta not involved (distal to takeoff of left subclavian artery)
• DeBakey:
– Type I: Ascending aorta, arch, descending aorta
– Type II: Ascending aorta only
– Type IIIa: Descending aorta only
– Type IIIb: Descending and abdominal aorta
TREATMENT
Premedications
• Short-acting drugs permit rapid termination of effect, if desired, and should be considered.
• Morphine, beta-blockers, and vasodilating drugs can be used to control pain and blood
pressure. Esmolol is ultra-short-acting and has organ-independent elimination (metabolized
within red blood cells).
• Sodium nitroprusside may cause an increase in aortic dP/dt; it is generally added only after
a negative inotrope is administered.
• Nicardipine may be preferred in patients intolerant of beta-antagonists and does not cause a
reflex tachycardia.
• Enalaprilat may be useful in refractory hypertension due to renal artery compromise.
• Phenylephrine and norepinephrine are preferred pressors due to a relative lack of associated
increase in aortic dP/dt.
INTRAOPERATIVE CARE
• No superiority has been demonstrated with any given anesthetic technique.
• For open repair, GETA is typically employed, alone or in combination with epidural
anesthesia; epidural placement may be precluded by hemodynamic instability.
• Evoked-potentials monitoring may influence technique (i.e., volatile anesthetic
concentration, use of muscle relaxant).
• For endovascular repair, local, regional, and general techniques may be used.
Monitors
• ECG with ST-segment analysis
• Temperature (central and peripheral sites if bypass is to be used)
• Foley catheter
• Arterial line: Right radial artery may be preferred if blood flow to the left subclavian artery
is disrupted due to dissection or cross-clamp placement. Femoral artery insertion may
permit monitoring of distal perfusion pressures.
• Central venous access may be appropriate for IV access and administration of vasoactive
medications.
• Pulmonary artery catheterization can provide SvO2, SVR, CO, PAP.
• TEE aids in diagnosis, anatomic localization, identification of complications, and
characterization of valvular and ventricular function in real time.
• Lumbar drains and evoked-potentials may be placed for patients at risk for spinal cord
ischemia.
• The potential for catastrophic hemorrhage necessitates appropriate vascular access,
availability of blood products, rapid infuser system, and autologous red cell salvage.
• Slow, controlled titration of medications to the desired effect can help maintain
hemodynamic stability. Hypertension and tachycardia increase shear stress and risk of
rupture.
• Single-lumen ETT may be typically placed for a median sternotomy approach.
• Lung isolation with a double lumen tube or bronchial blocker aids in the exposure of the
descending aorta and is preferred for procedures using the lateral thoracotomy approach.
Maintenance
• Thermoregulation: Forced air and fluid warming systems are necessary due to significant
heat loss with open procedures.
• Fluid management: Maintenance of intravascular volume may be challenging due to
significant hemorrhage and evaporative losses; no specific colloid or crystalloid strategy has
emerged as superior.
• Coagulation: Consumption and dilution of coagulation factors and platelets may be
significant; replacement is guided by conventional coagulation studies as well as TEG, if
available.
• Renal protection: Maintenance of renal blood flow and urine output is essential; IV mannitol
and fenoldopam can be employed to reduce the risk of kidney injury.
• Ongoing cardiac or pulmonary instability, bleeding, hypothermia, or neurologic injury may
necessitate continued mechanical ventilation; otherwise patients may be extubated at the
conclusion of the procedure.
• Pain, hypertension, and tachycardia should be anticipated and addressed.
POSTOPERATIVE CARE
BED ACUITY
Intensive care unit
COMPLICATIONS
• Aortic rupture
• Cardiac failure (ischemia, aortic insufficiency, tamponade)
• Postoperative pulmonary failure
• Neurologic deficits (stroke, paraplegia)
• Renal insufficiency
REFERENCES
1. Clouse WD, Hallett Jr JW, Schaff HV, et al. Acute aortic dissection: Population-based
incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc.
2004;79:176–180.
2. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic
Dissection (IRAD): New insights into an old disease. JAMA. 2000;283:897–903.
3. Golledge J, Eagle KA. Acute aortic dissection. Lancet. 2008;372:55–66.
4. Penco M, Paparoni S, Dagianti A, et al. Usefulness of transesophageal echocardiography in
the assessment of aortic dissection. Am J Cardiol. 2000;86:53G–56G.
5. von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection.
Arch Intern Med. 2000;160:2977–2982.
6. Isselbacher EM, Cigarroa JE, Eagle KA. Cardiac tamponade complicating proximal aortic
dissection: Is pericardiocentesis harmful? Circulation. 1994;90:2375–2379.
ADDITIONAL READING
• Nienaber CA, Eagle KA. Aortic dissection: New frontiers in diagnosis and management. Part
I: From etiology to diagnostic strategies. Circulation. 2003;108:628–635.
• Nienaber CA, Eagle KA. Aortic dissection: New frontiers in diagnosis and management. Part
II: Therapeutic management and follow-up. Circulation. 2003;108:772–778.
• Intubation/extubation criteria
• Aortic rupture
CODES
ICD9
• 441.00 Dissection of aorta, unspecified site
• 441.01 Dissection of aorta, thoracic
• 441.02 Dissection of aorta, abdominal
ICD10
• I71.00 Dissection of unspecified site of aorta
• I71.01 Dissection of thoracic aorta
• I71.02 Dissection of abdominal aorta
CLINICAL PEARLS
• Acute dissection of the proximal aorta is a surgical emergency, and preoperative evaluation
should be expedited.
• Preoperative management is directed at the reduction of arterial pressure and aortic dP/dt.
• Monitoring is essential to anesthetic management and should be individualized to the
specifics of the patient, nature of dissection, and surgical procedure.
AORTIC PRESSURE CURVE
Ryan Crowley, MD
BASICS
DESCRIPTION
• The aortic pressure curve is measured directly with an indwelling needle or catheter that is
inserted while the chest is open. The pressure in the aorta can also be directly measured by
percutaneous catheters advanced centrally from peripheral arteries.
• A transducer is then attached to the catheter to provide an arterial pressure tracing on a
physiologic monitor.
• Commonly, a more accessible central artery (femoral) or peripheral artery (radial) is
accessed using various techniques to place a catheter into the artery.
• Direct monitoring of the arterial pressure curve allows for beat-to-beat measurement of
blood pressure.
• Simultaneously measuring both the left ventricular and aortic pressures demonstrates that
pressure rapidly rises in the left ventricle (LV) during early systole (see Figure 1).
• Isovolumetric contraction is the period between mitral valve closure and aortic valve
opening. When the pressure in the LV exceeds the aortic diastolic pressure, the aortic valve
opens and the upslope of the aortic pressure tracing begins.
• The peak of the aortic pressure tracing is the systolic blood pressure and in the absence of
significant aortic valve disease, also represents the LV end-systolic pressure.
• As the ventricle stops contracting and begins to relax, the pressure falls in the aorta and the
LV. When the pressure in the aortic root exceeds the LV pressure, the aortic valve closes.
This represents the second heart sound (S2).
• The dicrotic notch on the downslope of the aortic pressure tracing represents the closure of
the aortic valve. The sudden closure of the valve briefly increases the pressure in the aortic
root.
• The pressure continues to fall after the dicrotic notch as blood “runs off” to the peripheral
circulation. The lowest pressure prior to the next ejection is the diastolic blood pressure.
• Mean arterial pressure (MAP) can be estimated by the calculation: MAP = (2DBP + SBP)/3;
where DBP is diastolic blood pressure and SBP is systolic blood pressure.
ANATOMY
• The aorta is an artery composed of 3 layers. From the lumen outward it is composed of the
intima, the media, and the adventitia.
• All arteries share a similar anatomical structure, but as arteries course to more peripheral
locations, the compliant media decreases in thickness. Consequently, peripheral arteries are
less compliant than central arteries. As measurements are made in progressively more distal
arteries, there is an increase in pulse pressure (increased systolic and decreased diastolic
pressure) with only a very slight decrease in MAP.
• Due to transmission of the pressure wave from a central to peripheral location, the onset of
the pressure curve is slightly delayed in peripheral locations as compared to the aorta.
• The aortic pressure curve can be suggestive of several pathologic states.
• A slow upstroke of the pressure tracing (decreased dP/dT) can be observed with:
– Poor LV contractility
– Aortic stenosis or arterial stenosis (e.g., coarctation of the aorta) if measured distal to the
obstruction
– Overdampening, however, can also present in this manner and should be ruled out.
• An extra wave may be seen in the aortic pressure curve, known as an anacrotic notch, which
occurs prior to peak systolic pressure. This phenomenon is most often observed in aortic
valve disease and is representative of high velocity flow.
• “Run off" describes the slope of the aortic pressure curve after the dicrotic notch and
corresponds to the afterload that the heart must contract against.
– Slow “run off" may be seen in high systemic vascular resistance (SVR) states such as
vasoconstrictor administration or a distal obstruction such as aortic coarctation
– Rapid “run off" may be seen with poor arterial compliance, aortic insufficiency, or a low
SVR state (e.g., sepsis, anaphylaxis)
• A wide pulse pressure can be indicative of very low arterial compliance (e.g., atherosclerotic
disease) or aortic insufficiency (good LV function with significant diastolic run-off due to an
incompetent aortic valve).
• Significant fluctuations in the aortic and arterial pressure tracings with respiration (>15%)
indicate decreased ventricular filling and may resolve with volume administration.
• The area under the curve (AUC) of the aortic pressure curve is proportional to stroke
volume.
• Given the same pressure, narrow curves with a small AUC represent smaller stroke volumes
than wide or “full” pressure tracings. This principle is the basis for various cardiac output
measurement devices that analyze the arterial waveform to estimate cardiac output.
• In aortic stenosis, the LV pressure tracing peak is significantly higher than the aortic
pressure peak.
– The area between the 2 tracings is the mean gradient.
– The difference between the 2 systolic peaks is the peak-to-peak gradient. The peak-to-peak
gradient is lower than the peak instantaneous gradient (PIG) derived from
echocardiography.
• Direct arterial blood pressure monitoring (typically peripherally) is indicated whenever
significant or rapid changes in blood pressure are anticipated.
• When displayed on a monitor with a static scale, the clinician can detect changes in systemic
blood pressure immediately by observing changes in the arterial pressure tracing.
• The blood pressure value displayed on physiologic monitors is averaged over many
preceding seconds while changes in the waveform are displayed without any delay.
• Continuous MAP determination can be utilized to ensure appropriate end-organ perfusion
pressures to the brain, kidneys, etc. in patients with limited reserve.
• Continuous diastolic blood pressure measurements can be used to ensure adequate LV
perfusion in patients at risk for ischemia (especially in conjunction with monitoring of
pulmonary capillary wedge pressure [PCWP], left atrial pressure [LAP], or pulmonary artery
diastolic pressure [PADP]).
• Continuous systolic blood pressure measurement can be used to minimize aortic wall tension
in patients with significant aortic disease (e.g., aneurysm or dissection).
EQUATIONS
• MAP = 2/3 DBP + 1/3 SBP; where MAP is mean arterial pressure, DBP is diastolic blood
pressure, and SBP is systolic blood pressure
• MAP = (2 [DBP + SBP])/3
• CO = (MAP – CVP) × SVR; where CO is cardiac output, MAP is mean arterial pressure, CVP
is central venous pressure, and SVR is systemic vascular resistance
GRAPHS/FIGURES
FIGURE 1. Aortic pressure curve (solid line) with the left ventricular pressure curve (dashed lines) superimposed.
REFERENCES
1. Marik PE, Cavallazzi R, Vasu T, et al. Dynamic changes in arterial waveform derived
variables and fluid responsiveness in mechanically ventilated patients: A systematic review
of the literature. Crit Care Med. 2009;37(9):2642–2647.
2. Morgan P, Al-Subaie N, Rhodes A. Minimally invasive cardiac output monitoring. Curr
Opin Crit Care. 2008;14(3):322–326.
• Cardiac output
• Aortic stenosis
CLINICAL PEARLS
• Blood is ejected from the left ventricle to the aorta during the period where the upstroke of
the aortic pressure curve meets the left ventricular pressure curve and until the dicrotic
notch.
• Respiratory variation in the aortic pressure tracing predicts for volume responsiveness.
• Direct measurement of arterial pressure allows for the continuous determination of
perfusion pressures to end-organs.
• As one measures arterial pressure from proximal to distal locations, the
– Systolic pressure increases
– Diastolic pressure decreases
– Pulse pressure increases
– MAP slightly decreases
AORTIC REGURGITATION
BASICS
DESCRIPTION
• The aortic valve, normally consisting of 3 leaflets, opens during ventricular systole and
closes during diastole. Valve closure prevents backflow of blood from the aorta to the left
ventricle (LV) and helps maintain aortic diastolic pressure and coronary perfusion pressure.
• Aortic regurgitation (AR) is the presence of a backflow leak through the valvular apparatus
during diastole.
– Ranges in severity from trace, mild, moderate, or severe; it is classified by the amount of
regurgitant volume, regurgitant orifice area size, and pressure equalization half-time by
echocardiography.
– Regurgitation may be associated with any condition that alters aortic valve closure. Aortic
dilation, aneurysm, dissection, and abscess are external causes of aortic valve dysfunction
and account for about half of all AR cases. Rheumatic valve disease, collagen vascular
diseases, connective tissue diseases (especially Marfan syndrome (1)[C]), congenital
malformations, senile degeneration, and infective endocarditis are direct valvular
conditions that commonly produce AR in the remainder of cases.
– Acute AR is the sudden onset of backflow leak usually due to an acute event such as aortic
dissection or valvular trauma.
– Chronic AR has a gradual onset and may be sustained for many years.
– May also accompany aortic stenosis—a narrowing of the open valvular area
EPIDEMIOLOGY
Prevalence
• Worldwide, rheumatic heart disease is the most common cause of AR.
• In the US, congenital and degenerative valvular and aortic disease is most common.
• Congenital bicuspid aortic valves occur in 1–2% of the US population and may contribute to
AR.
Prevalence
• 13% in men, 8.5% in women in a Framingham study (2)
• In the US population, severe AR is <1% (3).
• Chronic AR is more prevalent than acute AR.
Morbidity
• Acute AR has a higher rate of morbidity and mortality due to the underlying
pathophysiology. This can result in diastolic and systolic dysfunction and eventually
decompensation (CHF).
• Chronic AR mortality is related to the eventual decompensation of the LV; it is more
common in severe AR. Decreased ejection fraction and LV function have a poor prognosis
for recovery, even after repair.
• Surgical management becomes the common end point to both types of AR.
Mortality
• Acute AR has a high mortality due to sudden uncompensated cardiovascular changes usually
requiring immediate surgical management.
• Chronic AR mortality relates to eventual decompensation of the LV and may occur at any
age usually with severe AR. Decreased ejection fraction and LV function has a poor
prognosis for recovery even after repair.
• Yearly mortality risk relates to NYHA classification for chronic severe AR:
– Asymptomatic: 2.8%
– NYHA Class I: 3.0%
– NYHA Class II: 6.3%
– NYHA Class III–IV: 24.6% (4)
• Male gender has a greater risk for AR with a related increased risk of hypertension,
connective tissue and congenital valvular diseases, which may result in presentation at a
younger age.
• Severe AR is most commonly diagnosed at age 60 and above.
• Acute AR results in an acute increase in LV diastolic volume, decreased aortic diastolic
pressure (forward flow), decreased coronary perfusion pressure, volume overload, and
decreased diastolic function of the LV. This leads to an increase in myocardial demand,
acute fulminant CHF, and cardiogenic shock. Common causes of acute AR, including aortic
dissection, warrant emergent surgical repair.
• Chronic AR has a more insidious onset and may take years to become symptomatic. As
regurgitant volume and AR worsen over time, the LV has time to remodel with eccentric
hypertrophy and dilation. The increase in diastolic volume is compensated by the enlarged
LV, increased heart rate, and decreased systemic vascular resistance (SVR). Ejection fraction
is maintained and may prevent symptoms without exertion or positional changes. As time
passes, the ventricle becomes “too enlarged” with resultant increases in wall stress and
decreases in myocardial perfusion (leads to diminished EF, CHF, and end-organ
hypoperfusion). Recall Laplace’s law where Tension = (Pressure × Radius)/Wall Thickness;
as the radius increases, tension also increases (increases myocardial oxygen consumption).
Sympathetic stimulation increases SVR to maintain pressure but worsens AR; hinders
forward flow. Without timely surgical repair the heart may not be able to significantly
recover.
• Maintenance of cardiac output, coronary perfusion, and prevention of cardiac
decompensation are the primary goals.
• Normal sinus rhythm and avoidance of bradycardia to minimize regurgitant time
• SVR may be mildly decreased, but should be balanced between facilitating forward flow
(decreasing regurgitation) and maintaining adequate coronary and systemic perfusion
pressure.
• Careful fluid management and inotropic support to prevent cardiovascular overload or
collapse
SYMPTOMS
• Chronic AR may be asymptomatic for decades.
• Palpitations and tachycardia
• Fatigue
• Dyspnea on exertion
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Angina
History
• Family history of cardiac valvular disease, collagen or connective tissue disease, or
congenital malformations
• History of rheumatic disease or risk factors for endocarditis
• Commonly diagnosed after symptomatic exercise or during workup for diastolic or systolic
CHF
• May be discovered early after detailed physical exam and auscultation of heart murmur
• Usually classified by echocardiographic measurement of color Doppler flow across the valve
Signs/Physical Exam
• Syncope
• Cyanosis
• Decrescendo diastolic murmur
• Watson’s hammer pulse (bounding pulse)
• Corrigan’s carotid pulse
• Wide pulse pressure
• Signs of CHF
TREATMENT HISTORY
• Medical management of angina, CHF, diabetes, hypertension, and hyperlipidemia, if
associated
• Previous history of balloon aortic valvuloplasty or valve replacement
• Previous treatment of infective endocarditis
• Transesophageal echocardiography for diagnosis and risk stratification
MEDICATIONS
• Antihypertensives including calcium channel blockers; beta-blockers are usually not
prescribed since they may cause bradycardia.
• Anti-anginals including nitrovasodilators
• Heart failure treatments including digoxin, ACEI/ARB, and diuretics
• Statin therapy if indicated
Labs/Studies
• Basic metabolic profile: Monitoring electrolytes and kidney function
• CBC: Monitoring for preoperative infection and hematocrit and platelet counts adequate for
surgery
• CXR: Cardiopulmonary status
• CT scan for evaluation of aorta
• Echocardiogram: Diagnosis and classification of disease severity and ventricular function
• Basic coagulation studies: Adequate levels for surgery and evaluation of liver function
• Dilated cardiomyopathy and diastolic dysfunction
• Concomitant mitral stenosis or regurgitation in rheumatic heart disease
• Pulmonary hypertension, congestion, and pleural effusion
• Hypertension
• Unrelated end-organ failure
• Recent myocardial infarction or stroke
CLASSIFICATIONS
Severe AR criteria:
• >60 mL regurgitant volume
• >50% regurgitant volume
• Effective regurgitant orifice area >0.3 cm2
• Color Doppler Vena Contracta >0.6 cm
• Regurgitant jet >60% of LVOT diameter
• Aortic valve pressure half-time <250 ms
• Early closure of mitral valve and LV dilation
TREATMENT
Premedications
Midazolam to prevent anxiety and increased sympathetic tone, as appropriate
Risk for intraoperative stroke, myocardial infarction, and death should be discussed.
INTRAOPERATIVE CARE
• Depends on the procedure; sedation, general (endotracheal tube or laryngeal mask airway)
and regional anesthesia may be utilized.
• Neuraxial techniques can result in a sympathectomy and facilitate forward flow (reduce
regurgitation), but may reduce coronary perfusion pressure.
Monitors
• Invasive monitors may be chosen based upon the severity of AR and the surgical procedure.
• Smooth, controlled induction to maintain vital signs within normal limits
• Anticholinergic medications may be administered to maintain a NSR and slightly increase
the heart rate.
Maintenance
• Volatile and/or intravenous anesthetics may be utilized. Reductions in SVR are desirable to
facilitate forward flow; however, adequate cerebral and coronary perfusion should be
ensured. Total intravenous techniques may be associated with bradycardia, particularly if
utilizing high doses of remifentanil.
• Fluid balance includes maintaining normal preload and hematocrit >24–30 g/dL to
optimize forward flow and myocardial oxygen balance. Excessive preload may add to
regurgitant volume and cause LV failure.
No additional concerns
FOLLOW-UP
BED ACUITY
Depends on surgical procedure and severity of underlying disease
Standard postoperative fluid and electrolyte management and related laboratory studies
COMPLICATIONS
Perioperative arrhythmia
REFERENCES
1. Odili AN, Amusa GA. Aortic aneurysm with valvular insufficiency: Is it due to Marfan
syndrome or hypertension? A case report and review of literature. J Vasc Nurs.
2011;29(1):16–22.
2. Singh JP, Evans JC, Levy D, et al. Prevalence and clinical determinants of mitral, tricuspid,
and aortic regurgitation. Am J Cardiol. 1999;83:897–902.
3. Maurer G. Aortic regurgitation. Heart. 2006;92(7):994–1000.
4. Dujardin KS, Enriquez-Sarano M, Schaff HV, et al. Mortality and morbidity of aortic
regurgitation in clinical practice: A long-term follow-up study. Circulation.
1999;99(14):1851–1857.
ADDITIONAL READING
• 2006 American College of Cardiology/American Heart Association Guidelines
• Van Dyck MJ, Watremez C, Boodhwani M, et al. Review articles: Transesophageal
echocardiographic evaluation during aortic valve repair surgery. Anesth Analg.
2010;111:59–70.
CODES
ICD9
• 395.1 Rheumatic aortic insufficiency
• 424.1 Aortic valve disorders
• 746.4 Congenital insufficiency of aortic valve
ICD10
• I35.1 Nonrheumatic aortic (valve) insufficiency
• I06.1 Rheumatic aortic insufficiency
• Q23.1 Congenital insufficiency of aortic valve
CLINICAL PEARLS
• Aortic regurgitation (AR) is most commonly an acquired disease but may be related to
congenital malformations and several systemic conditions such as Marfan syndrome.
• Significant signs and symptoms include shortness of breath, angina, syncope, and systolic
and diastolic congestive heart failure with eccentric hypertrophy and a dilated LV.
• Severity is classified by echocardiographic criteria; 60 mL or 50% regurgitant volume being
severe AR.
• Acute AR is life-threatening and often requires immediate surgical management.
• Chronic AR requires medical or surgical management and may be asymptomatic until late
stages. Symptomatic, severe AR with below normal LV EF requires urgent treatment and has
poorer prognosis.
AORTIC STENOSIS
BASICS
DESCRIPTION
• The aortic valve normally consists of 3 leaflets which open during ventricular systole with
an area of >2.5 cm2 and close during diastole. Since the aortic valve is the smallest area
through which blood leaves the heart, its diameter determines maximum blood flow.
• Aortic valve stenosis is a narrowing of this area at the valve itself. New recommendations
classify severe aortic stenosis (AS) as an area <1.0 cm2 with a transvalvular mean gradient
>40 mm Hg, although symptoms may begin at much earlier stages. It is the most common
valvular lesion in the US.
EPIDEMIOLOGY
Prevalence
• Congenital AS occurs in 4–8 per 1,000 live births.
• Congenitally bicuspid aortic valves occur in 1–2% of the US population and later in life
accounts for 30–40% of AS.
• >50% of AS is acquired.
Prevalence
Present in 2–4% of adults aged 65 years and older (1)[B].
Morbidity
• Risk for acute myocardial infarction, syncope, congestive heart failure (CHF), and
endocarditis
• Low-grade severe stenosis with preserved ejection fraction has similar outcomes to those
with moderate stenosis (2)[B].
• Asymptomatic very severe AS (area <0.75 cm2) has a very poor prognosis and rapid
deterioration; elective valve surgery should be considered (3)[A].
Mortality
• 9% mortality per year
• Symptomatic AS sudden death risk is 15–20% with a 3-year mortality of 75%.
• When symptoms of angina, syncope, or CHF are present, 50% mortality is seen at
approximately 5, 3, and 2 years, respectively.
• Age <70 years: The etiology of AS is more commonly rheumatic or bicuspid aortic valve
disease.
• Age >70 years: The etiology of AS is more commonly calcific AS.
• Risk factors are similar to vascular disease and may include hyperlipidemia, hypertension,
and diabetes.
• The basic pathophysiology of AS stems from obstruction of cardiac output with a highly
resistant valve opening. As the stenosis becomes more severe, the left ventricle (LV)
compensates with concentric hypertrophy to overcome the increasing afterload/tension;
stroke volume is maintained. Additionally, cardiac output becomes fixed and highly
dependent upon heart rate and filling (diastolic dysfunction).
• Myocardial oxygen supply and demand
– Supply decreases from: A thickened myocardium (coronary blood flow must
perfuse/penetrate), increased left ventricular end diastolic pressure (decreased coronary
diastolic perfusion pressure), and limited cardiac output.
– Demand increases from: A thickened myocardium (more muscle equals increased energy
consumption) and increased afterload.
• Over time, systolic function can decrease as the LV decompensates and dilates or becomes
ischemic. Ventricular systolic and diastolic dysfunction can lead to pulmonary congestion
and CHF. Additionally, sympathetic tone increases and may contribute to symptoms.
• A slow heart rate is desired to allow time for forward flow after an adequate LV pressure has
been attained. Maintaining a sinus rhythm is necessary, as LV hypertrophy impairs filling
and the atrial kick is needed to maintain adequate LV end diastolic volume (preload).
• Both normal and congenitally bicuspid valves undergo degeneration through which scarring,
calcification, and sclerosis become the most common cause of acquired AS.
• Maintenance of cardiac output, coronary perfusion (diastolic perfusion pressure), normal
sinus rhythm, volume status, and prevention of cardiac decompensation are the primary
goals.
• Inotropic support may be necessary to prevent cardiovascular overload or collapse.
SYMPTOMS
• Severity of symptoms may be classified by NYHA I–IV. Early symptoms often include
exertional shortness of breath.
– Anginal pain may be an early symptom and may occur in the absence of coronary
occlusion.
– Syncope may occur due to a decrease in cardiac output and exertional systemic
vasodilation.
– CHF is often a late sign that signifies severe valve stenosis or cardiomyopathy.
History
• Commonly diagnosed after symptomatic exercising or during workup for diastolic or systolic
CHF
• May be discovered early after detailed physical exam and heart auscultation
Signs/Physical Exam
• Crescendo–decrescendo systolic murmur and decreased S2 sound
• Pulsus parvus et tardus with narrow pulse pressure
• Signs of CHF and increased sympathetic tone
TREATMENT HISTORY
Previous history of balloon aortic valvuloplasty or valve replacement
MEDICATIONS
• Antihypertensives including beta-blockers and calcium channel blockers
• Anti-anginals including nitrovasodilators
• Heart failure treatments including digoxin, ACEI/ARB, and diuretics
• Statin therapy
Labs/Studies
• Basic metabolic profile to monitor electrolytes and kidney function; aids with perioperative
management
• CBC: WBC to monitor for infection; Hct and platelet counts should be adequate for surgery.
• CXR to assess cardiopulmonary status
• Echocardiogram for diagnosis and classification of disease severity (valve area, transvalvular
gradient) and ventricular function
• Basic coagulation studies to evaluate liver function
• Cardiac: LV hypertrophy, diastolic dysfunction, hypertension, aortic regurgitation (due to
poor valve closure), mitral stenosis, or regurgitation in rheumatic heart disease
• Pulmonary: Hypertension, congestion, and pleural effusion
• Decompensated CHF
• Sepsis or infection
• Unrelated end-organ failure
• Recent myocardial infarction or stroke
CLASSIFICATIONS
• AS severity by valve area:
– >2.5 cm2: Normal
– 1.5–2.0 cm2: Mild stenosis
– 1.0–1.5 cm2: Moderate stenosis
– <1.0 cm2: Severe stenosis
• AS severity by mean pressure gradient:
– <25 mm Hg: Mild stenosis
– 25–40 mm Hg: Moderate stenosis
– >40 mm Hg: Severe stenosis
TREATMENT
Premedications
Benzodiazepines may be useful to prevent anxiety and tachycardia; however, they should be
titrated cautiously to avoid sympatholysis.
• Risk for intraoperative stroke, myocardial infarction, and death should be discussed.
• Arterial line placement if needed
INTRAOPERATIVE CARE
• Depends on the procedure: Sedation, general (endotracheal tube or laryngeal mask airway)
and peripheral nerve blocks may be utilized.
• Neuraxial techniques can result in a sympathectomy and decreased systemic vascular
resistance (SVR) that can impair coronary perfusion. This technique may be considered in
mild or moderate AS. Epidurals can allow for slower bolusing, time for fluid loading, and
treatment of hypotension with vasopressors (phenylephrine).
Monitors
• 5-lead EKG for arrhythmia and ischemia
• Arterial line for beat-to-beat BP monitoring
• Invasive monitors may be chosen based upon the severity of AS and the surgical procedure.
A smooth, controlled induction should be performed to maintain vital signs within normal
limits (heart rate and SVR) and allow time for treatment.
Maintenance
• Volatile anesthetics, intravenous, or a combination may be utilized. The goal should be to
maintain normal sinus rhythm and SVR.
– Total intravenous anesthesia with propofol and high-dose narcotics can result in
bradycardia and hypotension; consider concurrent phenylephrine, ephedrine, or an
anticholinergic.
– Volatile agents can decrease SVR and myocardial contractility; consider concurrent
phenylephrine.
• Preload. Because stroke volume is fixed, adequate filling volumes are essential in
maintaining a stable cardiac output. For patients at risk for ischemic events, hematocrit
values may also be of concern.
• Rhythm, rate, blood pressure
– Normal sinus rhythm may be maintained by minimizing cardiac stress and avoiding pro-
arrhythmic drugs
– Slight bradycardia may improve coronary perfusion time and LV filling but may decrease
total cardiac output (stroke volume is fixed). Conversely, tachycardia increases myocardial
oxygen consumption along with decreases in LV filling time and diastolic coronary
perfusion time. Caution should be exercised when using powerful chronotropes or
anticholinergics.
– Hypotension and hypertension should be managed with rate and rhythm in mind. All
inotropes and vasopressors may be used with caution.
• Ischemia usually occurs with arrhythmia, tachycardia, or hypotension, and the treatment
usually lies in the reversal of those conditions.
• Avoid tachycardia and hypotension
• Use standard extubation criteria
FOLLOW-UP
BED ACUITY
Depends on surgical procedure, severity of underlying disease, and intraoperative events
MEDICATIONS/LAB STUDIES/ CONSULTS
Cardiology consult may be considered in severe disease if ischemic events occurred
intraoperatively.
COMPLICATIONS
• Perioperative arrhythmia
• Mental status changes and stroke
• Myocardial infarction
REFERENCES
1. Freeman RV, Otto CM. Spectrum of calcific aortic valve disease: Pathogenesis, disease
progression, and treatment strategies. Circulation. 2005;111(24):3316–3326.
2. Jander N, Minners J, Holme I, et al. Outcome of patients with low gradient “severe” aortic
stenosis and preserved ejection fraction. Circulation. 2011;123(8):887–895.
3. Rosenhek R, Zilberszac R, Schemper M, et al. Natural history of very severe aortic stenosis.
Circulation. 2010;121(1):151–156.
ADDITIONAL READING
• Andritsos M, Singh N, Patel P, et al. The year in cardiothoracic and vascular anesthesia:
Selected highlights from 2010. J Cardiothorac Vasc Anesth. 2011;25(1):6–15.
• Aortic regurgitation
• Aortic valve replacement
CODES
ICD9
• 395.0 Rheumatic aortic stenosis
• 424.1 Aortic valve disorders
• 746.3 Congenital stenosis of aortic valve
ICD10
• I35.0 Nonrheumatic aortic (valve) stenosis
• Q23.0 Congenital stenosis of aortic valve
• I06.0 Rheumatic aortic stenosis
CLINICAL PEARLS
• Severity is classified by valve area and transvalvular gradients; values <1.0 cm2 and a mean
pressure gradient of 40 mm Hg indicate severe AS.
• Maintenance of general anesthesia includes supporting cardiac systolic function, optimizing
fluid management, sustaining normal sinus rhythm, and monitoring for ischemia.
AORTIC VALVE REPLACEMENT
Daniel Castillo, MD
BASICS
DESCRIPTION
General
• Aortic valve replacement is an open, intracardiac surgery procedure in which the stenotic or
regurgitant aortic valve is replaced with a healthy valve. The 2 basic artificial heart valves
are mechanical and tissues valves.
• Following sternotomy, opening of the pericardium, and routine venous and arterial
cannulation, the patient is taken onto full cardiopulmonary bypass (CPB). After the heart is
arrested, the aorta is opened to expose the aortic valve. The valve leaflets are excised and
the annulus is debrided. The annulus is then measured to properly match the prosthetic
valve. Interrupted sutures are placed through the annulus for its entire circumference and
then passed through the sewing ring. The prosthesis is tied securely in place.
• Systemic rewarming is initiated during the final stages of the valve implantation, and the
left ventricle is allowed to fill during aortic closure. With the patient in the head-down
position, all remaining air is vented from the left heart and aorta. The cross-clamp is
removed.
• Pacing wires and chest tubes are placed and the patient is weaned from bypass. Once the
patient is stable, decannulation and heparin reversal are accomplished in routine manner.
• Concomitant root replacement may be necessary in patients with aortic stenosis secondary
to bicuspid valve pathology and concurrent aortic root dilations.
• Pulmonary autograft (Ross procedure) involves replacing the aortic valve with a pulmonary
valve autograft and right-sided reconstruction with a homograft; it is used in children and
adolescents.
• Minimally invasive aortic valve surgery through smaller incisions with specialized
instruments is being explored; for the surgery on the valve itself conventional instruments
and techniques are used.
– Only selected patients are eligible for these approaches.
– Initial results are favorable in regard to clinical outcome, perioperative complications and
cost.
– No randomized controlled trials are available comparing minimally invasive and open
surgery.
• Transcatheter aortic valve replacement is a new catheter-approach that obviates the need for
open heart surgery. It is being used in Europe and parts of the world, but only tested in
clinical trials in the US. The results for high-risk patients with severe aortic stenosis who are
not surgical candidates are promising (1)[B].
Position
• Supine, arms tucked
• Temporary Trendelenburg at the time of left ventricle de-airing, prior to coming off bypass
Incision
• Standard: Median sternotomy
• Alternative incision sites (e.g., right second intercostal anterior thoracotomy) are used as
part of “minimally invasive aortic valve surgery.”
Approximate Time
4–8 hours, depending on the experience of the team and technical difficulties
EBL Expected
• CPB machine leads to dilution.
• Blood loss typically ranges from 1,000 to 2,000 mL.
Hospital Stay
Typical length of stay in the surgical ICU is 1–3 days and 3–7 days in the hospital overall.
• Valve (mechanical or tissue)
• CPB machine (operated by perfusionist)
• Minimally invasive approaches require special equipment.
• Transesophageal echocardiography probe (intraoperative examination performed by echo
trained anesthesiologists or cardiologist)
EPIDEMIOLOGY
Prevalence
In 2009 approximately 70,000 patients underwent aortic valve replacement in the US.
Morbidity
• The 2008 ACC/AHA Valvular Disease guidelines refer to risk stratification models to
estimate the risk of in-hospital mortality and morbidity of valve surgery with or without
coronary artery bypass (2). All models have drawbacks such as estimating risk for only one
specific procedure or not including patient’s variable like nutritional status. There are 3
major models:
– The US-based registry by the Society of Thoracic Surgeons (STS) (3)[B]. It includes data
from nearly 90% of cardiac surgery providers in the US and may provide the most
accurate risk stratification for aortic valve replacement.
– The European System for Cardiac Operative Risk Evaluation (“EuroScore")
– The scoring system developed from Great Britain’s and Ireland’s national database
Mortality
• Varies significantly with age, comorbidities, type of valvular lesion, ventricular function,
other concomitant valvular surgery, and/or bypass surgery
• Risk stratification models are useful to predict mortality risk for the individual patient.
Example: Mortality <1% in a 65-year-old patient with symptomatic severe aortic stenosis,
normal left ventricular function and otherwise healthy; however, mortality increases >1%
for the same patient with hypertension and diabetes.
• Hemodynamic stability from induction to the initiation of bypass. Management depends on:
The type of lesion (stenosis vs. regurgitation), right and left ventricular function, pulmonary
pressures, and other clinical factors.
• After successful replacement and completion of bypass, the goal is to maintain adequate
cardiac output and blood pressure; inotropes may be required if left ventricular function is
depressed.
SYMPTOMS
Vary depending on the type of lesion (stenosis vs. regurgitation) and the time course (acute
vs. chronic)
History
Determine if there is a history of esophageal strictures or other abnormality that would
prohibit placement of transesophageal echocardiography during the procedure.
Signs/Physical Exam
See “Aortic Stenosis” and “Aortic Regurgitation” chapters
MEDICATIONS
• Medical management depends on the type of lesion and other comorbidities.
• Initiation of statins may reduce the incidence of atrial fibrillation and mortality.
Labs/Studies
• Preoperative transthoracic echocardiography and sometimes a transesophageal
echocardiography are performed.
• Coronary angiography is routinely performed since significant coronary artery disease is a
common comorbidity and may require concurrent coronary bypass grafting.
• Renal dysfunction; further deterioration may be precipitated by contrast dye used during
catheterization (prior to the valve replacement) and increased bypass time.
• Chronic pulmonary disease may acutely worsen secondary to bypass and lead to hypoxemia
when coming off.
• Pre-existing neurologic deficits put the patient at great risk for further mental status
deterioration postoperatively.
TREATMENT
Premedications
Consider gentle anxiolysis with benzodiazepines
Morbidity and mortality risks vary with the extent of surgery (e.g., coronary bypass surgery
in addition to valve replacement) and pre-existing comorbidities.
Antibiotics/ Common Organisms
Skin flora poses the greatest concern; cefazolin is utilized if the patient is not a carrier of
multi-resistant bacteria and there is no allergy. It is administered intravenously within 60
minutes prior to incision and repeated q3–4h until chest closure.
INTRAOPERATIVE CARE
• General anesthesia in the US
• There are case reports of open heart surgery performed under epidural with sedation in
other parts of the world.
Monitors
• ASA standard monitoring; core and shell temperatures are measured.
• Arterial line placement most often prior to induction; the absence of pulsatile blood flow
during bypass precludes noninvasive blood pressure measurement.
• Central venous access is usually obtained after induction; pulmonary artery catheter
placement may be considered.
• Transesophageal echocardiography is frequently used intraoperatively to guide and assess
aortic valve replacement.
• Goal is to provide hemodynamic stability throughout the induction period. Gentle propofol
administration (with vasopressors and inotropes as needed) or etomidate in combination
with fentanyl.
• In the event of hemodynamic instability CPB may be instituted immediately.
Maintenance
• Patients are usually maintained with oxygen/volatile agents and intermittent doses of
opioids and non-depolarizing muscle relaxants.
• During bypass, volatile agent is added to the blood by the perfusionist through the bypass
machine.
• The management of patients during bypass varies substantially by institution and
practitioner.
• On bypass the target mean arterial blood pressure is typically between 50 and 80 mm▒Hg.
• On bypass the patient’s body temperature is cooled at the beginning and warmed to normal
body temperature before termination of bypass.
• Patients remain intubated and are transferred to the ICU.
• Sedation is typically provided with propofol or dexmedetomidine infusion. The latter
appears to have a lower risk for the development of postoperative delirium.
FOLLOW-UP
BED ACUITY
• Surgical ICU
• The time to extubation varies from a few hours to 24 hours and even days, depending on the
patient’s hemodynamic status, respiratory status, bleeding/coagulation, and other organ
systems.
ANALGESIA
• Usually provided by intravenous opioids either as intermittent boluses or as continuous
infusion until extubation
• Once the patient is extubated and bowel function has returned, oral opioids can be given.
COMPLICATIONS
• Bleeding, reoperation, heart block (requires insertion of permanent cardiac pacemaker),
stroke, renal failure, prolonged ventilation, infection; the incidence varies depending on
preoperative status, length and type of operation.
• Atrial fibrillation
• Replacement of a diseased heart valve with a prosthetic valve exchanges the native disease
for complications that are unique to the prosthetic valve.
– Structural failure, though not uncommon with bioprosthesis, is very rare with mechanical
valves.
– Severe and recurrent bleeding due to anticoagulant therapy: Mechanical valves require
long-term anticoagulation therapy, most often with warfarin, while patients with
bioprosthetic valves usually receive anticoagulation with warfarin only for 6 weeks to 3
months postoperatively and then aspirin lifelong.
– Valvular thrombosis and thromboembolic events, especially in patients with mechanical
valves and inadequate anticoagulant therapy
– Severe hemolysis is seen mostly with mechanical valves
– Endocarditis
• Complications associated with open heart surgery and CPB
PROGNOSIS
As survival after a first valve replacement has improved, more patients require a second
operation for replacement (about 2–3% during the first 10 years).
REFERENCES
1. Leon MB, Smith CR, Mack M. Transcatheter aortic-valve implantation for aortic stenosis in
patients who cannot undergo surgery. N Engl J Med. 2010;363(17):1597–1607.
2. Bonow RO, Carabello BA, Chatterjee K, et al. Focused update incorporated into the
ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A
report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. Circulation. 2008;118:e523–e661.
3. Shahian DM, O’Brien SM, Filardo G, et al. The Society of Thoracic Surgeons 2008 cardiac
surgery risk models. Part 2: Isolated valve surgery. Ann Thorac Surg. 2009;88:S23–S42.
ADDITIONAL READING
• Tabata M, Umakanthan R, Cohn LH, et al. Early and late outcomes of 1000 minimally
invasive aortic valve operations. Eur J Cardiothorac Surg. 2008;33:537–541.
• www.sts.org/quality-research-patient-safety/quality/risk-calculator-and-models/risk-
calculator
• www.euroscore.org
• www.ucl.ac.uk/research/riskmodel/index.html
• Aortic valve stenosis
• Aortic valve regurgitation
CODES
ICD9
• V42.2 Heart valve replaced by transplant
• V43.3 Heart valve replaced by other means
ICD10
• Z95.2 Presence of prosthetic heart valve
• Z95.3 Presence of xenogenic heart valve
• Z95.4 Presence of other heart-valve replacement
CLINICAL PEARLS
• Aortic valve replacement is an open, intracardiac surgery requiring CPB. The standard
approach is a median sternotomy; newer minimally invasive techniques are on the rise.
• Risk stratification models can help predict mortality and morbidity for the individual
patient.
• There is a significant rate of structural failure of bioprosthetic valves within the first 10–15
years that can require reoperation.
AORTOCAVAL COMPRESSION OF PREGNANCY
Kanishka Monis, MD
BASICS
DESCRIPTION
• Aortocaval compression refers to compression of the aorta and inferior vena cava (IVC) by
the gravid uterus.
• Supine hypotension syndrome describes the development of rapid hypotension or
cardiovascular collapse after placing the patient in a supine position with rapid recovery in
the lateral, sitting, or standing position. Classic signs and symptoms include bradycardia,
pallor, sweating, dizziness, and nausea.
EPIDEMIOLOGY
Prevalence
• 100% of parturients experience some degree of aortocaval compression at term.
• Approximately 15% of parturients experience supine hypotension syndrome at term.
Morbidity/Mortality
Compression of the aorta can lead to a decrease in uteroplacental perfusion and fetal
hypoxemia.
• Supine position
• Multiple gestations
• Obesity
• Polyhydramnios
• Uterine myomata (“fibroid tumors”)
• Fetal breech presentation, transverse and oblique, increases the risk of aortocaval
compression.
• Venous: Compression of the IVC leads to a decrease in venous return and an increase in
lower extremity venous pressure.
– The decreased preload can result in a 10–20% decline in stroke volume and cardiac
output.
– Blood return via collaterals (intraosseous vertebral veins, paravertebral veins, and epidural
veins) is less than would occur through the IVC.
• Aorta: Compression of the abdominal aorta can cause a decrease in peripheral perfusion.
– Uteroplacental insufficiency may be secondary to decreased perfusion pressure, and can
present as decelerations on the fetal heart monitor.
• Uterine contractions and fetal descent during labor typically reduce the risk of aortocaval
compression. However, there have been some case reports of aortocaval compression
occurring during labor and the postpartum period.
• Avoid the supine position:
– A full lateral position minimizes aortocaval compression.
– A left uterine displacement (with a pelvic wedge or table tilt) may be reduced to 15° to
improve comfort or facilitate Cesarean delivery.
– Flexing of the legs may decrease lumbar lordosis, thus reducing vena cava compression.
– Crossing one leg over the other tilts the pelvis and can relieve vena cava compression.
• Ensure adequate intravascular volume and vascular tone; aortocaval compression is
enhanced during periods of maternal hypotension.
• The speed of delivering the fetus is important if a Cesarean section is planned. Minimize any
delays and consider a wedge or table tilt.
• The severity of the aortocaval compression is greatest at about 38 weeks and decreases after
the engagement of the fetal head into the maternal pelvis.
• The onset of the symptoms is usually rapid (average of 3–10 minutes).
• The syndrome is initiated by placing the patient in the supine position.
• Maternal heart rate is invariably increased in most cases. Maximum heart rate or abrupt
bradycardia can ensue just before syncope.
• Fetal heart tones will often demonstrate decelerations that signify fetal distress.
• Symptoms:
– Dyspnea
– Nausea/vomiting
– Diaphoresis
– Dizziness
– Anxiety/agitation
– Loss of consciousness
• Signs:
– Maternal tachycardia or bradycardia
– Hypotension
– Pallor/cyanosis
– Cold clammy skin
– Non-reassuring fetal heart tracing
– Distension of lower extremity veins
• Amniotic fluid embolism
• High neuraxial block
• Uterine rupture
• Placental abruption
TREATMENT
• Lateral position or left uterine displacement (LUD): Some parturients may still experience
supine hypotension syndrome in LUD.
• Fluid boluses can minimize aortocaval compression.
• Vasopressor boluses (phenylephrine or ephedrine) for treatment of hypotension
FOLLOW-UP
• Parturients in late pregnancy should be advised to recognize the symptoms of aortocaval

compression and avoid lying supine.
• The anesthesia provider should be vigilant and prepared to recognize aortocaval
compression in parturients who are placed in the supine position. In particular, placement
of a laboring epidural and bolusing can result in hypotension (sympatholysis) and enhance
the effects of compression.
ADDITIONAL READING
• Cyna AM, Andrew M, Emmett RS, et al. Techniques for preventing hypotension during
spinal anaesthesia for caesarean section. Cochrane Database Syst Rev. 2006;4:CD002251.
• Kinsella SM, Lohmann G. Supine hypotensive syndrome. Obstet Gynecol. 1994;83(5 Pt
1):774–788.
• Levy DM. Emergency caesarean section: Best practice. Anaesthesia. 2006;61(8):786–791.
• Ngan Kee WD. Prevention of maternal hypotension after regional anaesthesia for cesarean
section. Curr Opin Anaesthesiol. 2010;23(3):304–309.
• Cardiovascular physiology in pregnancy
• Preload
• Fetal heart tones
CODES
ICD9
• 459.2 Compression of vein
• 671.80 Other venous complications of pregnancy and the puerperium, unspecified as to
episode of care or not applicable
• 671.81 Other venous complications of pregnancy and the puerperium, delivered, with or
without mention of antepartum condition
ICD10
• I87.1 Compression of vein
• O22.8X9 Other venous complications in pregnancy, unsp trimester
• O22.8X1 Other venous complications in pregnancy, first trimester
CLINICAL PEARLS
• Aortocaval compression is present after 20 weeks gestation and reaches its maximum effect
at 38 weeks gestation.
• Aortocaval compression is lessened once the fetal head is engaged in the pelvis.
• Supine hypotension syndrome manifests as profound hypotension and bradycardia.
• Uteroplacental insufficiency caused by compression of the aorta can manifest via a non-
reassuring fetal heart tracing.
• Lateral position or left uterine displacement relieves aortocaval compression.
APNEA OF PREMATURITY
Joel Stockman, MD
Samuel H. Wald, MD
BASICS
DESCRIPTION
• Apnea of prematurity (AOP) is defined as the cessation of breathing in premature infants
which lasts for:
– >20 seconds, or
– >10 seconds if associated with bradycardia (<80 beats per minute [bpm]) or oxygen
desaturation (O2 saturation <80–85%)
• It is categorized as central, obstructive, or mixed, with mixed apnea making up the majority
of cases (1)[C].
EPIDEMIOLOGY
Prevalence
• >50% of preterm infants have clinically significant apnea, bradycardia, or oxygen
desaturation, with a peak incidence occurring between 5 and 7 days after birth (2)[C].
– Essentially affects all neonates weighing <1,000 g at birth (1)[C]
• Incidence is inversely related to gestational age and postconceptual age.
– Postoperative risk is <5% at a postconceptual age of 48 weeks and gestational age of 35
weeks.
– Postoperative risk is <1% at a postconceptual age of 56 weeks with a gestational age 32
weeks or postconceptual age of 56 weeks and gestational age of 32 weeks (3)[A].
Prevalence
• Significant AOP will resolve by 40 weeks postconceptual age for a majority of those infants
at risk (1)[C].
• Of note, most severely premature infants (24–28 weeks gestation) may have apnea
persisting beyond 40 weeks postconceptual age (4)[C].
Morbidity
AOP is seen in most high-risk neonates, so there is great difficulty in separating its effects
from the consequences of prematurity. However, it is thought to increase the incidence of
intraventricular hemorrhage (IVH), hydrocephalus, prolonged mechanical ventilation, and
abnormal neurologic development after the 1st year of life (5)[C].
Mortality
No direct correlation found
• An associated risk factor for postsurgical apnea is the presence of an apneic episode at
home.
• Anemia (hemoglobin <10 g/dL) is a significant risk factor, especially for neonates >43
weeks postconceptual age (3)[A].
• AOP reflects the immaturity of the respiratory control system, which manifests as an
unstable respiratory rhythm. The neonatal neurotransmission pathway is underdeveloped,
and both central and peripheral chemoreceptors are impaired.
– The preterm neonate’s ventilatory response to hypercapnia is significantly reduced.
– Preterm infants express a biphasic response to hypoxia, with the initial response being an
increase in ventilation for 1 minute, followed by a phase of decreased ventilation.
Severely preterm infants typically do not display a period of hyperventilation.
– There is an enhanced inhibitory response by upper and lower airway afferent innervation
secondary to stimulation (i.e., negative pressure and positive airflow) (6).
• Sedative drugs/anesthetic agents create a significant risk for development of apnea.
• At-risk infants must be admitted and monitored in the immediate postoperative setting.
SYMPTOMS
• Cessation of breathing for more than 20 seconds
• Cessation of breathing for more than 10 seconds if accompanied by:
– Bradycardia (>30 bpm below resting heart rate)
– Oxygen saturation <85% for >5 seconds
History
• Discuss presence of apneic events with the bedside caregivers to note severity
• Assess other comorbidities related to the premature infant
• Note the current duration of ventilatory support
Signs/Physical Exam
• Observe respiratory effort
• Assess for any upper airway abnormalities
• Assess for conditions that may affect breathing (e.g., neurologic disorders, pulmonary
disorders, CHD)
TREATMENT HISTORY
• History of mechanical ventilation/support
• Methylxanthines (e.g., caffeine, theophylline) administration.
MEDICATIONS
• Methylxanthines are the mainstay of treatment.
– These drugs are thought to stimulate breathing efforts by an unknown mechanism (may be
due to increased chemoreceptor responsiveness, enhanced respiratory muscle
performance, and generalized nervous system excitation).
– Adverse effects include feeding intolerance and tachycardia.
– Effective in reducing apneic episodes and ventilator use in the first 2–7 days of treatment
– Caffeine is the Preferred Drug Due to its lower toxicity (7)[A].
Labs/Studies
• CBC
– A hemoglobin level <10 g/dL increases the risk of apnea to greater than the mean for
infants of all postconceptual ages (3)[A].
• Electrolyte panel
• Respiratory distress syndrome
• Infections
• Hypoglycemia
• Neurologic dysfunction (e.g., IVH, hydrocephalus, stroke)
• These infants should be cared for in an environment that has the capability to provide
continuous postoperative cardiorespiratory monitoring.
• Institutional practices may vary, but recommendations exist to delay elective cases up to 60
weeks postconceptual age. Clinicians must weigh the risk for unrecognized apnea versus the
cost savings through avoidance of overnight admission.
CLASSIFICATIONS
• Spontaneous:
– Minimal physiologic changes
– Events of brief duration and associated with self-recovery
– Events occurring once or twice in 24 hours
• Mild/moderate:
– Events involving apnea, bradycardia, and/or oxygen desaturation of intermediate duration
• Severe:
– Events of clinical significance with persistent bradycardia and oxygen desaturation
– Requires vigorous stimulation, oxygen administration, and/or assisted ventilation (2)[C]
TREATMENT
Premedications
• Consider:
– Atropine 10 mcg/kg
– Caffeine 10 mg/kg
• Need for possible continued postoperative intubation and ventilation
• Need for postoperative apnea monitoring
– Minimum observation period of 12–24 hours for those infants at increased risk
INTRAOPERATIVE CARE
• Less oxygen desaturation/bradycardia is associated with procedures completed under
regional anesthesia (spinal/caudal) and without sedation (8)[A].
• Use short-acting anesthetic agents
• Minimize long-acting intravenous and oral anesthetics
Monitors
• Appropriate IV access
Dictated by the patient’s comorbidities
Maintenance
Any form of sedation/general anesthesia carries an increased risk of postoperative apnea.
Extubation /Emergence
• Ensure the full reversal of muscle relaxant
• The preterm infant should be completely awake and vigorous prior to extubation.
FOLLOW-UP
BED ACUITY
Discharge to a monitored, inpatient unit for 12–24 hours
Postoperative respiratory support may be necessary, depending on the type of surgery.
COMPLICATIONS
Preterm infants may have a history of prior intubation and thus are at an increased risk for
subglottic stenosis.
REFERENCES
1. iner NN, Higgins R, Kattwinkel J, et al. Summary proceedings from the apnea-of-
prematurity group. Pediatrics. 2006;117:S47–S51.
2. Mayock DE. Apnea. University of Washington Division of Neonatology, 2011. Available at:
http://depts.washington.edu/nicuweb/NICU-WEB/apnea.stm
3. Cote CJ, Zaslavsky A, Downes JJ, et al. Postoperative apnea in former preterm infants after
inguinal herniorrhaphy: A combined analysis. Anesthesiology. 1995;82(4):809–822.
4. Baird TM, Martin RJ, Abu-Shaweesh JM. Clinical associations, treatment, and outcome of
apnea of prematurity. NeoReviews. 2002;3:66–70.
5. Butcher-Puech MC, Henderson-Smart DJ, Holley D. Relation between apnea duration and
type and neurological status of preterm infants. Arch Dis Child. 1985;60(10):953–958.
6. Mathew OP. Apnea of prematurity: Pathogenesis and management strategies. J Perinatol.
2010:1–9.
7. Henderson-Smart DJ, Steer PA. Methylxanthine treatment for apnea in preterm infants.
Cochrane Database Syst Rev. 2001;3:CD000140.
8. Krane EF, Haberkern CM, Jacobson LE. Postoperative apnea, bradycardia, and oxygen
desaturation in formerly premature infants: Prospective comparison of spinal and general
• Pediatric respiratory physiology
• Caudal epidural
CODES
ICD9
770.81 Primary apnea of newborn
ICD10
P28.3 Primary sleep apnea of newborn
CLINICAL PEARLS
• The risk of AOP is inversely correlated to postconceptual age.
• The anesthetic should be tailored to the use of agents with the least respiratory depression.
• Postoperative intubation may be necessary in high-risk patients.
• Inpatient admission and/or postoperative respiratory monitoring are highly recommended
in at-risk patients.
APPENDECTOMY
BASICS
DESCRIPTION
General
• Appendicitis is caused by an obstruction of the appendiceal lumen and can result in
inflammation, edema, and the potential for rupture of the viscus.
• Appendectomy is a surgical procedure that can be performed, open or laparoscopically, to
remove the appendix when infection and/or inflammation are suspected or present.
Removal is undertaken to avoid the complication of a ruptured appendix with resultant
peritonitis.
• Laparoscopic appendectomies are primarily performed today. Following trochar insertion
and the establishment of a pneumoperitoneum, the cecum is identified and retracted in
order to mobilize the appendix. An incision or window is made into the mesoappendix prior
to clamping and ligating the base. The appendix may be removed through the trochar or
placed into a bag depending on its size. Benefits over an open procedure include: Less
postoperative pain, smaller incisions (better cosmetic result), and reduced length of stay.
Drawbacks include: Greater cost, potentially longer operative time, and requirement of
general anesthesia due to insufflation.
• Open appendectomy involves adequate exposure of the cecum, followed by pulling of the
cecum through the incision site to expose the attached appendix. The base is clamped and
cut and drains are inserted prior to wound closure.
– Laparoscopic cases may be converted to open when operating conditions are suboptimal
for laparoscopy.
– It is commonly performed for complicated appendicitis or patients with extensive previous
intra-abdominal surgeries.
– May be performed under regional anesthesia for patients who are at high risk for
complications of general anesthesia (e.g., pregnancy, pulmonary hypertension).
Position
• Open: Supine with arms out or tucked
• Laparoscopy: Supine with arms tucked; surgeon stands on the left side of the patient.
Rightward tilt of the bed and Trendelenburg position may facilitate surgical exposure.
Incision
• Laparoscopy: 1 cm incision at the umbilicus, and two to three 5 mm incisions in the lower
abdomen for the insertion of trochars.
• Open: Transverse right lower quadrant incision (McBurney or Rockey-Davis)
Approximate Time
15–60 minutes for either approach
EBL Expected
Less than 75 mL
Hospital Stay
• 24 hours for uncomplicated appendicitis
• Ruptured or otherwise complicated appendicitis has an average length of stay of 5 days.
Laparoscopy equipment
EPIDEMIOLOGY
Prevalence
• In the US, ~250,000 cases of appendicitis annually
• Most common in 10–19 year olds
Prevalence
In the US, approximately 7% of people are affected at some point in their lives.
Morbidity
Varies from 5% to 11% and is related to the perforation of the appendix and degree of
peritonitis
Mortality
• Overall rate of 0.2–0.8% related to appendicitis, not surgical intervention
• Rate following appendectomy: 0–0.2%
• Elderly have the highest mortality rate.
• Consider preoperative nasogastric tube placement to decompress the stomach
• Patient may be hypovolemic from vomiting and/or poor PO intake.
• Counsel pregnant patients about the risk for preterm labor; discuss the option of an open
procedure with neuraxial anesthesia.
SYMPTOMS
• Abdominal pain
• Anorexia
• Nausea
• Emesis
History
Periumbilical pain that migrates to the right lower quadrant (RLQ) is present in
approximately 50% of cases.
Signs/Physical Exam
• RLQ pain, tenderness
• Guarding, rebound on abdominal exam
• Pain with rectal exam
• Psoas sign; inflammation from retrocecal appendix
• Palpation of the mass in the RLQ
MEDICATIONS
Antibiotic therapy may be considered for nonsurgical candidates, such as those with severe
lung disease or recent myocardial infarction.
Labs/Studies
• KUB, ultrasound, and/or CT scan have reduced the incidence of “normal” appendixes
mimicking appendicitis.
• WBC count with differential
• Beta-HCG, to rule out ectopic pregnancy as a cause of pain in females
• Concomitant organ dysfunction may necessitate additional preoperative assessment such as
EKG, basic metabolic panel, etc.
• Most common general surgery intervention during pregnancy with an incidence of 0.06–
0.1%
• Preoperative diagnosis is difficult in the setting of pregnancy. Additionally, the gravid
patient has an elevated WBC at baseline.
• An ultrasound diagnosis is preferred over CT scan to avoid radiation exposure.
• The appendix is located at the umbilical level in the second trimester and the RUQ in the
third trimester.
• 4% risk of pregnancy loss, 7% risk of early labor and delivery related to appendectomy
TREATMENT
Premedications
• GI prophylaxis including a H2 blocker, non-particulate antacid, and possibly a pro-motility
agent
• Preoperative hydration and electrolyte repletion, as needed
Patient should be consented for laparoscopic as well as open appendectomy.
Antibiotics/ Common Organisms
• One dose is adequate for uncomplicated disease.
• Metronidazole plus a first-generation cephalosporin, aminoglycoside, or quinolone
• Common organisms are Escherichia coli, Bacteroides, Klebsiella, Enterococcus, and
Pseudomonas.
INTRAOPERATIVE CARE
• Laparoscopic appendectomy:
– General endotracheal anesthesia (GETA)
• Open appendectomy:
– GETA
– Spinal or epidural anesthesia with a T10 level is also possible.
Monitors
• Foley, if patient has not voided in the immediate preoperative period, or per surgeon
request to improve visualization
• Sequential compression devices should be placed prior to induction.
• Rapid-sequence induction with endotracheal intubation is often required unless a difficult
airway is anticipated. If there is a potential for a difficult airway, consider an awake
fiberoptic intubation.
• Muscle relaxants: The speed of onset of succinylcholine is favorable; however, it may be
contraindicated in certain patients (e.g., children, stroke, etc.). Non-depolarizing muscle
relaxants administered at induction doses may not be reversible by the end of the case.
• Place an orogastric tube after intubation for gastric emptying
Maintenance
• Choice of inhalation agent
• Muscle relaxation can enhance surgical exposure. If succinylcholine was used at induction,
subsequent non-depolarizing administration may be needed.
• If a laparoscopic approach is used, the initial insufflation may lead to bradycardia from
vagal stimulation, which should resolve with time. Desufflation may be necessary if the
patient becomes hemodynamically unstable.
• As with other laparoscopic procedures, the pneumoperitoneum is created to enhance
visualization. However, it can impair ventilation by decreasing lung compliance and
functional residual capacity. Additionally, the Trendelenburg position is often implemented
to displace bowel with gravity and can further impair ventilatory efforts.
The patient should be fully awake, fully reversed, and capable of protecting their airway to
avoid aspiration.
• Appendicitis is more difficult to diagnose in children because of an inability to obtain a good
history. Younger children are more likely to present with perforated appendicitis because of
this diagnostic challenge.
• Surgery may be safely delayed until morning, without undertaking significant risk to the
child.
• Consider performing an ipsilateral transverse abdominal plane (TAP) block to improve pain
control and decrease postoperative narcotic requirements.
FOLLOW-UP
No need to continue antibiotics postoperatively for uncomplicated appendicitis

BED ACUITY
• Floor bed is typically sufficient.
• Telemetry or ICU may sometimes be necessary in the event of a perforated appendix or
other comorbid conditions.
ANALGESIA
• Generally mild-to-moderate pain, much improved after appendix removed
• Consider IV narcotic +/– ketorolac
• Regional techniques include TAP block or a thoracolumbar paravertebral block.
COMPLICATIONS
• Wound infection
• Intra-abdominal abscess
• Appendiceal stump leak
• Thromboembolism
• Injury to other structures in the surgical field
REFERENCES
1. Katkhouda N, Mason R, Towfigh S, et al. Laparoscopic vs. open appendectomy: A
prospective randomized double-blind study. Ann Surg. 2005;242(3):439–448.
2. McGory M, Zingmond D, Tillou A, et al. Negative appendectomy in pregnant women is
associated with a significant risk of fetal loss. J Am Coll Surg. 2007;205(4):534–540.
3. Sauerland S, Jaschinski T, Neugebauer EAM. Laparoscopic versus open surgery for
suspected appendicitis. Cochrane Database Syst Rev. 2010;10:CD001546.
4. Surana R, Quinn F, Puri P. Is it necessary to perform appendectomy in the middle of the
night in Children? BMJ. 1993;306(6886):1168.
Laparoscopy
CLINICAL PEARLS
• Appendicitis occurs most commonly in young patients; it has greater morbidity in those over
60 years of age.
• In the event of a ruptured appendix, immediate appendectomy is not the management of
choice. Antibiotic therapy, fluid resuscitation, and percutaneous drainage should be
undertaken with an interval appendectomy performed at a later date after the patient has
recovered.
• The open and laparoscopic approaches to an appendectomy are both appropriate; patient
comorbidities should play some role in the decision-making of the surgeon.
• A delay in proceeding to surgery does not affect patient outcome; it is a delay in diagnosis
that affects outcome.
ARTERIAL LINE WAVEFORM
John C. Frenzel, MD
BASICS
DESCRIPTION
• An arterial line is an invasive monitor that provides:
– Beat-to-beat numeric blood pressure values
– A waveform with arterial pressures (y-axis) as a function of time (x-axis)
– A means to attain arterial blood gas sampling
• An electromechanical transducer is coupled to the patient via a fluid column that is
generally composed of normal saline and heparin (4 units/mL).
• During the cardiac cycle, blood ejected from the left ventricle (LV) flows into the vascular
tree. A pressure wave is transmitted through the vessels and temporally leads the flow of
blood.
– Measurement of pressure occurs at the level of the transducer, not the location of the
cannula. This is in contrast to noninvasive blood pressure (NIBP) measurements, where
measurement occurs at the level of the cuff.
– The arterial waveform is a measure of pressure and does not necessarily correlate to
cardiac output (flow). For example, in patients with poor cardiac output and a high
systemic vascular resistance (SVR), pressure will be normal but perfusion inadequate.
• Anacrotic limb describes the first phase of the arterial pulse cycle and represents ventricular
ejection of blood. The highest point corresponds to the systolic blood pressure.
– Steep slopes can correspond to increases in HR and inotropy.
– Dampened slopes can correspond to decreases in HR and contractility.
FIGURE 1. Arterial line waveform. Point 1 to 2 represents the anacrotic limb. Point 2 to 3 represents the dicrotic limb,
with the dicrotic notch found along the way.
• Dicrotic limb describes the downstroke of the waveform; it begins at the peak, continues
through the dicrotic notch, and ends at the diastolic baseline. The dicrotic notch coincides
with closure of the aortic valve and the end of LV ejection. It is a result of the reflection of
the pressure wave created when the forward flow of blood out of the LV stops and the
elastic recoil of the aorta forces blood back against the closed aortic valve. Pressure decay is
the drop in pressure over time (dP/dT) from the dicrotic notch to diastolic pressure; it is a
function of SVR.
– Steep slopes correspond to decreased SVR/afterload. The waveform appears narrow.
– Dampened slopes correspond to increased SVR/afterload. The waveform may appear
widened.
• The highest fidelity of readings and waveform data occurs when utilizing:
– The largest diameter catheter that does not obstruct the lumen of the vessel
– The shortest length of high pressure (stiff walled) tubing between the transducer and the
patient
– Tubing that is free of gas bubbles
– Tubing that is free of other obstructions such as clotted blood
– A catheter that is placed closer to the central vascular tree
• Reflection and deflection occur as blood flows through the vasculature. Because the arterial
system undergoes constant pressure adjustments as well as has several bends and branches,
the flow of blood is turbulent as well as laminar. Turbulent flow results in pressure waves
being reflected much like waves in a pool of water are reflected off the concrete side. This
results in increased systolic pressures and decreased diastolic pressures in the more distal
arteries; the mean pressure is only minimally affected. Alternatively, if the vessels were
straight, and had no branches, flow would be laminar and the pressures would not change
in the more distal arteries.
FIGURE 2. Arterial line tracing from proximal to distal sites. Systolic pressures increase, diastolic pressures decrease, while
mean pressures remain mostly unchanged.
ANATOMY
• Although any artery can be used, the risk of distal thrombosis limits catheter placement to
larger vessels with adequate collateralization.
• The radial artery is the most common location for arterial monitoring.
• The ulnar artery is more difficult to cannulate because it is deeper at the wrist. It should not
be used if the ipsilateral radial artery has been punctured.
– Some suggest the use of the Allen Test to assess the adequacy of collateralization of the
hand.
– Recent studies have called this into question and if there is doubt, vascular ultrasound
should be used (1).
• Use of the femoral artery must be balanced against concerns of site and line infection,
pseudo-aneurysm formation, or distal embolization from plaque rupture.
• Other less frequently used sites for arterial wave monitoring include axillary, brachial, and
dorsalis pedis vessels.
• In neonates temporal and umbilical arteries are used.
• Dicrotic notch: The notch is a result of the reflection of the pressure wave created when the
forward flow of blood out of the LV stops and the elastic recoil of the aorta forces blood
back against the closed aortic valve.
– Patients with severe aortic insufficiency will have an indistinct notch. Since the aortic
valve is incompetent, blood flows freely backward, and no such pressure wave is
generated.
– A flat or absent notch may suggest low intravascular volume.
– A low or late notch may correlate to decreased SVR.
• Heparin-induced thrombocytopenia (HIT): In some patients, chronic exposure to heparin can
result in HIT (2). HIT results in thrombosis, not bleeding. Sodium citrate has been used as a
substitute for heparin in the flush (3).
• Thrombosis is an unusual complication but potentially devastating if it results in prolonged
ischemia (4). First-line therapy is systemic anticoagulation. Some studies have been
performed showing thrombolytics are effective as second-line therapy (5).
• Temporary occlusion of the radial artery following arterial line placement is not infrequent
and is reported in 1.5–35% (mean 19.7%) of studies on the subject. Generally temporary
occlusion has no serious consequences (6).
• Placement of arterial waveform monitoring is common when continuous beat-to-beat blood
pressure measurement is indicated. Changes in the waveform can be useful in cases where
rapid changes in volume status are occurring.
• Dampened waveforms result in underestimation of the blood pressure and can be seen with:
– Lumen occlusion due to thrombosis, clots, air bubbles, or kinking
– Loss of backpressure from the flush solution (low flush bag pressure, no fluid in pressure
bag)
– Troubleshooting involves inspection of the system starting from the placement site (if
possible) back to the electronics. On opening the transducer to air, the reading should
drop to zero. If not, this indicates the possibility of baseline drift and the system should be
re-zeroed. Next, the system should be flushed. If the reading does not move over 300
mm▒Hg, then the pressure bag should be checked. Otherwise the system should be
inspected distal to the transducer for obstructions, disconnections, or leaks.
– Tubing: overly compliant, distensible; incorrect tubing
FIGURE 3. Dampened tracing results in decreased systolic pressures, increased diastolic pressures, while mean pressures
remain mostly unchanged.
• Under-dampened or resonant waveforms result in overestimation of the blood pressure and

can occur due to:
– Tubing: Long, noncompliant, overly-stiff.
– “Ringing” describes exaggerated highs and lows that can occur when the measurement
system comes close to the natural underlying harmonic frequency of the waveform.
– Increased SVR
FIGURE 4. Under-dampened or resonant tracing results in increased systolic pressures, decreased diastolic pressures, while
mean pressures remain mostly unchanged.
• The electromechanical system must be zeroed prior to use by opening the transducer to air.
For neurosurgical cases, or cases where the patient is in the sitting position, the zero
reference is commonly set to the Circle of Willis at the level of the ear. Otherwise, the zero
reference is placed at the level of the heart. If the transducer is not physically attached to
the OR bed, the level must be adjusted when changes in patient position or vertical height
are made.
• Stroke volume variation describes changes in the systolic and diastolic pressure that
correlate with the respiratory cycle.
– Mechanical ventilation: Positive pressure inspiration corresponds with an increase in
airway pressures, compression of intrathoracic veins, and a decrease in transmural blood
flow. As a result, with inspiration, there is decreased preload that corresponds to
decreased blood pressure. Conversely, exhalation corresponds to a decrease in airway
pressures with increases in blood pressure.
– Spontaneous ventilation: Exhalation and the end of inspiration correspond to an increase
in airway pressures, compression of intrathoracic veins, and a decrease in transmural
blood flow.
FIGURE 5. Stroke volume variation with mechanical ventilation. Exhalation corresponds to decreased intrathoracic
pressures, allowing blood to return to the heart (increased preload, with resultant increase in cardiac output and blood
pressure). Inspiration corresponds to increased intrathoracic pressures with resultant decreases in blood return to the heart
(decreased preload that causes decreases in stroke volume, cardiac output, and blood pressure).
• Arterial line placement can be aided by ultrasound, but this is usually reserved for femoral
cannulation of pediatric patients and select adults.
• Newer methods of cardiac output monitoring use a peripheral arterial line and the pressure
waveform to calculate cardiac output. Unlike thermodilution methods, these devices use
advanced algorithms to assess vascular tone and sensing technology to indirectly measure
SVR.
• Arterial transducers are built to continually infuse a small volume (3 mL/hr) of flush
solution to reduce cannula thrombosis.
EQUATIONS
MAP = DBP(2/3) + SBP(1/3); where MAP is mean arterial pressure, DBP is diastolic blood
pressure, and SBP is systolic blood pressure. This represents the average, or mean, blood
pressure throughout the cardiac cycle.
REFERENCES
1. Jarvis MA, Jarvis CL, Jones PRM, et al. Reliability of Allen’s test in selection of patients for
radial artery harvest. Ann Thorac Surg. 2000;70(4):1362–1365.
2. Chong BH. Heparin-induced thrombocytopenia. J Thromb Haemost. 2003;1:1471–1478.
3. Branson PK, McCoy RA, Phillips BA, et al. Efficacy of 1.4 percent sodium citrate in
maintaining arterial catheter patency in patients in a medical ICU. Chest. 1993;103:882–
885.
4. Mangano DT, Hickey RF. Ischemic injury following uncomplicated radial artery
catheterization. Anesth Analg. 1979;58:55–57.
5. Geschwind JH, Dagli MS, Lambert DL, et al. Thrombolytic therapy in the setting of arterial
line-induced ischemia. J Endovasc Ther. 2003;10:590–594.
6. Scheer BV, Perel A, Pfeiffer UJ. Clinical review: Complications and risk factors of
peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and
intensive care medicine. Crit Care. 2002;6(3):199–204.
• Transducers
• Hypertension
• Heparin-induced thrombocytopenia
CLINICAL PEARLS
• Transducer systems can drift leading to erroneous readings. Leaving a NIBP cuff on the
patient and set to cycle every 15 or 30 minutes can help to more rapidly identify this
problem.
• Placing the pulse oximeter on the same hand as the arterial line can be helpful in
monitoring adequacy of perfusion distal to the arterial line.
• Check and tighten all connections after placement. Stopcocks that are not used for blood
sample draws should be taped in the vertical position and the draw port covered by a cap
and tape to avoid inadvertent injection of substances via the arterial line.
ASPIRATION
Kanishka Monis, MD
BASICS
DESCRIPTION
• Aspiration is defined as the inhalation of gastric, oropharyngeal, or other foreign contents
into the larynx and lower respiratory tract. It can be divided into 2 broad categories:
– Aspiration pneumonitis: Inhalation of sterile acidic gastric contents resulting in chemical
injury to the lung; also known as Mendelson syndrome
– Aspiration pneumonia: An infectious, pathologic process caused by inhalation of secretions
that have been colonized by microorganisms
• Although aspiration is rare during anesthesia, it is an important cause of anesthesia-related
mortality and ventilator-associated pneumonia (VAP) in the ICU setting.
EPIDEMIOLOGY
Incidence
3.1–10.2 per 10,000 patients receiving general anesthesia
Morbidity
• Pneumonia
• Lung abscess and empyema
• Acute lung injury (ALI)
• Acute respiratory distress syndrome (ARDS)
Mortality
3.8–4.6%; massive aspiration can reach 25%
• Extremes of age
• Full stomach at the time of anesthesia
• Pregnancy
• Critical illness
• Emergency surgeries
• Gastroesophageal reflux disease
• Diabetic gastroparesis
• Obesity
• Acidic gastric content pH <2.5
• Gastric volume >0.4 mL/kg
• Loss of airway reflexes
– Drug/alcohol overdose
– Unconscious patient from general anesthesia, deep sedation, trauma
• Neurologic dysphagia
• There are several structures and reflexes that protect against aspiration.
– Upper esophageal sphincter (UES)
The cricopharyngeus muscle acts as the constrictor muscle of the pharynx and divides
the upper esophagus from the hypopharynx.
Decreased tone is seen with sodium thiopental, succinylcholine, midazolam, and
halothane.
Increased tone is seen with the use of ketamine.
– Lower esophageal sphincter (LES)
Located at the border between the stomach and the esophagus
Composed of the right crux of the diaphragm and the acute angle of the left margin of
the esophagus with the gastric fundus; it forms a sling around the lower esophagus.
Decreased tone is seen with opioids, inhalation agents, and sodium thiopental.
Increased tone is seen with antiemetics (metoclopramide), cholinergic drugs, and
succinylcholine.
– Airway reflexes
Laryngospasm: Hypoxia results from the closure of the false and true vocal cords;
however, this prevents aspiration of foreign contents.
Coughing: Forceful expiratory flow can aid with removal of foreign contents.
Expiration: Describes a forceful expiratory effort without preceding inspiration
Spasmodic panting: Episodes of shallow breathing result in rapid vocal cord opening and
closing and reduce the aspiration of foreign material.
• Consequences of aspiration
– Large particles will cause airway obstruction. Areas of lung that are not being ventilated
are still perfused leading to ventilation/perfusion (V/Q) mismatching, shunting,
hypoxemia, and death.
– In aspiration pneumonitis, acid-related effects of gastric contents will cause inflammatory
reactions and direct lung tissue injury, airway constriction, and edema. Release of
cytokines and chemokines attract inflammatory mediators, neutrophils, and macrophages.
Altered lung defenses may lead to bacterial infection.
– In aspiration pneumonia, the aspiration of oropharyngeal secretions and contaminated
gastric contents will elicit an acute inflammatory lung response to bacteria and bacterial
products. The pathogens that are frequently associated with aspiration pneumonia are
Gram-positive cocci, Gram-negative rods, and (rarely) anaerobes.
• Pregnant patients in labor have an increased risk of aspiration due to:
– Slow gastric emptying time
– Increased gastric volume
– Relaxation of the LES due to progesterone’s effect and the upward pressure of the
enlarging uterus on the LES. Patients are typically considered a “full stomach” beginning
their second trimester.
• Adequate preoperative fasting to control gastric content and volume:
See Table
• Decrease gastric acidity:
– Sodium citrate is a nonparticulate antacid that functions to raise gastric pH as well as
increase gastric motility.
– H2 antagonists inhibit secretion of acid, thereby reducing acidity of stomach contents and
gastric volume.
• Decrease gastric volume:
– Metoclopramide is an antidopaminergic and cholinergic which speeds gastric emptying
and increases LES tone.
– Nasogastric tube insertion and suctioning prior to or after induction for gastric
decompression
– In situ nasogastric tubes should be suctioned prior to induction. Of note, it can form a
mechanical barrier to LES protection against aspiration.
• Application of cricoid pressure/Sellick maneuver:
– Described by Sellick in 1961 as a way to prevent aspiration during the rapid sequence
induction phase of anesthesia
– The upward and backward directed pressure on the cricoid cartilage compresses the
esophagus against the vertebral bodies, thus occluding the esophagus. The recommended
pressure is 30–40 Newtons (difficult to ascertain while performing the technique).
– Theoretically, this will prevent passage of gastric content into the pharynx and subsequent
aspiration into the tracheobronchial tree.
– Minimizes gastric insufflation and aspiration in unconscious patients; however, it may also
prevent effective mask ventilation by reducing airway patency. It may cause discomfort to
the patient if applied too early.
• Early endotracheal intubation with a cuffed endotracheal tube will decrease but not
eliminate the risk of gastric aspiration.
– Excessive cuff pressure may compromise the microcirculation of tracheal mucosa leading
to necrosis. Insufficient cuff pressure may impair ventilation and allow leakage of
supraglottic material into the tracheobronchial tree.
– A better seal can be achieved by using the ultra thin cuff (low pressure, high volume). This
prevents the formation of folds that can lead to longitudinal channels for supraglottic
material to enter the tracheobronchial tree.
• Consider all laboring patients as having a "full stomach," irrespective of the last meal time.
– Avoid general anesthesia, if possible
– If general anesthesia is necessary, consider metoclopramide, sodium citrate, and H2
antagonists.
• Semi-recumbent position has been endorsed by the Centers for Disease Control and
Prevention (CDC) as an effective measure to decrease the risk of aspiration and VAP.
– Reflux of gastric contents is counterbalanced by the effect of gravity in the semi-
recumbent position.
– Prone position in patients with ARDS has been reported to reduce gastric aspiration and
risk of VAP in some studies.
DIAGNOSIS
• Vomiting at the time of induction or following extubation
• Symptoms:
– Postoperative coughing, hoarseness, night sweats, shortness of breath, pleuritic chest pain,
myalgia, and malaise
• Signs:
– Intraoperatively: Hypoxemia, wheezing, bronchospasm/laryngospasm
– Postoperatively: Fever, cyanosis, tachypnea, inspiratory wheezing (in lesions where the
obstruction is in proximal trachea) or expiratory wheeze (distal obstruction), rales,
irritability
• Diagnostic tests and imaging:
– ABG with an increased alveolar–arterial oxygen gradient and hypoxia
– CXR may reveal consolidation and opacities. Changes may be delayed and not appear for
12–24 hours after initial aspiration.
– CBC with differential
– Sputum culture
• Pulmonary air embolism
• Pulmonary tuberculosis
• ARDS
• Drug reaction
• Asthma
• Bronchospasm
• Laryngospasm
TREATMENT
• Vomiting at induction
– Immediately place the patient in the Trendelenburg position to prevent aspiration into the
trachea
– Suction the upper airway
– Endotracheal intubation and inflation of the cuff
– Endotracheal suctioning with a soft suction tube; bronchoscopy and removal of large
inhaled particles
• Vomiting intraoperatively (with a supraglottic device or mask ventilation)
– Remove supraglottic device and have an assistant maintain cricoid pressure
– Head down/lateral position
– Suction and clear the upper airway
– Administer 100% oxygen
– Administration of succinylcholine and endotracheal intubation for airway protection
– Expedite surgery
• Vomiting at emergence
– Head down or lateral position to prevent the entry of aspirated contents into the airway
– Gentle suctioning of the pharynx
– Consider reintubation for airway protection
• There is no data to support the use of steroids in the treatment of aspiration.
– Antibiotics should be considered once a specific organism is identified.
– In situations that involve bowel obstruction and aspiration of bowel contents, Gram-
negative and Gram-positive antibiotic coverage should be considered if the patient
develops signs of aspiration pneumonia.
• There is no data to support use of steroids in treatment of aspiration pneumonitis or
pneumonia.
FOLLOW-UP
CLOSED CLAIMS DATA

• In 4,459 total anesthesia-related claims:
– Aspiration was the primary or secondary cause of morbidity in 158 (3.5%) of all claims.
– Aspiration was the primary source of adverse events in 1.75% of these patients.
– The majority of aspiration events (42%) occurred during the induction of anesthesia.
– Obstetrical related aspiration accounted for 21% of all claims.
REFERENCES
1. Yoshikawa H, Yamazaki S, Abe T. Acute respiratory distress syndrome in children with
severe motor and intellectual disabilities. Brain Dev. 2005;27(6):395–399.
2. Brownlee IA, Aseeri A, Ward C, et al. From gastric aspiration to airway inflammation.
Monaldi Arch Chest Dis. 2010;73(2):54–63.
3. Beck-Schimmer B, Bonvini JM. Bronchoaspiration: Incidence, consequences and
management. Eur J Anaesthesiol. 2011;28(2):78–84.
4. Paintal HS, Kuschner WG. Aspiration syndromes: 10 clinical pearls every physician should
know. Int J Clin Pract. 2007;61(5):846–852.
5. Kluger MT, Visvanathan T, Myburgh JA, et al. Crisis management during anaesthesia:
Regurgitation, vomiting, and aspiration. Qual Saf Health Care. 2005;14(3).
ADDITIONAL READING
• ASA NPO Guidelines
• Ventilator-associated pneumonia
• Asthma
CODES
ICD9
• 482.9 Bacterial pneumonia, unspecified
• 507.0 Pneumonitis due to solids and liquids
ICD10
• J15.9 Unspecified bacterial pneumonia
• J69.0 Pneumonitis due to inhalation of food and vomit
CLINICAL PEARLS
• All patients with stroke should be screened for swallowing abnormalities to prevent
aspiration.
• Patients with decreased sensorium are unable to protect the airway, thus are at an increased
risk for aspiration.
• Mechanically ventilated patients with risk factors of aspiration should be nursed by placing
the head of the bed elevated at 30–35°.
ASSESSMENT OF ACUTE POSTOPERATIVE PAIN
BASICS
DESCRIPTION
• Pain is defined as “an unpleasant sensory and emotional experience associated with actual
or potential tissue damage or described in terms of such damage” by the International
Association for the Study of Pain (ISAP).
• It is often referred to as the “fifth vital sign,” and relief from pain is seen as a basic human
right. Pain is by its very nature an entirely subjective experience and should always be
regarded as such!
• Anesthesia providers and pain medicine physicians encounter pain in the acute and chronic
setting:
– Acute pain is of recent onset and probable limited duration.
– Chronic pain commonly persists beyond the time of healing of an injury; frequently there
may not be any clearly identifiable cause.
EPIDEMIOLOGY
Prevalence
• Annually in the US, there are >73 million surgical procedures. An expected 80% of patients
experience acute pain with up to 87% of those being moderate and severe.
• Following an ICU stay, approximately 75% of patients report to have suffered from
moderate-to-severe pain.
• Children especially suffer from postoperative pain unnecessarily, with approximately 15%
experiencing severe pain.
Prevalence
Every day in the US, approximately 175,000 patients suffer from moderate or severe
postoperative pain.
Morbidity
• Under-treatment of acute pain has significant consequences:
– Increased length of hospital stay and rehabilitation leading to high socioeconomic cost
– Progression to chronic pain may result in catastrophic personal and socioeconomic
consequences.
– Triggering of sleep deprivation and anxiety disorders can result in significant personality
changes.
– Greatly decreased patient satisfaction
– Increased overall postsurgical stress response with elevated plasma levels of catabolic
hormones, hypercoagulopathy, and increased myocardial oxygen consumption
– There is no clear correlation between pain treatment and overall postsurgical mortality
due to a lack of randomized controlled studies.
• Over-treatment of acute and chronic pain also has undesired consequences:
– Respiratory depression with subsequent hypoxia that can lead to brain damage or death
may result from the inappropriate use of opioids; increased occurrence in high-risk
patients (e.g., sleep apnea, elderly).
– Other adverse events with opioid treatment include constipation, itching, nausea, and
vomiting.
– Adverse events with NSAIDs include GI ulceration and bleeding.
• Acute postoperative pain depends on the degree of surgical tissue trauma, but is also
affected by individual patient factors such as:
– Previous experiences
– Personality, anxiety, catastrophizing, neuroticism, depression
– Cultural background
• Risk factors for misdiagnosis of pain:
– Inability to communicate verbally (e.g., young children, patients with dementia or
delirium, and sedated patients in the ICU)
– Medical myths (e.g., infants do not feel pain as much as adults)
– Using “objective” physiologic parameters (heart rate, blood pressure) to assess the severity
of pain and make treatment decisions; pain is SUBJECTIVE!
Adverse physiologic effects in patients with postoperative pain include:
• Pulmonary system: Atelectasis, V/Q mismatching, hypoxemia, hypercapnia
• Cardiovascular system: Hypertension, tachycardia, increased myocardial oxygen demand
• Hematologic system: Decreased immune function, hypercoagulable state
• GI system: Ileus
• The assessment of pain should be a holistic approach involving patient self-rating, whenever
possible. It should also include obtaining a thorough medical and pain history, behavioral
observation and, with caution, monitoring of physiologic parameters (e.g., blood pressure,
respiration rate).
• Pain assessment and treatment by a dedicated acute pain service may result in better pain
relief and less side effects.
• An initial assessment of postoperative pain must commence as early as possible and consists
of a medical (type of surgery, comorbidities) and pain history:
– Location
– Quality; dull visceral, stabbing, shooting, or neuropathic pain
– Intensity
– Provoking factors (coughing) versus continuous pain
– Chronic pain history; especially which medications have been used
– Factors influencing pain treatment; patient’s beliefs and expectations, knowledge, coping
strategies
• Reassessment should be repeated regularly at appropriate intervals (e.g., recovery room
every 3–5 minutes, ward every 0.5–4 hours).
• Physiologic parameters can be used as indicators of pain and include heart rate, blood
pressure, and respiration rate.
– Although physiologic parameters are often used as a “crutch” to assess pain in
unconscious patients, they should only be used with extreme caution to guide therapeutic
decisions. None of them have been validated as accurate measures of pain!
• A variety of pain scales are available. They range from scales “objectively” measuring pain
in conscious patients to scales used in unconscious and pediatric patients.
• Verbal descriptor scale (VDS): Conscious patients. Pain is described as absent, mild,
moderate, severe, and agonizing/unbearable.
– Quick and easy
– Useful in elderly patients with cognitive impairment; use familiar words such as no, mild,
moderate, unbearable (2)[C]
– Less sensitive to pain changes and dependent on higher verbal skills (e.g., a patient who
barely speaks English may not understand the term “agonizing”)
• Visual analogue scale (VAS): Conscious patients. Consists of a 100 mm long horizontal line
with the words “no pain” on the left (0) and “worst pain imaginable” on the right (100).
The patient marks his/her actual severity of pain on the scale (pen/paper or ruler/sliding
marker system).
– Helpful in most conscious subjects
– A reduction of pain by approximately 30% has been rated meaningful by patients.
– Clinical use may be hindered by anesthesia-related cognitive impairment in the immediate
postoperative period.
– Requires basic motor skills; 0–5 mm commonly signify “no”, 5–45 mm “mild”, 45–74 mm
“moderate” and 75–100 mm “severe” pain
• Numeric rating scale (NRS): Conscious patients. Commonly 0–10 points, hence an 11-point
scale. 0 means no pain, 10 worst pain imaginable; 4 is often used as the threshold for
treatment intervention (e.g., opioid administration).
– The NRS correlates well with the VAS but is easier to administer with consistent results.
• Multidimensional pain scales (e.g., McGill Pain Questionnaire); conscious patients
– Helpful to evaluate more complex pain issues (e.g., chronic or neuropathic pain)
– Due to their complexity, these pain scales are usually not useful in the acute postoperative
context.
• Functional pain scales: Conscious patients. Assesses a patient’s ability to perform certain
tasks (e.g., coughing, physiotherapy). Commonly rated as “no” (performance unhindered by
pain), “mild” (moderate-to-severe pain during task), and “significant” limitation (unable to
perform task).
– The ability to perform a certain task may be influenced by more factors than just pain, but
such scales can be useful to trigger pain therapeutic intervention.
• Behavioral pain scale (BPS): Sedated or semi-conscious patients. 3 components are analyzed:
Facial expression (relaxed, partially tightened, fully tightened, grimacing), upper limb
movement (none, partially bent, fully bent, permanently retracted), and compliance with
ventilation (tolerant, mostly tolerant, fighting ventilator, unable to control ventilation).
Each component is rated from 1 to 4; hence, a total BPS score of 12 (maximum pain) can be
achieved.
– BPS is reliable and valid for pain assessment in sedated adult ICU patients (3)[B].
• Critical care pain observation tool (CPOT): Sedated or semi-conscious patients. 4 domains:
Facial expression (relaxed, tense, grimacing), body movement (none, protective, restless),
muscle tension (relaxed, tense, rigid), compliance with ventilation (tolerant, coughing,
fighting), or, in extubated patients, vocalization (normal, moaning, crying); rated from 0 to
2 points each. CPOT ranges from 0 to 8 (maximum pain).
– The CPOT correlates with the VAS which supports its clinical use (4)[C].
• Premature infant pain profile (PIPP) has been validated for postoperative pain in both
premature infants and term newborns. Indicators: Gestational age, behavioral state, heart
rate, oxygen saturation, brow bulge, eye squeeze, nasolabial furrow; all marked with 0–4
points with a total score of 0–21 points (moderate-to-severe pain if >12).
• Children’s Revised Impact of Event Scale (CRIES). Indicators: Crying, oxygen requirement,
increased heart rate and blood pressure, expression, sleeplessness; all marked 0–2 points,
total score 0–10.
• Faces Legs Activity Cry Consolability Scale (FLACC). Indicators (1–3 year olds): Facial
expression, leg movement, overall activity, crying, consolability; each factor scores 0–2
points, with a total score of 0–10 points.
• Faces Pain Scale-Revised (FPS-R). Indicators (4–7 year olds): Showing 6 faces (very happy to
very sad/crying); shown to be equivalent to a 5-step scale graded 0–10 VAS on paper/ruler.
• When solely based on clinical observation and the monitoring of physiologic parameters,
pain assessment may be confounded by a range of other factors including:
– Arousal (potent sympathetic stimulus)
– Anxiety (especially children)
– Confusion (especially elderly patients, emergence delirium in children)
– Co-medication (antihypertensive drugs, sympatholytic [e.g., beta-blockers, clonidine] and
sympathomimetic drugs [e.g., catecholamines, ketamine])
• Hence, get a patient self-rating whenever possible.
TREATMENT
Consists of a multimodal approach including:

• Oral and parenteral analgesics (opioids, NSAIDs, acetaminophen)
• Patient-controlled analgesia (PCA)
• Regional and neuraxial blocks
• Non-conventional therapies (e.g., transcutaneous electrical nerve stimulation)
FOLLOW-UP
In-hospital postoperative patients may have their pain managed by either the surgical team,
primary service, anesthesia service, or acute pain team.
CLOSED CLAIMS DATA
• From 1985 to 2007, there were 150 out of 7,328 closed claims related to acute pain
(American Society of Anesthesiologists Closed Claims Project).
– Although this may appear to be a low percentage, the outcome in approximately 30% of
cases was death or brain damage.
– The median payment was $211,650 ($627–14,880,000).
• Pain mismanagement has been viewed as “unprofessional conduct” by state medical boards
with individual doctors being disciplined.
REFERENCES
1. esonen A, Kauppila T, Tarkkila P, et al. Evaluation of easily applicable pain measurement
tools for the assessment of pain in demented patients. Acta Anaesthesiol Scand.
2009;53:657–664.
2. Pesonen A, Suojaranta-Ylinen R, Tarkkila P, et al. Applicability of tools to assess pain in
elderly patients after cardiac surgery. Acta Anaesthesiol Scand. 2008;52:267–273.
3. ade CH. Clinical tools for the assessment of pain in sedated critically ill adults. Nurse Crit
Care. 2008;13:288–297.
4. Tousignant-Laflamme Y, Bourgault P, Gelinas C, et al. Assessing pain behaviours in healthy
subjects using the critical care pain observation tool (CPOT): A pilot study. J Pain.
2010;11:983–987.
ADDITIONAL READING
• Macintyre PE, Scott DA, Schug SA, et al. Acute pain management: Scientific evidence, 3rd
ed. Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine,
2010.
• Complex regional pain syndrome I
• Complex regional pain syndrome II
• Epidural
CODES
ICD9
338.18 Other acute postoperative pain
ICD10
G89.18 Other acute postprocedural pain
CLINICAL PEARLS
• Pain is a SUBJECTIVE experience.
• Pain is often misdiagnosed in young children, as well as demented and sedated patients.
• Pediatric pain scales should be age-adequate; there is no “one-fits-all” scale.
• Physiologic parameters as well as newly introduced monitoring solutions (e.g., skin
conductance or surgical pleth index) are influenced by many factors other than pain; if
used, they require caution and support from other methods of pain assessment (e.g.,
observation).
• The adequacy of pain relief should be checked regularly.
• Assessment alone is not enough. Clear orders and policies must also define which level of
pain triggers and which response/medication to alleviate it.
ASSIST CONTROL VENTILATION
Daniel Castillo, MD
BASICS
DESCRIPTION
• Assist control ventilation (A/C) or assisted mechanical ventilation (AMV) is a full support
mode of mechanical ventilation that is used preferentially across the intensive care units
(ICU) in the US and around the world (1)[B]. Spontaneous breathing modes have been
shown to decrease atelectasis and can improve V/Q matching.
• In this mode, the breath can be triggered by the set rate (ventilator-triggered) or by the
patient; the “interactive” element of this mode allows the patient to receive a “fully
supported” breath when they initiate one.
• Patients ventilated with A/C can go from total ventilatory rate control when apneic,
sedated, or paralyzed to full patient trigger rate control when spontaneously breathing (2)
[B],(3)[B]; this change will occur seamlessly without changing the ventilator settings.
• In A/C, as in other modes of ventilation, it is necessary to set parameters such as:
– FIO2
– Positive end expiratory pressure (PEEP)
– Pressure-targeted or volume-targeted
– Respiratory rate
– Mode of triggering: Negative pressure- triggering or flow-triggering
– Peak flow
• Mechanical ventilation (MV) parameters: MV is based on the equation of motion, where
pressure, volume, and flow change continuously during the respiratory cycle, assuming that
compliance and resistance remain constant (4)[A].
• Physiologic ventilatory control: The respiratory center in the brain stem controls ventilation.
Signals are delivered to the respiratory muscles to contract and create a negative
intrapleural pressure, resulting in lung expansion and airflow entering the airways.
• Interactive components of AC ventilation: During MV, if the patient initiates a breath, the
ventilator is triggered to deliver a preset breath to the patient.
• Backup rate: When the patient is unable to initiate a breath, the set ventilatory rate delivers
the breaths. This functions as a backup or “safety-net” when the patient’s breathing rate
drops below the ventilator set rate (5)[C],(6)[B],(7)[B],(8)[B].
• Patient-triggered versus ventilator-triggered breaths: The delivered breath in A/C is equally
supported regardless if it is patient or ventilator initiated; they are identical in duration and
magnitude.
• Work of breathing: Contrary to popular belief, A/C does not abolish the work of breathing
because breaths remain initiated by the patient; it does, however, decrease it. As a result,
there is decreased fatigue and shallow breaths that can result in atelectasis and shunting.
• Settings:
– FIO2: As with most modes of ventilation, this needs to be selected. Patients are often
started at an FIO2 of 1.0 with downward titration to avoid oxygen toxicity and decreased
surfactant production.
– PEEP: Reduces atelectasis during expiration with resultant improvement in oxygenation,
lung volumes (by increasing FRC), and lung compliance. PEEP also antagonizes auto-
PEEP. In acute respiratory distress syndrome (ARDS), it can decrease atelectrauma (the
opening and closing of airways) and the effects of volutrauma. Initially, PEEP is typically
set at the lower inflection point (LIP) of a pressure-volume curve and then titrated
upwards to produce the best PaO2 with an FIO2 <0.6.
– Method of support (tidal volume vs. pressure targeted): In tidal volume support, a volume
is set for each breath. The volume set is delivered using a fixed flow (flow × time).
Airway pressure is not set and will depend on the elastic and resistance component of the
lung. Inspiratory time is determined by the VT delivered and the flow rate: Ti = VT/flow
rate. In pressure-targeted support, the ventilator utilizes flow (adjustable) to generate a set
pressure in the airway for a period of time determined by the inspiratory time of the I:E
(inspiration:expiration) ratio. The pressure generated is the same for patient- and
ventilator-initiated breaths. The VT generated is not fixed and will depend on the elastic
and resistance components of the lung. For ARDS patients, the goal is to attain a tidal
volume of 5–7 mL/kg with peak pressures <30 mm Hg.
– Respiratory rate: Some machines set a minute volume that determines the respiratory rate:
MV/VT.
– Mode of triggering: Negative pressure sensors are typically found on anesthesia machines
and are set at –2 cm H2O. However, because they place an unnecessary workload on
breathing, they have been replaced by flow triggers on ICU ventilators. Flow triggers
implement a continuous flow of gas and when patient-triggered inspiration (negative
pressure) deflects this flow, the ventilator is triggered. If the trigger is too sensitive, the
patient can hyperventilate. If it is not sensitive enough, the patient becomes
dyssynchronous.
– Peak flow is measured as liters per minute (L/min) and is typically set at 4 times the
minute ventilation; this parameter is utilized as opposed to an I:E ratio. In adults, 50
L/min is initially chosen; higher levels may be selected in patients with airflow
obstruction. If the flow rate is too high, the volume is rapidly delivered to the most
compliant lung tissues (not to the inelastic diseased tissues) at very high peak pressures. If
the peak flow is too low, the patient will demand more gas than the ventilator is setup to
supply and dyssynchrony with the machine occurs; this is referred to as “air hunger.”
Pressure augmentation allows the ventilator to sense that the patient’s demands exceed
the peak flow, and automatically increases the flow.
• Ventilatory settings are adjusted based upon the patient’s plateau pressure, inspiratory flow
demand, and blood gas targets.
ANATOMY
• The airway tree starts with the trachea and divides approximately 23 times (dichotomous
divisions) to form alveolar sacs that contain 17 alveoli in average.
• The average adult has a gas exchange surfaces in the lungs of about 50–100 m2 (300 million
alveoli).
• Respiratory failure: Respiratory rate >35 breaths/min or <6 breaths/min; oxygen
saturation <90% despite adequate supplemental oxygen; tidal volume <5 mL/kg; vital
capacity <15 mL/kg; pH <7.20; PaCO2 >50 mm Hg; A-a gradient >350 mm Hg on an
FIO2 1.0
• Pulmonary consequences and ventilator-associated lung injury
– Barotrauma can be seen with excessive pressures and can lead to pneumothorax,
pneumomediastinum, subcutaneous emphysema, and pneumopericardium.
– Volutrauma can be seen with high-end inspiratory volumes that can lead to alveolar stress
injury and increased lung water; can be reversed by PEEP.
– Atelectrauma; decreases in surfactant result in less “patent” alveoli, or alveolar collapse.
The repeated opening and collapsing results in shear stress to the alveoli.
– Biotrauma describes the maladaptive inflammatory release that occurs secondary to
mechanical factors or biophysical injury. Cytokines, complement, prostanoids,
leukotrienes, proteases, and reactive oxygen species can result in damage to distal organs.
Tissue injury can result from these inflammatory mediators as well as impaired oxygen
delivery and bacteremia.
– Hyperventilation and significant respiratory alkalosis can develop, particularly with CNS
disorders, febrile states, or sepsis. An alarm can be set if the ventilator cycles too
frequently.
– Air trapping and breath stacking can occur with obstructive airway disease or with
increased respiratory rates (not enough time to exhale the full tidal volume).
– Muscle atrophy resulting from disuse develops if used for long, thus the need for gradual
weaning of pressure or volume support before extubation.
• Cardiovascular effects: Increased intrathoracic pressure
– Decreases venous return to the right atrium (preload) and can potentially decrease cardiac
output. This can be significant in patients that are hypovolemic, have low ejection
fractions, or are preload-dependent (pericardial tamponade).
– Can decrease left ventricular afterload by increasing the transmural pressure (less
negative). In patients with LV dysfunction, the negative inspiratory pressures that are
needed to maintain adequate inspiratory volumes are greater (due to pulmonary edema,
the lung volume and compliance decrease). Positive pressure ventilation functions on the
principle of increasing intrathoracic pressures and hence makes the transmural pressure
less negative.
• Renal function has been shown to decrease with positive pressure ventilation (decreased
urine output and sodium excretion).
• Hepatic function may be affected due to decreased cardiac output, increased hepatic
vascular resistance, and elevated bile duct pressure.
• A/C is useful for rapid weaning at the end of a case where the patient is not yet breathing
spontaneously but expected to shortly (muscle relaxant reversal, decreasing volatile or IV
anesthetic levels). Patients can be extubated directly from A/C or switched to pressure
support prior to extubation.
• In patients not breathing spontaneously (neuromuscular blockade, opioids), there is no
difference in minute ventilation between SIMV, AC, or CMV.
EQUATIONS
Equation of motion of the airway: P = VT/C + R × F (P = transpulmonary pressure, VT =
tidal volume, C = compliance, R = resistance, F = flow) (3)[A]
Volume-targeted assist control ventilation. On the left, the patient is receiving controlled, set breaths at a rate of 12/min.
On the right, the patient is receiving assisted breaths as can be seen by the small downward deflection produced by a
patient-triggered breath. All breaths have an identical tidal volume.
Pressure-targeted assist control ventilation. On the left side, the peak flow is set at 30 L/min, and the scooped out
appearance of the pressure trace indicates that the patient is slightly dyssynchronous. On the right side, pressure
augmentation has been added and increases the peak flow rate in response to the patient’s demand. Results in improved
dynamics in regard to the pressure and flow waveforms and resembles pressure support, rather than assist control.
REFERENCES
1. steban A, Anzueto A, Alia I, et al. How is mechanical ventilation employed in the intensive
care unit? Am J Respir Crit Care Med. 2000;161(5):1450–1458.
2. hiumello D, Pelosi P, Calvi E, et al. Different modes of assisted ventilation in patients with
acute respiratory failure. Eur Respir J. 2002;20:925–933.
3. Tejeda M, Boix JH, Alvarez F, et al. Comparison of pressure support ventilation and assist-
control ventilation in the treatment of respiratory failure. Chest. 1997;111:1322–1325.
4. Nikischin W, Gerhardt T, Everett R, et al. A new method to analyze lung compliance when
pressure–volume relationship is nonlinear. Am J Respir Crit Care Med. 1998;158:1052–
1060.
5. Sassoon CSH, Zhu E, Caiozzo VJ. Assist-control mechanical ventilation attenuates
ventilator-induced diaphragmatic dysfunction. Am J Respir Crit Care Med.
2004;170(6):626–632.
6. Tobin MJ, Jubran A, Laghi F. Patient–ventilator interaction. Am J Respir Crit Care Med.
2001;163:1059–1063.
7. Tobin MJ. Mechanical ventilation N Engl J Med. 1994;330:1056–1061.
8. Toublanc B, Rose D, Glerant JC, et al. Assist-control ventilation vs. low levels of pressure
support ventilation on sleep quality in intubated ICU patients. Intensive Care Med.
2007;33(7):1148–1154.
• Continuous positive airway pressure
• Positive end expiratory pressure
• Intubation and extubation criteria
CLINICAL PEARLS
• A/C does not abolish the work of breathing; it can reduce it.
• It provides a seamless transition from ventilator-controlled respiration to ventilator-
supported, patient-initiated breaths.
ASTHMA
BASICS
DESCRIPTION
• Asthma describes bronchial hyper-reactivity with reversible airflow obstruction in response
to various stimuli. Despite its reversible nature, chronic airway inflammation is a hallmark.
• A reactive airway, or bronchial hyper-responsiveness, is also seen in chronic bronchitis,
emphysema, allergic rhinitis, and respiratory infections.
EPIDEMIOLOGY
Prevalence
7% of US population, increasing yearly
Prevalence
• 1/2 of all cases develop before the age of 10 years
• 1/3rd occur after the age of 40 years
• 2:1 male:female preponderance up to the age of 30 years, then equalizes
Morbidity
• Perioperative occurrence is seen in 0.17–2.4% of asthmatics.
• 40,000 missed school or work days each day
• 30,000 asthma attacks daily
• 5,000 ER visits daily
• 1,000 hospital admissions daily
Mortality
5000/year
• Allergens
• Pharmacologic agents (aspirin, beta-blockers, NSAIDS, sulfa)
• Infections (viral airway infections increase airway resistance even in non-asthmatics,
possibly due to a cholinergic mechanism in the bronchial smooth muscles)
• Exercise (post-exercise)
• Emotional stress
• Cold weather
• Abnormal autonomic nervous system regulation
• Endotracheal tube, mucus, saliva (anesthetic related)
• Pregnant patients administered prostaglandins for abortion or operative delivery
• The above-mentioned triggers can elicit bronchial smooth muscle contraction. Additionally,
vagal and sympathetic factors directly modulate airway tone (1,2,3).
• Acutely, inflammatory edema and mucus plugging exacerbate airflow limitation.
Chronically, airway remodeling, thickening, and abnormal communications occur in the
epithelium of the injured airway and in the pulmonary mesenchyma; changes are
permanent and can result in progressive damage (1,2,3).
• Immunologic–inflammatory pathways involve lymphocytes, eosinophils, neutrophils, mast
cells, leukotrienes, and cytokines (1,2,3).
• Bronchoconstriction increases (3):
– Work of breathing
– Air trapping
– V/Q mismatch (reduced ventilation that causes shunting)
– Pulmonary vascular resistance (PVR)
– Right ventricle afterload
– Residual volume (RV)
– Functional residual capacity (FRC)
– Total lung capacity (TLC)
– Oxygen consumption
– Carbon dioxide production
• Bronchoconstriction decreases:
– Airflow
– FEV1
– Expiratory reserve volume (ERV)
– Inspiratory reserve volume (IRV)
– FEV1/FVC
– FEV25-75%
– Dynamic compliance of lungs
• Accessory muscles are recruited to preserve tidal volume (TV) despite increased ERV (from
increased FRC and air trapping) (1,2).
• Initially, hyperventilation causes respiratory alkalosis. Over time, increased air trapping and
respiratory muscle fatigue increase CO2 retention; therefore, normalization of PaCO2 reflects
decompensation. Extreme air trapping can restrict cardiac filling and “pulmonary
tamponade” that can result in pulse-less electrical activity.
• Assess severity of disease, optimize pulmonary function, and treat acute exacerbation
• The anesthetic plan should prevent, suppress, and blunt airway hyper-reactivity; stimuli that
do not ordinarily evoke airway responses can precipitate life-threatening
bronchoconstriction in the asthmatic.
• Diagnose and treat perioperative bronchoconstriction
SYMPTOMS
• Shortness of breath
• Chest tightness
• Cough
History
• Age of onset
• Triggers
• Treatment history
– Frequency of exacerbations
– Nighttime awakenings
– Rescue inhaler use
– Steroids pulse dose
– ER visits
– Hospitalizations
– ICU admissions
– Intubations
Signs/Physical Exam
• Expiratory wheezing
• Accessory muscle use
• Tachypnea
• Diminished or inaudible breath sounds
MEDICATIONS
• “Controller” to modify airway environment
– Inhaled steroids
– Theophylline
– Leukotriene modifiers
– Cromolyn
• “Rescue” for acute bronchospasm (quick onset)
– Beta-adrenergic agonists
– Anticholinergics
Labs/Studies
• Pulmonary function tests can aid with diagnosis, and objectively assess severity and
response to treatment (FEV, FEV1/FVC)
• CXR (hyperventilation, pneumonia, CHF)
• EKG (acute right heart failure, PVCs)
• Eosinophilia
• ABGs (pCO2 and pO2)

77% have gastroesophageal reflux disease (GERD); control of GERD may improve asthma
symptoms.
• Acute exacerbation
• Chronic sinus infection
• Upper respiratory infection
• Pneumonia
CLASSIFICATIONS
• Based on symptoms, nighttime awakenings, short-acting beta-agonist symptoms,
interference with normal activity, lung function, oral steroid use
– Mild
– Moderate
– Marked
– Severe/status asthmaticus
TREATMENT
Premedications
• Consider beta-agonists (MDI, nebulizer)
• Consider a steroid stress dose (avoid Addisonian crisis if recent therapy and major surgery)
• Consider a steroid pulse dose (avoid perioperative exacerbation in severe disease, or major
surgery)
• Anxiolysis
INTRAOPERATIVE CARE
• Consider regional anesthesia to avoid airway instrumentation and stage II emergence
(increased risk for bronchoconstriction)
• Consider LMA, which sits supraglottically and is associated with less airway irritation than
ETT
Monitors
• Consider augmenting the ETCO2 waveform to improve detection of obstruction; a slow rise
to the peak indicates expiratory obstruction.
• Consider an arterial line in high-risk patients to allow for ABG monitoring
• Laryngoscopy, intubation, suctioning, and cold inspired gases can exacerbate hyper-
reactivity.
• Patient should be “deep” prior to airway instrumentation. Ensure that an adequate dosage of
induction medications and neuromuscular blockade have been administered, as well as an
appropriate amount of time for onset. Induction medications should be titrated to blunt
bronchial smooth muscle responsiveness, and NMBD should be titrated to block coughing,
gagging, or bucking. Although these are skeletal muscle phenomenon, when provoked, they
can precipitate irritant receptors and airway hyper-reactivity.
• Consider bag mask ventilating with volatile agents (potent bronchodilators) for 2–3 minutes
prior to airway instrumentation
• Ketamine is the only bronchodilating IV induction agent; propofol and etomidate blunt
airway reflexes to a greater extent than thiopental.
• Lidocaine blunts airway response to irritation. However, caution is advised when topically
applied; spraying can cause irritation and precipitate bronchospasm.
• Succinylcholine has histamine release; however, studies have not shown this to be clinically
relevant.
• When considering a RSI, the risk of aspiration needs to be weighed against the risk of
bronchoconstriction from airway manipulation prior to the patient being “deep.”
Maintenance
• Keep the patient “deep” or adequately anesthetized. Otherwise, innocuous stimuli can result
in increased airway resistance (saliva, mucus, ETT).
• I:E ratio should be reduced (increased time for exhalation to avoid air trapping; similar to
phenomenon of “pursed lip breathing” in patients with emphysema).
• Humidify, warm inspiratory gases
• Fluid hydration to soften mucus secretions
• Consider “deep” extubation (removing airway while anesthetic is sufficient to suppress
hyper-reactivity)
• When it is unwise to extubate before the patient is fully awake, consider suppressing airway
reflexes (IV lidocaine, bronchodilators, epinephrine IV/SQ, dexmedetomidine).
• Neostigmine may bronchoconstrict if not administered with adequate antimuscarinics.
• Antimuscarinics can thicken secretions.
FOLLOW-UP
BED ACUITY
• Vigilance for bronchospasm
• Consider scheduled bronchodilator treatments
• Incentive spirometry and deep breathing
• Early mobilization
• Good pain control
• Control GERD
COMPLICATIONS
• Intraoperative bronchospasm is diagnosed by:
– Increased peak inspiratory pressures (PIP)
– ETCO2 sloping
– Expiratory wheezing
• Treatment consists of:
– Deepening the anesthetic with inhaled volatile agents. Volatile agents are potent
bronchodilators and cause direct bronchial smooth muscle cell dilation by altering
intracellular calcium regulation. However, if there is little or no airway movement, this
may not be effective.
– Deepening the anesthetic with intravenous agents. Propofol does not bronchodilate, but it
can suppress airway reflexes.
– Inhaled beta-agonists. Albuterol causes bronchodilation, but may require several puffs (8–
10) to ensure delivery through a long narrow ETT. There are several devices available that
can facilitate delivery.
– Steroids intravenously. Administration should not preclude more immediate therapy.
– Epinephrine (IV bolus, SQ, drip); sympathomimetic that decreases bronchospasm via beta-
2 agonist.
– Theophylline may be considered; however, it is more common for symptom control and
prevention. Additionally, it has a narrow therapeutic index and levels need to be
monitored if continued postoperatively.
– Heliox can promote laminar airflow, but reduces FIO2, and has not been shown to be
therapeutic.
– Magnesium (drowsiness and NMBD potentiation)
– Avoid histamine-releasing medications (e.g. morphine, vancomycin)
REFERENCES
1. Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and
bronchospasm. Br J Anaesth. 2009;103(S1):i57–i65.
2. Fanta CH. Asthma. N Engl J Med. 2009;360:1002–1014.
3. Tirumalasetty J, Grammer LC. Asthma, surgery, and general anesthesia: A review. J
Asthma. 2006;43(4):251–254.
ADDITIONAL READING
• Asthma and Allergy Foundation of America
• Burburan SM, Xisto DG, Ferreira HC, et al. Lung mechanisms and histology during
sevoflurane anesthesia in a model of chronic allergic asthma. Anesth Analg.
2007;104(3):631–637.
• Overview of Changes to Asthma Guidelines. www.aafp.org
• Ventilation perfusion matching
• Ventilation perfusion mismatching
• End tidal CO2
• I:E ratio
• Deep extubation
• Laminar flow
CODES
ICD9
• 493.90 Asthma,unspecified type, unspecified
• 493.92 Asthma, unspecified type, with (acute) exacerbation
ICD10
• J45.901 Unspecified asthma with (acute) exacerbation
• J45.909 Unspecified asthma, uncomplicated
CLINICAL PEARLS
• Assess the severity of disease in order to plan an appropriate anesthetic technique.
• Stimuli that do not ordinarily evoke airway responses can precipitate life-threatening
bronchoconstriction in asthmatics. Ensure that the patient is adequately induced prior to
airway manipulation, as well as remains adequately anesthetized during the surgery;
consider a “deep" extubation.
• Intraoperative bronchoconstriction presents as increased PIP, a sloping ETCO2 waveform,
and wheezing.
• All that wheezes is not asthma; rule out other causes prior to treating for bronchospasm.
• Asthma increases the risk of bronchospasm, hypoxemia, hypercapnia, inadequate cough,
atelectasis, and pulmonary infection following surgery.
ATELECTASIS
Arun Alagappan, MD
BASICS
DESCRIPTION
• Atelectasis refers to a collapse of lung tissue from compression, absorption, or loss of
surfactant; it is very common in the perioperative setting.
• Atelectasis from anesthesia:
– Occurs with both inhalational and intravenous anesthetics
– Appears within minutes after induction (1)
– Occurs with spontaneous and mechanical ventilation
– Primarily affects lung tissue in the basal regions adjacent to the diaphragm
– Can be worsened with positioning (supine and Trendelenburg)
– Can persist for days after major surgery
EPIDEMIOLOGY
Prevalence
• Atelectasis is found in 90% of anesthetized patients (2).
• Infants are at a greater risk secondary to their decreased lung compliance relative to their
chest wall. Additionally, their closing volume is greater due to incomplete development of
the elastic supporting structures of the lung, and as a result, they are at risk for airway
closure during tidal volume breathing (2).
• Atelectasis is most common after cardiac surgery with CPB (3).
Prevalence
• Observed in all age groups
• Magnitude is independent of age in adults (2).
Morbidity
Hypoxemia, right ventricular dysfunction, lung injury
Mortality
Pulmonary complications account for 24% of deaths within 6 days of surgery (2). Atelectasis
causes physiologic impairments that contribute to the development of these pulmonary
complications.
• There are 3 mechanisms by which atelectasis can develop:
– Compression
– Absorption
– Loss of surfactant
• Compression atelectasis: Occurs when the transmural pressure that distends the alveolus is
reduced. During anesthesia, the diaphragm is relaxed and is cephaledly displaced making it
less effective at maintaining distinct pressures in the extrathoracic and abdominal cavities.
Abdominal pressures are transmitted to the pleural space and promote collapse of adjacent
lung units (3).
• Absorption atelectasis: Occurs when less gas enters the alveolus than is removed by uptake
of blood. This can happen when there is complete airway occlusion creating a pocket of
trapped gas in a distal lung unit that continues to be perfused. Gas uptake from the pocket
continues without inflow of gas, and the pocket collapses. Alternately, in the absence of
complete airway occlusion, if the VA/Q is reduced, there is a point reached at which the
rate of inspired gas entering the alveolus is balanced by gas uptake from the alveolus. Below
this critical ratio, the lung unit will collapse. This becomes more likely with increasing FIO2
(2). May be seen when nitrous oxide is changed to 100% oxygen at the end of a case.
• Loss-of-surfactant atelectasis: Occurs when the alveolar-stabilizing function of surfactant is
depressed by anesthesia or by a lack of intermittent deep breaths. Surfactant is a surface-
active lipoprotein that is produced by alveolar type 2 cells and acts to reduce alveolar
surface tension. The surface tension of the alveolar air–water interface provides a retractive
force opposing lung inflation. The presence of surfactant can lower the air–water surface
tension to near zero, ensuring that the alveolar space remains open. Abnormalities in the
amount or composition of surfactant are seen in certain conditions including neonatal
respiratory distress syndrome and acute respiratory distress syndrome (ARDS), as well as
secondarily from inflammatory processes in the lung (4).
• Other contributing factors to atelectasis under general anesthesia include:
– Obesity: The weight of the chest wall and abdomen makes diaphragmatic excursion more
difficult and promotes atelectasis (5). Studies have shown that atelectasis resolves more
slowly compared to nonobese patients.
– Positioning: In the supine position, abdominal contents have cephalad invasion against the
relaxed diaphragm. In Trendelenburg, gravity further accentuates this.
– Laparoscopy: Pneumoperitoneum promotes atelectasis. Studies have also shown that it is
associated with an increased incidence of postoperative atelectasis (5).
• Atelectasis causes several physiologic impairments in respiratory function resulting in a
range of clinical findings including:
– Hypoxemia
– Decreased pulmonary compliance
– Right ventricular dysfunction
– Worsening of lung injury
• Hypoxemia results from ventilation perfusion mismatching or shunt. Perfusion to the
alveolar unit continues despite the lack of ventilation.
• Decreased pulmonary compliance is primarily through a reduction in lung volume (3). This
increases the work of breathing by requiring an increased transpulmonary pressure to
achieve a given tidal volume.
• Right ventricular dysfunction: Atelectasis contributes to regional hypoxia that in turn
contributes to hypoxic pulmonary vasoconstriction and increased pulmonary vascular
resistance. This can result in right ventricular dysfunction and increased microvesicular
leakage (3).
• Lung injury: Atelectasis can potentiate existing lung injury in both high and low tidal
volume ventilation strategies. In high tidal volume ventilation with zero PEEP, atelectasis
causes increased serum cytokine concentrations as well as impaired lung compliance (3).
During low tidal volume ventilation in the presence of atelectasis, there was shown to be a
decrease in survival (3).
• Chronic obstructive pulmonary disease actually reduces the amount of atelectasis that
develops due to hyperinflation of the lungs and prevents lung collapse. However, these
patients develop a more severe V/Q mismatch (2).
Prevention of atelectasis starting at induction of anesthesia is important.
• Induction:
– Application of CPAP (6 cmH2O) for 5 minutes prior to induction, followed by mechanical
ventilation with PEEP has been suggested to be superior to PEEP alone (1).
– Although studies have suggested that using lower FIO2 during preoxygenation prevents
atelectasis formation during induction, it is not recommended. The apnea time before
hypoxia develops is decreased; hence the margin of safety is decreased (6).
• Intraoperative:
– Lower levels of FIO2 may decrease absorption atelectasis (6).
– Application of PEEP (6 cmH2O) can prevent formation of atelectasis and reduction of FRC
(increased lung volume and oxygen storage) (2). It may also be an effective strategy to
avoid atelectasis when higher FiO2 is required.
• Atelectasis should be considered whenever there are alterations in lung physiology in a
setting where atelectasis is likely.
• Hypoxemia secondary to atelectasis is reflected in an increased A-a gradient. It is important
to note other causes of hypoxemia, as seen below in differential diagnosis.
• Confirmation of the diagnosis, if needed, can be obtained with imaging.
– On CXR, atelectasis will have features similar to consolidation with opacification of the
lung parenchyma (3).
– CT scan is superior to CXR based on the resolution, and ability to measure whole and
regional lung volumes. Atelectasis on CT scan has been defined as pixels with attenuation
values of –100 to +100 Hounsfield units (a measure of density as seen on CT) (3).
– Thoracic ultrasound is emerging as a way to rapidly assess regional consolidation (3).
Atelectasis should be distinguished from other causes of hypoxemia including:
• Hypoxic delivery
• Hypoventilation
• Diffusion impairment
• Right-to-left intracardiac shunting
TREATMENT
• A vital capacity maneuver (VCM) can offset the atelectasis that develops after induction of
general anesthesia. A pressure of 40 cmH2O maintained for 7–8 seconds is needed to re-
expand previously collapsed lung tissues (2).
– Laparoscopy: The recruitment effect of a single VCM may be lost after pneumoperitoneum
and requires additional maneuvers to keep the alveoli open (5).
– Lower FIO2: When the inflation and succeeding ventilation are performed with a lower
FIO2, atelectasis reappears more slowly. One study demonstrated that when 40% was
used, only 20–25% of the initial area was atelectatic 40 minutes after the VCM. When
100% oxygen was used, however, atelectasis recurred within 5 minutes (7).
– Drawbacks of VCM include a decreased preload, and potentially cardiac output.
• A PEEP of 10 cmH2O will consistently reopen collapsed lung tissue. However, those lung
units may re-collapse after discontinuation of PEEP. It has been shown that PEEP applied
immediately following a VCM will completely prevent recurrence of atelectasis, even when
100% oxygen is used (2).
• Postoperatively, techniques or devices that encourage or force patients to inspire deeply are
beneficial, with a goal of producing a large, sustained increase in transpulmonary pressure
to distend and re-expand collapsed lung units. Techniques include intermittent positive-
pressure breathing, deep-breathing exercises, incentive spirometry, and chest physiotherapy.
All these techniques were shown to be equally efficacious in reducing the frequency of PPC
following abdominal surgery (3).
FOLLOW-UP
• Most perioperative atelectasis resolves within 24 hours after surgery (2). However, the
normal coordination of respiratory muscle action is disrupted in the postoperative period,
and this predisposes to decreases in FRC and VC which can contribute to development of
atelectasis for days following major surgery (8).
• Patients should be monitored for development of postoperative pulmonary complications.
REFERENCES
1. rismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with
muscular relaxation: A proposal of atelectasis. Anesthesiology. 1985;62:422–428.
2. Magnusson L, Spahn DR. New concepts of atelectasis during general anesthesia. Br J
Anesth. 2003;91:61–72.
3. Duggan M, Kavanagh BP. Pulmonary atelectasis. Anesthesiology. 2005;102:838–854.
4. Griese M. Pulmonary surfactant in health and human lung diseases: State of the art. Eur
Resp J. 1999;13:1455–1476.
5. Talab HF, Zabani IA, Abdelrahman HS, et al. Intraoperative ventilatory strategies for
prevention of pulmonary atelectasis in obese patients undergoing laparoscopic bariatric
surgery. Anesth Analg. 2009;109(5):1511–1516.
6. Reber A, Englberg G, Wegenius G, et al. Lung aeration: The effect of pre-oxygenation and
hyperoxygenation during total intravenous anaesthesia. Anaesthesia. 1996;51:733–737.
7. Rothen HU, Sporre B, Engbert G, et al. Prevention of atelectasis during general anesthesia.
Lancet. 1995;345:1387–1391.
8. Weiskopf RB. Preventing postoperative pulmonary complications. Anesthesiology.
2000;92:1467–1472.
9. Ho-Tai LM, Devitt JH, Noel AG, et al. Gas leak and gastric insufflations during controlled
ventilation: Face mask versus laryngeal mask airway. Can J Anaesth. 1998;45:206–211.
10. Hedenstierna G, Edmark L. Mechanisms of atelectasis in the perioperative period. Best
Pract Res Clin Anesth. 2010;24:157–169.
• Pulmonary ventilation perfusion matching
• Surfactant
• Hypoxemia intraoperatively
CODES
ICD9
518.0 Pulmonary collapse
ICD10
J98.11 Atelectasis
CLINICAL PEARLS
• Ketamine is the only anesthetic that does not produce atelectasis when used alone (3).
• Infants are at a greater risk for atelectasis secondary to decreased lung compliance relative
to the chest wall (2).
• Gastric insufflation may result from the application of PEEP during induction if peak
pressures exceed 20 mm Hg (9).
ATRIA
Ali Salehi, MD
BASICS
DESCRIPTION
• The atria:
– House the sinoatrial (SA) node that initiates electrical impulses
– Are responsible for the active filling of the ventricles during diastole
– Play an important role in the neurohormonal regulation of sodium (Na+) and fluid
balance
• SA node: The primary pacemaker of the heart; located at the junction of the superior vena
cava (SVC) and the right atrium (RA). The action potential is initiated in the SA node which
has an automaticity of 70–80 pulse per minute (ppm) and a conduction velocity of 0.05
m/s.
• Internodal bundles: There are 3 bundles that connect the SA node to the atrioventricular
(AV) node (anterior internodal bundle of Bachman, middle internodal bundle of
Wenckebach, and posterior internodal bundle of Thorel). The action potential is conducted
via these bundles through both atria to the AV node simultaneously. The conduction
velocity in these bundles is 0.8–1 m/s.
• AV node: Located in the right posterior portion of the interatrial septum (IAS). It is the only
conducting pathway between the atria and the ventricles. Its conduction velocity is slower
(0.02–0.05 m/s) than the rest of the heart, allowing the ventricles sufficient diastolic filling
time. The AV node can act as a latent pacemaker with an automaticity of 40–60 ppm.
• His bundle: Divides at the top of the interventricular septum into the left bundle branch and
right bundle branch; has an automaticity rate of 40 ppm. The left bundle divides into
anterior and posterior fascicles. These bundles run subendocardially and come in contact
with Purkinje fibers that spread throughout the myocardium. Conduction velocity in this
system is fast (1–1.5 m/s for the bundles and 3–3.5 m/s for Purkinje fibers).
• Innervation: Embryologically, the SA node develops from the structures on the right side of
the heart and the AV node from the left side of the heart. This results in the SA node being
innervated by the right vagus nerve and the AV node by the left vagus nerve. Sympathetic
innervations (T1–T4, cardioaccelerator fibers) follow the same distribution. The majority of
sympathetic fibers come from the ipsilateral stellate ganglion.
• Endocrine physiology: Atrial myocytes are responsible for the production and release of
atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). ANP and BNP are
polypeptides that are released from the atria in response to increases in extracellular fluid
(ECF) volume due to Na+ retention. They function to increase the glomerular filtration rate
(GFR) via renal glomerular afferent arteriole vasodilatation and efferent arteriole
vasoconstriction; decrease the reabsorption of Na+ from the distal convoluted tubule and
collecting ducts (causing a net increase in Na+ excretion and volume loss); and increase
capillary permeability and relax vascular smooth muscle in arterioles and venules, causing
decreases in blood pressure.
ANATOMY
• The walls of all heart chambers consist of 3 layers: Endocardium (inner layer of the heart,
comprises endothelial cells and subendocardial connective tissue), myocardium (middle
layer of the heart, comprises myocardial muscle cells), and epicardium (outer layer of the
heart, formed by the visceral layer of the pericardium).
• Right atrium: The chamber forming the right upper border of the heart.
– Systemic venous return from the SVC and inferior vena cava (IVC) enter the posterior,
smooth wall of the RA (SVC enters at the level of the 3rd costal cartilage; IVC enters at the
level of the 5rd costal cartilage on the same line as the SVC). The coronary sinus (CS)
carries cardiac venous return into the posterior wall between the orifice of the IVC and
tricuspid valve. The IVC is protected by the Eustachian valve and the CS is protected by
the Thebesian valve.
– Pectinate muscles are found on the anterior portion of the RA; they are rough,
trabeculated, and made of parallel muscle bundles.
– The anterior and posterior portions are separated on the right by the sulcus terminalis
externally and crista terminalis internally.
– The posteromedial wall of the RA is the IAS.
– The base of the RA is the tricuspid valve and has 3 leaflets (anterior, posterior, and
septal).
• Left atrium (LA): A smooth-walled chamber that forms the base of the heart.
– Receives pulmonary venous return through the right upper and lower pulmonary veins
(RUPV, RLPV) and the left upper and lower pulmonary veins (LUPV, LLPV).
– The left atrial auricle (LAA), or appendage, forms the superior part of the left border of
the LA and has a rough trabeculated wall comprising pectinate muscles.
– The LA wall is slightly thicker than the RA.
– Unlike the right-sided veins, pulmonary veins do not have valves.
• Interatrial septum: Separates the 2 chambers and extends posteriorly and to the right
causing most of the LA to be posterior to the RA.
– Embryologically, the IAS is formed by the septum primum and septum secundum (1).
– The septum primum starts to develop in the 5th week of gestation and grows towards the
endocardial cushion (1).
– The septum secundum, at the same time, develops to the right of the septum primum as an
invagination of the atrial wall. It stops growing in the 7rd week of gestation. It leaves a
posterior inferior gap called the “fossa ovalis (1).”
– The lower portion of the septum primum persists into adulthood as the “flap valve." Upon
birth and expansion of the lungs, right-sided pressures drop below left-sided pressures and
the flap valve is pressed against the septum secundum. In 66% of people they fuse
together forming the “fossa ovalis." In 33% they fail to fuse resulting in a “patent foramen
ovale” (PFO) (1).
• Abnormal pulmonary venous return (congenital defect): One or more pulmonary veins that
carry oxygenated blood from the lungs enter the RA instead of the LA; this can be partial
anomalous pulmonary venous return (PAPVR) or total anomalous pulmonary venous return
(TAPVR). PAPVR presents with symptoms of right-sided volume overload, pulmonary
hypertension, and right heart failure. TAPVR is a cyanotic disorder and a true surgical
emergency needing an atrial septostomy in the newborn. Since all of the pulmonary venous
flow returns to the RA, presence of an atrial septal defect (ASD) or patent ductus arteriosus
(PDA) is essential to sustain life after birth.
• Atrial septal defect: An abnormal connection between the LA and RA that is associated with
a left-to-right shunt. Patients present with symptoms of right-sided volume overload (JVP
elevation, hepatic congestion, lower extremity edema, shortness of breath, pulmonary
congestion). Over time, if not corrected, it can cause right ventricle (RV) failure and
elevation of RA pressures with resultant shunt reversal (right-to-left shunt; Eisenmenger’s
syndrome). This will lead to hypoxemia and cyanosis. There are 4 major types:
– Septum secundum ASD: Results from inadequate growth of the septum secundum,
enlarged foramen ovale, or excessive absorption of the septum primum. Most common
ASD (80–90%), usually seen in women in the 5th or 6th decade of life, and rarely
associated with other cardiac defects (1).
– In addition to the septum primum, the endocardial cushion is responsible for the
development of the medial portion of the mitral and tricuspid valves, and the inlet portion
of the interventricular septum. A complete endocardial cushion defect is associated with a
septum primum ASD, a common AV valve, and an inlet VSD. It comprises 2–3% of all
ASDs and can be associated with a mitral (anterior leaflet) or tricuspid valve (septal
leaflet) cleft (1).
– Sinus venosus ASD: The failure in separation between the right-sided pulmonary veins and
the SVC, IVC, or RA. It comprises 2–10% of all ASDs. The superior type is a defect at the
junction of the SVC and RA leading to anomalous pulmonary venous return of the RUPV
into the RA. The inferior type is a defect in the junction of the IVC and RA leading to
anomalous pulmonary venous return of the RLPV into the RA (1).
– Coronary sinus ASD: Results from the unroofing of the CS which leads to a connection
between the inferior part of the LA and CS; associated with left-sided SVC. It is the least
common form.
• Atrial bradycardia: Sinus bradycardia (SB) is a heart rate <60 bpm. It can be seen normally
in athletes due to preconditioning and increased stroke volume due to exercise. SB can also
result from conditions involving the SA node such as inferior myocardial infarction;
medications (beta-blockers, inhalational anesthetic agents, narcotics, anticholinesterase
agents, and succinylcholine); and vagus nerve stimulation from carotid sinus message,
tension on the extra-ocular muscles (oculocardiac reflex) or omentum. Additionally, reflex
bradycardia can result from a sudden rise in BP that is detected by the carotid sinus. Causes
include a rise in intracranial pressure (Cushing’s reflex from tumors, intracranial bleed), use
of alpha-agonists (phenylephrine, norepinephrine), and increases in cardiac output.
• Atrial tachycardia is a heart rate >100 bpm with a narrow complex QRS on ECG.
– Sinus tachycardia is due to an increase in output (automaticity rate) of the SA node. Heart
rate is usually 100–180 bpm with a “P” wave seen on the ECG. Common causes include
sympathetic stimulation (hypoxia, hypercarbia, acidosis, ischemia), hypotension or
hypovolemia, anemia, anxiety, fever, anaphylactic reactions, sepsis, medications
(dopamine, epinephrine), hyperthyroidism, and physical activity.
– Supraventricular tachycardia (SVT) includes all forms of tachycardia originating above the
bifurcation of the His bundle. They have a regular rate of 150–220 bpm. The most
common type is AV nodal re-entrant tachycardia (60%). Another 30% are due to an AV
re-entry pathway connecting the atria to the ventricles. The remaining etiologies include
pre-excitation syndromes such as Wolff–Parkinson–White and paroxysmal atrial
tachycardia.
– Atrial flutter occurs at a rate of 200–350 bpm. It is usually associated with a circuit
movement of the right atrial tissue causing the saw tooth pattern on ECG. Atrial flutter is
almost always associated with a 2:1 or greater AV block because the AV node is not able
to conduct more than 220 bpm.
– Atrial fibrillation occurs at a rate of 300–500 bpm in a completely irregular and
disorganized fashion. It is the result of multiple, concurrent, circulating re-entrant
excitation waves in both atria; seen as an irregular pattern of AV node conduction at
irregular intervals about 80–160 bpm. A-fib can be acute, chronic, or paroxysmal. Most of
the foci responsible for a-fib appear to originate from atrial smooth muscle at the junction
of the pulmonary veins and the LA. Other foci that can be involved include the mitral
valve isthmus, orifice of CS, and SVC.
• Conduction abnormalities:
– First-degree heart block: All impulses are conducted to the ventricles but the PR interval
on the ECG is prolonged.
– Second-degree heart block (2 types): Type 1 (Wenckebach) is associated with gradual
prolongation of the PR interval and eventual drop of a ventricular beat. Type 2 has a
normal PR interval with sudden dropped ventricular beats; it has the potential to progress
into complete heart block.
– Third-degree (complete) heart block is associated with total dissociation of the atria and
ventricles. The ventricles beat at a rate lower than the atrial rhythm. The block can be at
the level of the AV node (nodal block) or lower (infranodal). In nodal block the remaining
AV node becomes the pacemaker of the ventricles at a rate of 40–50 bpm. In infranodal
block the pacemaker will be further down the conduction system with a lower rate of 15–
30 bpm which can result in significant hypotension, dizziness, and syncope. Complete
heart block usually occurs due to myocardial infarction, cardiac surgery, or ventricular
septal defects.
– Right or left bundle branch block (RBBB, LBBB): Impulse is conducted through the intact
bundle into the normal side and then through the ventricular myocardium to the blocked
side. Ventricular rate is normal but there is a wide QRS complex on the ECG.
• Sinus bradycardia: Intraoperative medical management should be administered when
associated with hemodynamic changes; treatment may include anticholinergic agents
(atropine, glycopyrrolate), beta-agonists (isoproterenol), and volume resuscitation. If
medical management fails, the use of temporary pacing devices should be considered, such
as cutaneous pacing pads, esophageal pacing leads, intravenous pacing wires and pacing
pulmonary artery catheters (PAC, or epicardial pacing placed prior to closure of the chest in
cardiac surgery).
• LBBB: Avoid placement of a PAC due to the risk of complete heart block. Detection of a new
onset LBBB in the perioperative period is suggestive of an ischemic event.
• Atrial contraction (P wave on ECG) is responsible for 20% of LV filling during diastole. This
percentage increases in patients with mitral stenosis (30%) and aortic stenosis (40%), so
maintaining sinus rhythm in these patients is of utmost importance. If a-fib or atrial flutter
occurs, medical or electrical cardioversion should be attempted. If attempts for
cardioversion are unsuccessful, ventricular response rate should be controlled to allow for
adequate ventricular filling.
• Atrial tachycardias in the perioperative period should be managed based upon the
appropriate ACLS protocols.
• Serum BNP level is an indicator of heart failure. Normal serum BNP levels are <100 pg/dL.
Levels >100 pg/dL suggest heart failure. Its sensitivity, specificity, and positive predictive
value are higher than cardiomegaly on CXR or rales on physical exam in diagnosing heart
failure. It also serves as an objective means to assess treatment.
GRAPHS/FIGURES
• SVC: Superior Vena Cava

• AAo: Ascending Aorta
• RAA: Right Atrial Appendage
• CT: Crista Terminalis
• ER/EV: Eustachian Valve/Eustachian Ridge
• CS/ThV: Coronary Sinus/Thebesian Valve
• SI: Septal Isthmus
• STV: Septal leaflet of Tricuspid Valve
• RV: Right Ventricle
• RCA: Right Coronary Artery
• OF: Oval Fossa (Fossa Ovalis)
REFERENCES
1. Rojas CA, El-Sherif A, Medina HM, et al. Embryology and Developmental defects of the
interatrial septum. Am J Roentgenol. 2010;195(5):1100–1104.
2. Linton NWF, Dubrey SW. Narrow complex tachycardias. Postgrad Med J. 2009;85:546–
551.
ADDITIONAL READING
• Costanzo LS. Physiology, 4th ed. Philadelphia, PA: Elsevier, 2010, chap. 4, 111–181.
• Ganong WF. Review of medical physiology, 20th ed. New York, NY: McGraw-Hill
Companies, 2001, chap. 24, 439–451.
• Ganong WF. Review of medical physiology, 20th ed. New York, NY: McGraw-Hill
Companies, 2001, chap. 28, 528–544.
• Moore KL, Dalley AF, Agur AMR. Clinically oriented anatomy, 6th ed. Philadelphia, PA:
Lippincott Williams & Wilkins, 2010, chap. 1, 135–160.
• AV conduction blocks
• Vagal response
• Tachycardia
• Bradycardia
CLINICAL PEARLS
The atria of the heart function as priming pumps, house the sinoatrial node, and are involved
in several congenital and rhythm disturbances.
ATRIAL FIBRILLATION
BASICS
DESCRIPTION
• Atrial fibrillation (AF) is a supraventricular arrhythmia characterized by uncoordinated
atrial activation and consequent deterioration of mechanical function.
• AF is associated with a high risk of stroke as well as increased mortality and health
expenditures; as such, it is a major public health issue.
EPIDEMIOLOGY
Incidence
• General population: ∼1% per year
– Age <40 years: ∼0.1% per year
– Age >80 years: ∼2% per year (1)[A]
• Postoperatively:
– Noncardiac surgery: Up to 8%
– Thoracic surgery: Up to 30%
– Cardiac surgery: Up to 46% (2)[A]
Prevalence
About 2.2 million patients in the US and 4.5 million in the European Union have either
persistent or paroxysmal AF (1)[A]
Morbidity
• Stroke, cerebral thromboembolic complications, myocardial ischemia, CHF, hypotension
• Ischemic stroke: 5% per year (2–7 times more frequently than those without AF)
Mortality
• Doubled compared to age-matched controls in NSR
• Related to the severity of underlying heart disease
• Congestive heart failure is a strong predictor of mortality
• Only a minority of patients die of thromboembolic complications
• Cardiovascular: HTN, CAD, CHF, valvular (mitral stenosis), and pericardial heart disease
• Non-cardiovascular: DM, hyperthyroidism, alcohol abuse, COPD, age
• Iatrogenic: Surgery, medications (beta-agonists, cold medications, antihistamines, local
anesthetics)
• Familial: Na+ and K+ channel mutations
• Perioperative: Atrial injury or ischemic inflammation, increased adrenergic tone, atrial
stretch from volume overload, and electrolyte disturbances
PATHOPHYSIOLOGY
• Re-entry is the main electrophysiologic mechanism of AF, and is secondary to structural or
electrical remodeling.
• Atrial dilation and inflammation can result in interstitial fibrosis and is the most common
substrate predisposing to AF.
• Channelopathies involving both K+ and Na+ channels are responsible for most familial
forms of AF.
• Triggers include alcohol, sleep deprivation, emotional stress, caffeine, and exercise.
• Maintain rate control in patients presenting with AF; maintain NSR in patients with
recurrent or paroxysmal AF.
• Perioperative anticoagulation strategy should balance the risk of bleeding related to the type
of surgery and the individual patient’s risk of thrombosis (3)[B].
• Optimization of comorbidities
• Implement preventative strategies in surgical patients who are at a high risk for the
development of AF (e.g., thoracic and cardiac procedures).
SYMPTOMS
• Palpitations, shortness of breath
• Neurologic symptoms
History
• Duration and type of AF (see “Classification”)
• Assess CHADS2 score
Signs/Physical Exam
• Irregularly irregular heart rate
• Signs of CHF, orthopnea, heart murmurs and gallop, rales and crackles
• Consider common comorbidities: COPD, hyperthyroidism, DM, valvular disease
TREATMENT HISTORY
• Length of treatment
• Antiarrhythmics: Class, efficacy, side effects
• Previous electrical cardioversion
• Electrophysiological ablation
• Percutaneous closure of the left atrial appendix
• Anticoagulation regimen; INR if on warfarin
MEDICATIONS
• For rhythm control, Class III antiarrhythmics (amiodarone, sotalol) are preferred due to
their decreased toxicity, however they should be used with caution in patients with LQT.
For rate control, beta-blockers, calcium channel blockers, and digitalis are commonly used.
• Amiodarone is effective for both rate control and pharmacological cardioversion (up to 90%
success if bolused followed by infusion). It is considered safe in patients with LV
dysfunction, unlike class IC drugs. Acute side effects: Hypotension, bradycardia.
• CHADS2 provides an objective score for estimating the risk of stroke in non-valvular AF.
Points for individual stroke risk factors are assigned as follows: 1 point is assigned for CHF,
HTN, age >75, or DM; and 2 points are assigned for a history of CVA/TIA. A CHADS2 score
of 0 denotes low risk, 1–2 intermediate risk, and 3–6 high risk of stroke (4)[A].
• Anticoagulation regimens are based upon the risk of stroke (CHADS2 or other scores) and
are balanced against the risk of bleeding.
– Aspirin if CHADS2 score ≤1
– Warfarin if CHADS2 score ≥2
– Dabigatran is a direct selective thrombin inhibitor. Stroke prevention is equal to that of
warfarin and fewer bleeding complications are seen with low doses. It is dosed twice per
day, orally. For a CHADS2 score = 1, the dose is 110 mg PO and for a CHADS2 score ≥2,
the dose is 150 mg PO (4)[A].
– The CHADS2 score has not been validated in valvular AF where there is a high risk of
stroke; thus, anticoagulation is always required.
• Statins
• Palpation or auscultation: Irregular heart rate
• EKG: Uneven R-R interval with occasional f waves
• CXR: Pulmonary vasculature congestion and cardiomegaly
• Echocardiogram and stress testing may be considered to rule out underlying structural or
ischemic myocardial disease, left atrial enlargement, thrombus, RV strain if PE is suspected.
• Holter monitor in suspected paroxysmal AF or if evaluating the efficacy of rate control
treatment
• Pacemaker may be in place.
Labs/Studies
• Serum or whole-blood (point-of-care) INR if on warfarin, or PTT/ACT if on heparin; there is
no valid point-of-care test for direct thrombin inhibitors.
• Electrolytes, including magnesium
• Digoxin levels
• Thyroid function tests if on amiodarone
• EP studies, if available
Evaluate cardiopulmonary, neurologic, and endocrine systems for known associated
comorbidities
• Poor rate control
• Signs and symptoms of CHF
• New-onset AF of unknown etiology (rule out ischemic or structural heart disease)
• Delay DC cardioversion until therapeutic INR or TEE evidence of atrial thrombus
CLASSIFICATIONS
• Newly discovered AF is the first presentation of AF for which the actual onset is not known.
• Paroxysmal and persistent AFs are both recurrent, but the former is self-terminating within
7 days, while the latter requires cardioversion to restore sinus rhythm.
• Permanent AF describes unsuccessful or abandoned attempts to convert to sinus rhythm.
• Etiologically, AF can be valvular or non-valvular. Patients with mitral valve disease are at an
increased risk for stroke.
TREATMENT
Premedications
• Anxiolysis as needed
• Caution with possible triggering agents (glycopyrrolate, albuterol)
• Ideal resting heart rate is 60–80 bpm. Consider optimizing existing antiarrhythmic therapy.
• In cardiac surgery, corticosteroids should be considered; they have been shown to reduce
the incidence of AF postoperatively (5)[A].
• Statins, given 7 days preoperatively, reduce the incidence of postoperative AF in thoracic
and cardiac surgery, and should be considered (5)[A].
• Increased risk of thromboembolic or hemorrhagic (if on anticoagulant) complications
• Increased risk of ventricular arrhythmias, CHF
• Possible need for intraoperative DC cardioversion in recurrent AF
• Possible TEE to rule out atrial clots in a patient who is not anticoagulated
INTRAOPERATIVE CARE
• Regional or neuraxial anesthesia may be contraindicated due to anticoagulants. If warfarin
has been held for surgery, PT/PTT/INR should be checked prior to placement. In patients
with thrombin inhibitors (Dabigatran) ASRA recommends against the use of neuraxial
anesthesia.
• For MAC cases, consider dexmedetomidine to maintain rate control.
Monitors
• Noninvasive BP measurement is adequate for most routine cases. Highly irregular pulses
may result in the NIBP cuff reading taking more time to cycle and may give unreliable
measurements.
• Arterial line is not necessary in stable hemodynamics and routine cases. However, a lower
threshold should exist for placing an arterial line when hemodynamic instability is
anticipated.
• Central venous catheters, pulmonary artery catheters, and TEE may be indicated based on
the type of surgery and comorbidities. TEE is a superior monitor of preload and
contractility, particularly in the absence of atrial contraction. TEE may be beneficial in
guiding fluid administration and vasopressor therapy in critical patients with AF.
• Esophageal Doppler and arterial pressure based cardiac output monitors do not work well in
AF.
• Avoid excessive sympathetic stimulation prior to airway management by ensuring adequate:
– Depth of anesthesia with induction agents, volatile agents, opioids, and lidocaine
– Oxygenation and ventilation
– Time for full onset of muscle relaxants when intubating
• Have rate control drugs ready and available
Maintenance
• MAC/sedation: Caution with, or avoidance of, epinephrine in local anesthesia
• General anesthesia may be provided with either a balanced inhalational or intravenous
technique.
• Rate control: Adequate depth of anesthesia, cautious use of positive chronotropes (e.g.,
ephedrine, albuterol, vagolytic agents, etc.)
• Rapid ventricular rate (RVR) with instability warrants immediate DC cardioversion.
• For RVR with hemodynamic stability, rate control may begin with diltiazem or beta-
blockers. Reserve amiodarone for patients with poor LV function. Caution: Amiodarone may
convert into NSR and “eject” a clot into the systemic circulation.
• New-onset AF: Pharmacological conversion if stable, DC cardioversion if unstable. Caution:
Successful DC cardioversion may still require anticoagulation due to atrial stunning.
• Avoid excessive sympathetic stimulation (see “Induction”)
• Slow titration of reversal agents
• Consider deep extubation, if appropriate, to avoid coughing and bucking
POSTOPERATIVE CARE
BED ACUITY
• Routine postoperative care is usually appropriate in stable patients.
• Telemetry or ICU care may be warranted in poorly controlled AF and hemodynamic
instability.
• Reinstitute rate control, antiarrhythmic, and/or anticoagulants as soon as appropriate
• Labs: Electrolytes, glucose in DM, INR/PTT
• Troponins if underlying cause for AF is CAD
COMPLICATIONS
• RVR with hypotension, CHF
• Ventricular arrhythmias
• Bleeding versus stroke and other thrombotic complications
• Postoperative cognitive dysfunction
REFERENCES
1. Fuster V, Ryden L, Cannom D, et al. 2011 ACCF/AHA/HRS Focused Updates Incorporated
Into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial
Fibrillation: A Report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines. Circulation. 2011;123(10): e269–e367.
2. Mayson SE, Greenspon AJ, Adams S, et al. The change in face of postoperative atrial
fibrillation prevention. Cardiol Rev. 2007;15:231–241.
3. Mannucci C, Douketis JD. The management of patients who require temporary reversal of
vitamin K antagonists for surgery: A practical guide for clinicians. Intern Emerg Med.
2006;1:96–104.
4. Medi C, Hankey G, Freedman S. Stroke risk and antithrombotic strategies in atrial
fibrillation. Stroke. 2010;41:2705–2713.
5. Jongnaranggsin K, Hakan O. Postoperative atrial fibrillation. Med Clin N Am. 2008;92:87–
99.
ADDITIONAL READING
• Horlocker T, Wedel D, Rowlingson J, et al. Regional anesthesia in the patient receiving
antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and Pain
Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med. 2010;35:64–
101.
• Kaatz S, Douketis JD, Zhou H, et al. Risk of stroke in patients with and without chronic
atrial fibrillation. J Thromb Haemost. 2010;8:884–890.
• Lip GH, Huang-Fat T. Management of atrial fibrillation. Lancet. 2007;370:604–618.
• Atrial flutter
• Cerebrovascular disease
• Postoperative stroke
CODES
ICD9
427.31 Atrial fibrillation
ICD10
• I48.0 Paroxysmal atrial fibrillation
• I48.2 Chronic atrial fibrillation
• I48.91 Unspecified atrial fibrillation
CLINICAL PEARLS
• Assess for the underlying structural, valvular, or coronary artery ischemic disease.
• Perioperative anticoagulation and rate control management should be addressed in
consultation with the surgeon, anaesthetist, and cardiologist.
• Risk of stroke is higher in valvular AF.
• Atrial thrombi may be seen in 14% of patients in whom AF lasted >2 days.
• Statins may be protective: Risk of postoperative AF is inversely related to the duration of
preoperative statin prophylaxis. Additionally, statins improve outcomes in the surgical
ablation of AF.
ATRIAL FLUTTER
BASICS
DESCRIPTION
• Atrial flutter (AFL) is a paroxysmal, regular, macro re-entrant arrhythmia most often
occurring in patients with structural heart disease. The re-entrant circuit is classically
confined to the right atrium with typical rates from 240 to 320 beats per minute (bpm).
• Ventricular rate is determined by AV node conduction; thus a 2:1 AV block results in a
ventricular rate of 120–160 bpm. Rapid AV node conduction is responsible for
hemodynamic deterioration and AFL-related fatalities.
• AFL is usually short-lived and closely related to atrial fibrillation (AF). If present for a
prolonged period, AFL usually evolves to AF.
EPIDEMIOLOGY
Incidence
• Incidence of ∼1% in the general population
• Incidence >5% in patients >80 years old
Prevalence
Uncertain since AFL is rarely a chronic condition
Morbidity/Mortality
• Based on the integrity of the myocardial conduction system, ventricular function, age at
presentation, duration of arrhythmia, and presence of other coexisting diseases.
• Associated with a 1.7-fold increase in mortality over a mean period of 3.6 years. The risk is
higher if AFL coexists with AF.
• Male gender: AFL ∼5-fold more common in men.
• Cardiac procedures:
– Pericarditis following cardiac surgery can lead to atrial inflammation and AFL.
– Myocardial scar formation following atrial ablation procedures can instigate AFL.
• Cardiovascular diseases:
– Structural heart disease leading to right atrial enlargement (valvular heart disease,
pulmonary embolism, or cardiomyopathy).
– Slowing of cardiac conduction (fibrosis or antiarrhythmic agents).
• Other disease: Chronic obstructive pulmonary disease (COPD), thyrotoxicosis, and chronic
alcoholism.
• Iatrogenic: Digitalis toxicity.
PATHOPHYSIOLOGY
• AFL describes a class of re-entrant arrhythmias localized to the atria.
– Typical AFL (isthmus-dependent, Type I): Right atrial re-entrant circuit that travels around
the tricuspid valve either counterclockwise or clockwise.
The flutter wave circuit is bounded by the caval veins, crista terminalis, and the
Eustachian ridge (the “isthmus” of slow conduction).
The direction of the re-entry circuit determines polarity of typical “sawtooth” flutter
waves (Ta). The Ta waves, which reflect atrial repolarization, are positive in the inferior
leads with counterclockwise re-entry. Clockwise re-entry results in negative Ta deflection
in the inferior leads. If discernable, P’ waves (atrial depolarization) have reverse polarity
in the same leads.
Cycle length of 200–400 ms depends on atrial size and the presence of antiarrhythmic
drugs.
– Atypical AFL (non-isthmus dependent, Type II): Right or left atrial re-entrant circuits that
travel around a region of atrial scarring.
Atrial scar secondary to myocardial disease, surgical procedure, or extensive
radiofrequency atrial ablation.
Difficult to treat: Ablation, cardioversion, and pharmacologic interventions are often
unsuccessful.
• AV conduction ratio (1:1, 2:1, 4:1, 6:1) influences the physiologic consequences of AFL.
– 1:1 AV node conduction results in a rapid ventricular rate and hemodynamic compromise.
Occurs in the setting of accessory pathways or exogenous catecholamines.
Rapid ventricular rate may lead to myocardial ischemia, malignant ventricular
arrhythmias, and death.
– 2:1 AV node conduction results in a fixed and regular ventricular rate.
– Variable AV block produces an irregular ventricular rhythm.
Occurs with nodal disease, increased vagal tone, and in the presence of nodal blocking
agents.
• AFL and AF have similar pathophysiology and coexist in many patients.
– ∼50% of patients with AFL will develop AF over a 5-year period.
– The arrhythmia-related “remodeling” caused by one arrhythmia AFL leads to progression
of the other AF. “Remodeling” is characterized by structural (increased atrial size),
electrical (shortening of atrial refractory period), and ultrastructural (promoting atrial
fibrosis) changes.
• AFL with atrial rates of 400–600 bpm and 2:1 conduction is common in neonates.
Termination of the arrhythmia can be accomplished with transesophageal pacing or external
synchronized cardioversion.
• Mustard, Senning, or Fontan cardiac procedures dramatically increase the risk for
development of AFL.
• The underlying medical condition or inciting event should be optimized.
• Control the ventricular rate to enhance ventricular filling and sufficient stroke volume.
– Calcium channel blockers or beta-blockers can be used to increase AV conduction block
and slow ventricular rate.
– Carotid sinus massage may increase the AV conduction ratio and temporarily slow the
ventricular rate.
• Conversion to sinus rhythm via synchronized cardioversion:
– Monophasic shocks in the following sequence: 100 J, 200 J, 300 J, 360 J.
– If AFL duration is >48 hours, confirmation via transesophageal electrocardiography (TEE)
to confirm the absence of atrial thrombus and/or anticoagulation must precede
cardioversion.
• Anticoagulation is typically via heparin or warfarin.
– Patients with AFL are at similar risk of stroke as patients with AF and should be
anticoagulated if AFL lasts >48 hours.
SYMPTOMS
• The hemodynamic consequences of AFL depend on the flutter rate, AV conduction ratio,
ventricular rate, and presence of ventricular dysfunction.
• Symptoms depend on the ventricular rate.
– Increased ventricular rates (1:1 or 2:1 AV conduction) are often perceived as palpitations,
chest discomfort, or dizziness.
– Decreased ventricular rates (8:1 AV conduction) may manifest as fatigue and exercise
intolerance.
History
• Evaluation of risk factors: Open heart surgery, cardiac valvular disease, myocardial
ischemia, pulmonary embolism, COPD, hyperthyroidism, and/or digitalis toxicity.
• History of AFL: Duration, current management, and previous treatment.
• Presence of coexisting diseases: Pharmacologic management depends on myocardial
function.
Signs/Physical Exam
• Tachycardia with regular, usually fixed, ventricular rate of 140–160 bpm. Irregularly
irregular pulse is rare, but may occur if AV conduction ratio is variable.
• Rapid, rippling flutter waves may be seen in the jugular venous pulse with an AV
conduction ratio of 4:1 but not with 2:1 ratio.
• Cardiac decompensation leads to dyspnea, hypoxemia, rales, and crackles.
• Previous radiofrequency ablation
– AFL ablation has a >90% long-term success rate. Best results are seen with isthmus-
dependent AFL, normal right atrial size, and no history of AF.
MEDICATIONS
• Rate control: Amiodarone, diltiazem, verapamil, or beta-adrenergic blockers slow down AV
conduction and control the ventricular rate.
– Amiodarone, diltiazem, and digoxin are preferred in the presence of impaired myocardial
function.
– Beta-blockers are effective in the setting of increased sympathetic tone and thyrotoxicosis.
– Vagolytic effects of class I antiarrhythmic drugs administered for AFL may result in
reduction of atrial rate to 180-200 bpm, consequential 1:1 AV nodal conduction, and
resultant increase of ventricular rate. Thus, AV blocking drugs should be administered
before the administration of class I antiarrhythmic drugs.
• Convert rhythm: Ibutilide, amiodarone, dofetilide, sotalol, flecainide, propafenone,
procainamide, and disopyramide have variable success (50–60%) in terminating AFL.
• Approximately 15% of patients treated with class IC antiarrhythmic agents or amiodarone
for AF will develop AFL. This led to the development of a “hybrid" management strategy of
antiarrhythmic drugs to treat AF with subsequent ablation to treat AFL.
Labs/Studies
• Labs: Electrolytes, cardiac enzymes, digoxin level, and thyroid function tests.
• ECG: Atrial rate ranges from 240 to 340 bpm, “sawtooth” pattern in the inferior leads, and
regular ventricular response with a discernable and consistent relationship between flutter
waves and QRS complexes.
– Flutter waves can be obscured by the T waves. Infusion of adenosine or vagal maneuvers
will briefly stop or decrease AV conduction, allowing recognition of the flutter waves.
– In the setting of an accessory pathway, the ECG pattern is indistinguishable from
ventricular tachycardia, even with 2:1 conduction.
– Atrial rate of >340 bpm may be seen with atypical AFL.
• Echocardiogram: Evaluate atrial size and ventricular function
– TEE is used to evaluate for the presence of atrial thrombus prior to synchronized
cardioversion in patients with AFL lasting longer than 48 hours.
• Uncontrolled ventricular rate, myocardial ischemia, or cardiac decompensation.
• Synchronized cardioversion in hemodynamically unstable patients.
TREATMENT
Premedications
• Anxiolytics can decrease sympathetic output.
• Rate control: Calcium channel blockers or beta-adrenergic blockers can be titrated to effect.
• Increased risk of intraoperative rapid ventricular rate, myocardial ischemia, cardiac
decompensation, and thromboembolic events.
• Risks and benefits of delaying the surgery to evaluate and treat paroxysmal AFL must be
explained. Non-urgent surgery should be postponed until adequate control of the ventricular
rate has been achieved.
INTRAOPERATIVE CARE
Insufficient evidence to suggest that either general or regional anesthesia is preferred for
patients with AFL.
Monitors
• Standard ASA monitors including ECG with ST segment analysis.
• Arterial catheter for close monitoring of blood pressure or frequent blood gas evaluation.
• Central venous catheter for infusion of vasopressors or transvenous pacing.
• Pulmonary artery catheter for evaluation of cardiac output or mixed venous oxygenation, if
indicated.
• Transesophageal echocardiography, if indicated.
• Risk of hemodynamic instability
– Vasodilation and myocardial depression from induction agents (propofol and thiopental).
– Sympathetic stimulation from laryngoscopy.
– Dexmedetomidine is associated with prolonged hypotension and increased AV nodal
blockade.
• Avoid pharmacologic agents associated with sympathetic activation (ketamine) or vagolytic
effects (pancuronium).
Maintenance
• Use of either volatile anesthetic or total intravenous anesthetic is acceptable.
• Conservative fluid management in the setting of reduced myocardial function.
• Intraoperative occurrence may be treated with rate control medications, vagal maneuvers,
or cardioversion if the patient is hemodynamically unstable.
• Avoid sympathetic stimulation.
• Ensure adequate analgesia.
• Balance reversal of neuromuscular block (excessive anticholinergics can provoke AFL);
consider slow titration to reduce incidence.
POSTOPERATIVE CARE
BED ACUITY
ICU with hemodynamically unstable or poorly controlled AFL
• Medications: Rate control agents and anticoagulation as indicated.
• Labs: Electrolytes, digoxin level, cardiac enzymes, and thyroid function tests.
COMPLICATIONS
• Systemic thromboembolism
• Coronary and/or cerebral ischemia secondary to hemodynamic insufficiency
• Tachycardia-induced cardiomyopathy
• Sinus bradycardia following administration of AV nodal blocking agents
REFERENCES
1. Lee KW, Yang Y, Scheinman MM. Atrial flutter: A review of its history, mechanism, clinical
features, and current therapy. Curr Probl Cardiol. 2005;30:121–168.
2. Nattel S, Singh BN. Evolution, mechanisms, and classification of antiarrhythmic drugs:
Focus on class III actions. Am J Cardiol. 1999;84:11R–19R.
3. Van Gelder IC, Hagens VE, Bosker HA, et al. Pharmacologic versus direct-current electrical
cardioversion of atrial flutter and fibrillation. Am J Cardiol. 1999;84:147R–151R.
• Electrical cardioversion
• Wolff–Parkinson–White
CODES
ICD9
427.32 Atrial flutter
ICD10
• I48.3 Typical atrial flutter
• I48.4 Atypical atrial flutter
• I48.92 Unspecified atrial flutter
CLINICAL PEARLS
• Atrial flutter (AFL) commonly occurs in patients after open heart surgery and those with
underlying cardiac disease.
• ECG manifestations include flutter waves with variable AV conduction.
• Ventricular rate control is achieved with beta-blockers or calcium channel blockers.
• Hemodynamically unstable patients require immediate synchronized cardioversion.
ATRIAL SEPTAL DEFECT (ASD)
Jason Choi, MD
John G. T. Augoustides, MD, FASE, FAHA
BASICS
DESCRIPTION
• A defect of the interatrial septum that allows communication between the right and left
atria. It is the most common congenital heart defect in adults.
• 3 types:
– Ostium secundum (75% of all ASDs): Patent foramen ovale (PFO) is a subtype of ostium
secundum and is the most common ASD.
– Ostium primum (15%): Associated with mitral regurgitation from the cleft mitral valve
– Sinus venosus (10%): Associated with anomalous partial drainage of the pulmonary veins
into the right atrium or superior vena cava
• ASD is often benign and asymptomatic until the 4th or 5th decade of life. Virtually all adults
with an ASD become symptomatic by the 6th decade.
– Moderate or severe defects present in a child with congestive heart failure (CHF).
– First presentation of ASD in adults may be a stroke or transient ischemic attack (TIA).
– Diagnosis is common during pregnancy due to increased blood volume.
• Clinical sequelae of ASD correspond to the degree and direction of shunting.
– Most common is left-to-right cardiac shunt.
– Right-to-left shunt indicates a more severe disease.
– PFO is the main cause of transient right-to-left shunt and paradoxical emboli.
EPIDEMIOLOGY
Incidence
ASD is diagnosed in 1 out of 1,500 live births.
Prevalence
• ASDs account for 10% of all congenital heart diseases and 30% of adult congenital heart
diseases (1)[A].
• ASDs are 2–3 times more common in women.
• PFOs present in about 25% of adults (2)[A]. A majority of PFOs are undiagnosed.
Morbidity
• ASDs have low morbidity.
• Pulmonary hypertension is rarely seen before the 3rd decade of life (3)[B].
Mortality
• ASDs are associated with low mortality.
• Decreased life expectancy is seen with ASD, but patients can reach advanced age without
intervention. Mortality rate from ASD repair is close to zero if performed before the 4th
decade in patients without significant pulmonary hypertension (2)[B].
• Spontaneous genetic mutations lead to aberrant embryologic septal development (4)[B].
• Inheritance of ASD is not fully understood.
• Ostium primum is associated with Down syndrome.
• CHF symptoms in an infant with ASD indicate additional congenital heart defects (3)[C].
PATHOPHYSIOLOGY
• Size of defect, ventricular compliance, and direction of venous inflow determine the degree
and direction of interatrial shunting.
– Defects <5 mm are hemodynamically insignificant, while defects >20 mm cause
clinically significant shunting (1)[A].
• Left-to-right shunt is a result of greater right ventricle compliance and lower pulmonary
vascular resistance (PVR).
– Chronic left-to-right shunt increases pulmonary blood flow and can lead to pulmonary
vascular congestion and right ventricular strain.
– Severe pulmonary hypertension and right heart failure may develop. Pulmonary flow can
reach 4 times that of systemic flow in severe disease. Right-to-left shunt (Eisenmenger
syndrome) can develop over time secondary to increased pulmonary pressures. This
“shunt reversal” results in cyanosis as a significant fraction of blood bypasses the
pulmonary circulation and gets ejected into the systemic circulation, unoxygenated.
• Patients most commonly present with dyspnea, palpitations, and decreased exercise
tolerance. Atrial arrhythmias, especially atrial fibrillation, are commonly seen in the 4th
decade.
• PFO is unique as a dynamic shunt occurring under certain physiologic situations that
transiently elevate right atrial pressures (e.g., coughing, Valsalva maneuver, and increased
PVR).
– All other ASDs can have transient right-to-left shunting, but usually shunt left-to-right
continuously.
• Decrease the risk of paradoxical emboli (e.g., avoid air entry in IV lines).
• To prevent worsening of left-to-right shunt, avoid increases in systemic vascular resistance
(SVR), fluid overload, steep Trendelenburg positioning, and over-transfusion.
• Be aware of scenarios that cause transient right-to-left shunting: Pulmonary embolism, high
positive end-expiratory pressure (PEEP), venous air embolism, pneumoperitoneum with
laparoscopy, and cardiac tamponade.
• Be prepared to treat pulmonary hypertension with direct pulmonary vasodilators.
SYMPTOMS
• ASD is an acyanotic defect (left-to-right shunt).
• Cyanosis and clubbing with only an ASD reflect right-to-left shunt and severe disease.
• CHF symptoms: Orthopnea
History
• Clinical presentations of ASD vary.
• ASD is often undiagnosed until adulthood due to a lack of symptoms and physical findings.
• Rule out a history of stroke, TIA, new onset dyspnea on exertion, and palpitations from
atrial arrhythmias.
• Assess progression/worsening of symptoms.
• Ask about a history of murmur or previous assessment by a cardiologist.
Signs/Physical Exam
• Fixed-split S2 heart sound on auscultation is pathognomonic for ASD.
• Systolic ejection murmur is heard from increased output through the pulmonic valve.
• Ostium primum is associated with significant mitral regurgitation.
• S4 heart sound reflects right ventricular hypertrophy and pulmonary hypertension.
TREATMENT HISTORY
Closure of the defect with open heart surgery or cardiac catheterization. If the patient has not
had an ASD closure, they are most often asymptomatic.
MEDICATIONS
There is no specific medical therapy.
Labs/Studies
• ECG: Incomplete right bundle branch block (invariably present), atrial arrhythmia (e.g.,
atrial fibrillation), prolonged PR interval, right ventricular hypertrophy, or right axis
deviation
• CXR: Prominent pulmonary vasculature often noted from vascular congestion
• Echocardiography: Important to note the degree of shunting, size and strain of right
ventricle, and pulmonary artery pressures
– TEE with bubble study is the gold standard diagnostic study (4)[A].
• Cardiac catheterization: Pulmonary artery pressures should be recorded.
Other organ dysfunction, such as pulmonary edema, pulmonary hypertension, or
complications of right heart failure, is only seen with moderate/severe disease from ASD.
• Presence of right-to-left shunt requires correction or medical optimization prior to elective
surgery (4)[B].
• Pulmonary blood flow >1.5 times the systemic flow warrants closure of the ASD (1)[A].
CLASSIFICATIONS
• Asymptomatic
• Symptomatic left-to-right shunt
• Right-to-left shunt with pulmonary hypertension
TREATMENT
Premedications
• For most patients with ASD, there is no restriction on premedication.
• Premedication with midazolam can help with facilitating parental separation in the
pediatric population.
Risk of paradoxical emboli leading to stroke is minimal but present.
INTRAOPERATIVE CARE
For the typical asymptomatic ASD patient, choice of anesthesia and technique can be tailored
to provider and/or patient preference.
Monitors
• Standard ASA monitoring
• Monitors should be tailored to extent of surgery and its risks.
• For open ASD repair on bypass, TEE, arterial line, and central line +/– pulmonary artery
catheter are recommended for intra-operative management.
• No special airway considerations
• Drug dilution occurs from increased pulmonary blood flow, but is unlikely to have clinical
relevance or to affect induction time.
• There is no indication for endocarditis prophylaxis (4)[B], unless concomitant valvular
disorder warrants it.
Maintenance
• Imperative to prevent air emboli
• Prevent increases to the left-to-right shunt
– Use techniques that decrease the SVR (promotes forward flow into the aorta) or increase
the PVR
– Avoid a high FiO2 and hyperventilation; they can cause pulmonary vasodilatation.
– Maintain higher mean airway pressures
– Avoid fluid overload and over-transfusion
Bucking and coughing upon emergence increases the risk of paradoxical emboli by causing
transient right-to-left shunting.
POSTOPERATIVE CARE
BED ACUITY
ICU postoperative care is not warranted unless the patient has significant pulmonary
hypertension or has had closure of the ASD.
If symptoms or complications of ASD manifest during the perioperative period, cardiology
should be consulted.
COMPLICATIONS
• Paradoxical embolism: Stroke, TIA, fat embolism
• Transient supraventricular dysrhythmias and atrioventricular conduction defects are
common post-closure of ASD.
• Post-ASD closure, interpretation of central venous pressure (CVP) must account for a
previously dilated right atrium. Maintaining normal CVP values may cause volume
overload.
REFERENCES
1. Rigatelli G, Ronco F. Patent foramen ovale: A comprehensive review for pulmonologist.
Curr Opin Pulm Med. 2010;16:442–447.
2. ensley FA, Martin DE, Gravlee GP. A practical approach to cardiac anesthesia, 3rd ed.
Philadelphia: Lippincott Williams and Wilkins, 2003.
3. Augoustides JG, Ochroch EA. Assessment of intracardiac shunts: Perioperative
echocardiography. Int Anesthesiol Clin. 2008;46:83–95.
ADDITIONAL READING
• Warnes CA, Williams RG, Bashore TM, et al. ACC/AHA 2008 guidelines for the management
of adults with congenital heart disease: Executive summary. A report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2008;118(23):2395–2451.
• Ventricular septal defect
• Patent foramen ovale
• Chest x-ray
CODES
ICD9
• 745.5 Ostium secundum type atrial septal defect
• 745.8 Other bulbus cordis anomalies and anomalies of cardiac septal closure
ICD10
• Q21.1 Atrial septal defect
• Q21.2 Atrioventricular septal defect
CLINICAL PEARLS
• 25% of adults have patent foramen ovale (PFO) and most are undiagnosed.
• Avoid air entry in IV lines in ASD patients.
• A fixed-split S2 heart sound is pathognomonic for ASD.
• PFOs can transiently shunt right-to-left during the anesthetic course (high peak inspiratory
pressure [PIP], coughing, abdominal insufflation, Trendelenburg positioning, etc).
ATRIAL TACHYCARDIAS
BASICS
DESCRIPTION
• Atrial tachycardias (ATs) encompass several types of arrhythmias driven by one or more
ectopic sources outside the sinus node and do not require the participation of the AV node
for maintenance of tachycardia. ATs may be based on micro-reentrant, triggered, or
automatic mechanisms causing focal atrial tachycardia (FAT) or multifocal atrial
tachycardia (MAT) (1)[A].
• FAT may present as transient, recurrent, sustained, and incessant with usual rates of 130–
250 bpm. MAT may be persistent and easily misinterpreted as atrial fibrillation (2)[A].
EPIDEMIOLOGY
Prevalence
FAT accounts for 5–15% of patients undergoing electrophysiologic studies. The rates are
higher in children (1)[A].
Prevalence
• FAT: 0.34% in asymptomatic individuals and 0.46% in symptomatic patients (1)[A]
• MAT in the hospitalized population has been estimated to be 0.05–0.32% (2)[A].
Morbidity/Mortality
• Incessant AT may result in dilated cardiomyopathy, which may be reversible after the
tachycardia has been terminated.
• Patients being hospitalized with MAT are usually elderly and may have high mortality as a
consequence of underlying chronic obstructive pulmonary disease (COPD) (2)[A].
• FAT: Open heart surgery (especially for correction of CHD), younger age, and disturbances
of the autonomic nervous system
• MAT: COPD, congestive heart failure (CHF), hypoxemia, use of theophylline, electrolyte
abnormalities (hypomagnesemia, hypokalemia), and increased age (2)[A].
• FAT is characterized by atrial activation starting rhythmically at a small area (focus) from
which it spreads out centrifugally. Usual locations of such foci are the area along the crista
terminalis and near the right and left pulmonary veins. It may be caused by micro-reentrant,
triggered, or automatic mechanisms (3)[A].
– Micro-reentry may be initiated and terminated with programmed electrical stimulation.
Verapamil, adenosine, and dipyridamole can terminate this arrhythmia.
– Triggered activity may also be initiated and terminated with electrical stimulation (atrial
extrastimuli or rapid atrial pacing). Verapamil, propranolol, adenosine, carotid sinus
massage, and dipyridamole can terminate triggered FAT.
– Automatic FAT cannot be initiated or terminated with programmed electrical stimulation,
but it can be initiated by isoproterenol infusion and terminated with propranolol. The
rhythm is insensitive to adenosine, verapamil, and carotid sinus massage. Episodes of
automatic FAT commonly show a “warm-up” phenomenon at the beginning (the rate
gradually increases) and a “cool-down” phenomenon at termination (the rate gradually
slows down with transition to normal sinus rhythm). Since automaticity decreases with
aging, automatic FAT is less common in geriatric patients (1)[A].
• MAT (chaotic AT) may be initiated by delayed after-depolarizations arising from multiple
atrial foci. The definition of MAT requires at least 3 distinct P’ wave morphologies (2)[A].
FAT during infancy is typically incessant. Patients often present with tachycardia-induced
cardiomyopathy. MAT is an uncommon, well-tolerated, and self-limiting rhythm in most
pediatric patients.
• Drugs that modulate the autonomic nervous system may be useful in the anesthetic regimen
of patients presenting with FAT.
• Treatment of the underlying medical diseases is the primary and the most successful therapy
for MAT. It is also important to avoid hypoxemia as well as medications or procedures that
could worsen the pulmonary status.
• Cardioversion has no effect on the sites of ectopy that produce automatic FAT and is not
effective in converting MAT to sinus rhythm (1)[A], (2)[A].
SYMPTOMS
• Symptoms of ATs may range from none to syncope to symptoms of heart failure.
• The severity of FAT presentation depends on the ventricular rate and presence of ventricular
dysfunction.
• The gradual increase in heart rate at the beginning and slowing at termination may make it
difficult for a patient to recognize the tachycardia.
• Some patients may perceive fast ventricular rates as palpitations, chest discomfort, or
dizziness. Exercise intolerance results from the inappropriately high ventricular rate that
does not change with increasing workload.
• Symptoms or signs of CHF are due to decreased left ventricular contractility, AV valve
regurgitation, and atrial dilatation.
History
• Review for presence of a cardiac or pulmonary disease, recent heart surgery, and the
arrhythmogenic effects of current medications.
• Review for previous episodes, management, and current duration of AT.
• FAT may resolve spontaneously. However, failure to perceive the FAT of incessant nature
can lead to depression of myocardial function and tachycardia-induced cardiomyopathy. If
the tachycardia is not treated aggressively, the myocardial function can continue to decline,
resulting in an irreversible cardiomyopathy. This occurs in 80% of cases due to FAT of
abnormal automaticity. Patients with faster rates may be at higher risk (1)[A].
• The MAT usually occurs in elderly and seriously ill patients. It may resolve within days
following successful management of the underlying disease. If management of the
underlying disease is not successful, onset of MAT implies a poor prognosis. MAT may be
preceded by or progress to atrial fibrillation or atrial flutter in 50% of cases. The choice of
pharmacologic agents may depend on the presence of coexisting medical diseases.
Signs/Physical Exam
• The pulse rate may not be reflective of the atrial rate because of variable AV node
conduction.
• The heart rates seen in FAT vary based on the patient’s age and catecholamine state. In case
of chronic FAT the rate tends to vary from hour to hour influenced by a variety of
physiologic factors modifying autonomic tone. Ventricular rate is usually regular.
• In MAT, the rhythm is irregular and the physical examination findings clinically resemble
atrial fibrillation.
• Dyspnea, hypoxemia, rales, and crackles are signs of cardiac decompensation.
TREATMENT HISTORY
• Review type, length, success of treatment, and recurrence of symptoms
• History of interventional management: Overdrive pacing and cardioversions are usually not
successful in automatic FAT and MAT.
• History of arrhythmia ablation: The treatment of choice for poorly controlled FAT and MAT
has become radiofrequency catheter ablation.
MEDICATIONS
• Termination of AT using adenosine makes it highly unlikely that automatic FAT is present.
• Primary acute treatment strategy of FAT is slowing or terminating the tachycardia. AV nodal
blocking is the secondary strategy. IV beta-adrenergic blockers may terminate automatic
FAT while nonautomatic FATs are frequently terminated by verapamil (1)[A].
• Class I antiarrhythmic medications may decrease automaticity, prolong refractory period,
and can terminate FAT.
• Class III drugs that slow myocardial conduction and AV conduction have had modest success
in treatment of ATs. These medications, except amiodarone, have the potential to decrease
myocardial performance and must be used with caution in patients with decreased LV
function.
• Digoxin slows AV conduction by enhancement of vagal activity and is a positive inotropic
agent.
• Calcium channel blockers (Class IV drugs) slow the AV conduction, but are negative
inotropes and should be used selectively and cautiously.
• The management strategies of MAT also rely on suppression of the tachycardia focus and/or
slowing of AV conduction. It may take a combination of drugs to control the rate.
• Metoprolol and high doses of IV magnesium can be useful in treating MAT.
Labs/Studies
• Electrolytes, digoxin level
• The majority of FATs can be diagnosed from the ECG; however, differentiation from other
forms of supraventricular tachycardia (SVT) may be difficult.
– FAT presents on the ECG with P’ waves that generally show an abnormal axis and
configuration, but remain similar in shape. When the focus arises from the left atrium, the
P’ wave is negative in lead I; those with focus in the low right atrium show a negative P’
wave axis in the lead aVF with a positive wave in lead I. Occasionally, the focus is in an
area close to the sinus node or in the high right atrium and the P’ wave axis is similar to
sinus tachycardia. When the rhythm resembles sinus tachycardia, it can lead to a delay in
diagnosis and institution of therapy.
– The atrial rate during FAT is generally between 100 and 180 bpm. Each P’ wave is usually
followed by a QRS complex, and the PR interval is typically not prolonged. Thus the P’P’
intervals do not vary by more than 50 ms unless an exit block from the focus of FAT is
present.
– AV block may be present during FAT and is due to decreased sympathetic tone or digitalis
toxicity.
– Tachycardia-induced ST segment depression and T wave inversion may occur and may
persist for some time after the cessation of long-lasting FAT.
– During MAT there are ≥3 distinct P’ waves of varying morphology in the same ECG lead;
there is no dominant atrial pacemaker (difference from sinus rhythm with frequent
premature atrial complexes and focal AT); AV conduction may be variable; and there is an
isoelectric baseline with varying PP, PR, and RR intervals. Multiple P’ wave morphologies
and variable P-R and R-R intervals may contribute to confusion of MAT and atrial
fibrillation. The ventricular rate is usually 100–150 bpm but may be as high as 250 bpm.
• Ambulatory (Holter) monitoring is very helpful in establishing the FAT diagnosis.
• Exercise testing is frequently not useful because the sinus heart rate increases and the
automatic focus is suppressed.
• COPD, pulmonary infection
• Uncontrolled ventricular rate, hemodynamic instability, signs of myocardial ischemia, or
cardiac decompensation
• Cardiac consultation may be necessary.
CLASSIFICATIONS
Varies; depends on pathophysiologic characteristics or clinical presentation
TREATMENT
Premedications
• A combination of benzodiazepines and opioids will decrease anxiety and modulate
sympathetic tone.
• Anticholinergic agents may worsen AT.
• Consider medications that decrease automaticity and AV conduction without decreasing
cardiac output.
Increased risk of cardiac complications
INTRAOPERATIVE CARE
Depends on the surgical procedure. There is insufficient evidence to suggest that either
general or regional anesthesia is more beneficial for patients with ATs.
Monitors
• Standard ASA monitors including ECG with ST segment and T wave trends
• Arterial catheter for cases of expected blood pressure instability or need for frequent blood
gas evaluation (COPD)
• Central venous catheter is optional, but if utilized, intracardiac stimulation should be
minimized during catheter placement.
• Pulmonary artery catheter may be used in cases of cardiomyopathy.
• Increased risk of hemodynamic instability due to cardiac depression caused by intravenous
or inhalational anesthetics
• Consider administration of higher doses of benzodiazepines and opioids to decrease
sympathetic tone
• Dexmedetomidine, an alpha-2 agonist, may be useful in decreasing the sympathetic tone and
the heart rate, but the loading dose may cause significant hypotension.
• Ketamine and pancuronium are relatively contraindicated.
• Minimize the length of laryngoscopy or avoid laryngoscopy with the use of a laryngeal mask
airway or intravenous sedation.
Maintenance
• Neither propofol nor volatile agents have significant electrophysiologic effects and are
adequate maintenance agents.
• Conservative fluid management in case of cardiomyopathy
• Balanced reversal of neuromuscular block, with slow administration
• Avoid sympathetic stimulation
• Complications:
– Hemodynamic instability, coronary ischemia
– Tachycardia-induced cardiomyopathy
FOLLOW-UP
BED ACUITY
Poorly controlled AT will dictate ICU care.
• Rate control as indicated
• Electrolytes, digoxin level, cardiac enzymes
COMPLICATIONS
• Hemodynamic instability, coronary ischemia
• Tachycardia-induced cardiomyopathy
REFERENCES
1. Roberts-Thomson KC, Kistler PM, Kalman JM. Atrial tachycardia: Mechanisms, diagnosis
and management. Curr Probl Cardiol. 2005;30:529–573.
2. McCord J, Borzak S. Multifocal atrial tachycardia. Chest. 1998;113:203–209.
3. Saoudi N, Cosio F, Waldo A, et al. A classification of atrial flutter and regular atrial
tachycardia according to electrophysiological mechanisms and anatomic bases. Eur Heart
J. 2001;22:1162–1182.
CODES
ICD9
427.89 Other specified cardiac dysrhythmias
ICD10
I47.1 Supraventricular tachycardia
CLINICAL PEARLS
• FAT usually occurs in young patients and may resolve spontaneously; however, failure to
perceive an incessant FAT (e.g., in small children) can lead to a cardiomyopathy that may
become irreversible if the tachycardia is not aggressively pharmacologically treated.
• MAT usually occurs in elderly and seriously ill patients. It may resolve within days following
successful management of the underlying disease. If management of the underlying disease
is not successful, onset of MAT implies a poor prognosis.
• Cardioversion has no effect on the sites of ectopy that produce automatic FAT and is not
effective in converting MAT to sinus rhythm. Radiofrequency catheter ablation may be
curative.
AUTOLOGOUS BLOOD TRANSFUSION
Andrew A. Klein, MD
BASICS
DESCRIPTION
• Transfusion of the patient’s own blood or blood components back to them has the
theoretical advantages of:
– No risk of transmission of infection
– No blood transfusion reaction
– No graft versus host disease
– No storage of blood required (except with preoperative autologous blood donation
[PABD])
• There are 4 types of autologous blood transfusion:
– Preoperative autologous blood donation
– Intraoperative hemodilution
– Cell salvage or saver
– Postoperative blood collection and re-transfusion
• Allogeneic transfusions are the “opposite” of autologous transfusions and involve giving a
patient blood collected from another person and has been stored in the blood bank.
• “You know what you’ve got inside you and therefore what you’re getting.”
• Oxygen-carrying capacity: In a normal person breathing room air, arterial blood carries
approximately 20 mL O2/100 mL; 19.7 mL combined with hemoglobin (Hb) and only 0.3
mL dissolved in plasma. Hemoglobin molecules within red blood cells contain iron that can
bind reversibly to oxygen molecules to form oxyhemoglobin. Normal Hb is 13–16 g/dL in
men and 12–16 g/dL in women.
• Viscosity is the tendency of fluids to resist flow. Blood viscosity depends largely on
hematocrit (increasing exponentially as hematocrit increases), red cell characteristics, and
blood protein concentration. Increasing viscosity (from blood transfusion) leads to reduced
flow, especially in vessels <0.3 mm in diameter. This causes an increase in resistance with
a resultant increase in blood pressure (blood pressure is equal to cardiac output multiplied
by resistance: BP = CO × R).
• Transfusion, even of autologous blood, should be reserved for when it is needed, and local
protocols should be followed. The ACC/AHA Guidelines recommend that blood is given
when the Hb <6 g/dL; as this is described as lifesaving. They also state that transfusion in
most postoperative patients with a Hb <7 g/dL is reasonable and that in select patients
with critical end-organ ischemia, it may be necessary to transfuse at a Hb of 10 g/dL.
• Preoperative autologous blood donation (PABD): 1–2 units of blood are collected from the
patient 2–4 weeks before surgery.
– The goal is to remove red blood cells and plasma, process it, and store it until the day of
surgery. The blood is not separated into components and is re-administered as whole
blood. Thus, it contains some or all of the blood components needed by the patient.
– Preoperative donation allows the patient time to recover and begin red cell regeneration,
provided that iron stores are adequate. Thus, levels should be checked and iron
supplementation administered if necessary.
– Guidelines state that patients should be in good health to tolerate phlebotomy of around
450 mL and autologous blood collection should only be offered to those patients in whom
there is a reasonable expectation that blood will be required.
– Patients who would not normally require cross-matched blood (e.g., Group and Save only)
should not be considered, unless there is a specific clinical reason. Direct patient requests
should be discouraged after adequate explanation.
– Contraindications include anemia (Hb <11 g/dL), current infection, no definite surgical
date, severe cardiac, respiratory, or cerebrovascular disease, and pregnancy.
– Autologous blood should be stored in a refrigerator at a controlled temperature between 2
and 8°C, with alarms set at 3–7°C, and physically separated from homologous blood stocks
and cross-matched blood. This refrigerator should be equipped with a recorder and an
alarm similar to those on other fridges used for blood storage.
– The autologous label for each unit should include all necessary information for correct
identification of the patient and should have a suitable adhesive for refrigerated storage.
• Intraoperative hemodilution consists of blood collection immediately before surgery (usually
after induction of anesthesia), followed by IV fluid replacement to prevent hypovolemia.
Blood is then re-infused at the end of, or after, surgery. Blood is kept warm in the operating
theatre (can be stored for up to 8 hours in blood collection [containing citrate] bags without
refrigeration).
– Popular in cardiac surgery before or immediately after commencing cardiopulmonary
bypass
– Usually acceptable to Jehovah’s Witnesses if blood is kept in continuous contact with the
patient
– Less metabolic derangements due to the shorter storage time; hyperkalemia does not
develop in <24 hours but hemolysis can occur during blood removal if too small a line is
used.
– Hematocrit before blood removal should be >30%, and generally >36%. After blood
removal, hematocrit should be >24%.
• Cell salvage is the most common method of autologous blood transfusion. Blood lost during
or immediately after surgery is suctioned and collected into a designated reservoir. Heparin
is added to prevent clotting and is processed and transfused back to the patient.
– May commonly be utilized in cardiac, vascular, and orthopedic surgery
• Postoperative blood collection (most often after orthopedic surgery) and re-transfusion of
unprocessed blood back to the patient. It has been used in cardiac and orthopedic surgery,
as well as traumatic hemothorax. During total knee replacement, the surgery is most
commonly performed with a tourniquet in place, and this is then deflated at the end of the
procedure after a drain has been placed in the joint. This drain is then opened after 30–60
minutes, and the blood collects into a specifically designed collection reservoir (bellows)
using vacuum suction (as opposed to wall suction). The collected blood is filtered before
being immediately transfused back to the patient; this is performed on an hourly basis. This
system is low-cost, easy to perform, and with minimal side effects. Blood is
defibrinogenated and thus does not require anticoagulation prior to transfusion;
additionally, it is sterile.
• Autologous platelet-rich plasma is collected from the patient intraoperatively via apheresis
equipment. When used for cardiac surgery patients, it is removed prior to heparin
administration and the onset of cardiopulmonary bypass. It is returned after heparin
reversal. Studies have not shown improved benefit in regard to hemostasis and/or decreased
need for transfusion.
• PABD can have disadvantages, problems, and/or challenges including:
– Wastage of blood due to cancellation of surgery
– Inability to utilize the blood for another patient, in the event that it is not given to the
donor patient. A small number of autologous units are administered to other patients;
however, due to the donor’s comorbidities, autologous units are often unsuitable for
allogeneic donation.
– The need for storage
– Metabolic derangements still exist, such as hyperkalemia and loss of 2,3 DPG (related to
length of storage)
– Potential for administrative error
– Blood must still be warmed during infusion to prevent hypothermia.
– Donation may predispose to deterioration in medical condition (e.g., severe ischemic heart
disease).
– Contraindicated in patients with anemia
– Unacceptable to Jehovah’s Witnesses
– Not often practiced due to logistical reasons, particularly scheduling of surgery, collecting,
and storing blood (different locations)
– Does not guarantee that allogeneic blood will not be transfused
– Vasovagal reactions during collection from hypotension and bradycardia
– Increased cost compared to allogeneic blood units
• Intraoperative hemodilution can have disadvantages including:
– Hemodynamic instability: Removal of up to 500 mL of blood is possible; however, loss of
volume may cause hypotension unless fluid is replaced immediately.
– Precipitation of myocardial ischemia or worsening tissue oxygenation from acute anemia
– Need for wide-bore vascular access; central venous may be necessary if the arm IV is
insufficient or unreliable.
– Blood storage time is limited to a few hours. It should not be stored in the blood fridge,
but kept in the patient’s immediate vicinity and transfused within 8 hours.
• Cell salvage can have disadvantages including:
– Loss of plasma containing clotting factors and platelets leading to coagulopathy and
bleeding. This is only relevant after at least 50% of a patient’s blood volume has been
processed.
– Requires “enough” blood loss in order to prepare a unit
• Postoperative blood collection can have disadvantages including:
– Risks of fluid overload with rapid re-infusion
– Clotting of blood in re-transfusion bag if not administered to patient immediately after
filtration
• Direct re-infusion of shed mediastinal blood from postoperative chest tube drainage is not
recommended as a means of blood conservation and may cause harm (Level B evidence).
• Autologous transfusion can optimize or increase Hb while reducing the risk and amount of
allogeneic blood transfusion.
• Allogeneic blood is strongly associated with increased risk of death (1)[B] and
complications, including postoperative infection (2)[A], cancer recurrence, acute lung injury
(TRALI) (3)[B], and increased length of stay in the intensive care unit and hospital. Risk
correlates with the number of units of allogeneic blood transfused and length of time that
the blood is stored (4)[B]. These risks are NOT associated with autologous transfusion.
• Needs advance planning and preparation before surgery
• Discuss with the surgeon and patient
REFERENCES
1. Karkouti K, Wijeysundera DN, Yau TM, et al. The independent association of massive blood
loss with mortality in cardiac surgery. Transfusion. 2004;44:1453–1462.
2. Duffy G, Neal KR. Differences in post-operative infection rates between patients receiving
autologous and allogenic blood transfusion: A meta-analysis of published randomized and
nonrandomized studies. Transfusion Med. 1996;6:325–328.
3. Brander L, Reil A, Bux J, et al. Severe transfusion-related acute lung injury. Anesth Analg.
2005;101:499–501.
4. Koch CG, Li L, Sessler DI, et al. Duration of red-cell storage and complications after cardiac
surgery. N Engl J Med. 2008;358:1229–1239.
• Cell salvage
• Blood transfusions
• Transfusion-related infections
• Blood substitutes
CLINICAL PEARLS
• Autologous blood transfusion is commonly considered in coronary artery bypass, major
vascular surgery, primary and revision hip or total knee replacements, hepatic resections,
radical prostatectomies, and major spine surgery with instrumentation.
• Directed donation describes blood donated by a friend or family member for a designated
patient. This may be used when the patient’s health or baseline hemoglobin may not be
suitable for autologous donation. Drawbacks, however, are that it is not as safe as the
patient’s own blood and is handled as an autologous donation.
AUTONOMIC HYPERREFLEXIA
John F. Bebawy, MD
Antoun Koht, MD
BASICS
DESCRIPTION
• Autonomic hyperreflexia (AH) is a syndrome characterized by profound and imbalanced
reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) at or above
the T6 level.
– Inciting stimulus ranges from innocuous to noxious.
– Unchecked sympathetic discharge occurs below the level of injury in response to a
stimulus also below the level of injury.
– Compensatory hemodynamic responses occur above the level of injury.
– Also known as “autonomic dysreflexia”
• Patients with SCI commonly present to the operating room for urologic and other lower
extremity procedures (e.g., decubitus ulcers) that can elicit AH.
EPIDEMIOLOGY
Prevalence
• Associated with the incidence of SCI at or above the T6 level; in the US, there are 12,000
new cases of SCI annually.
• Pregnant women with SCI at or above the T6 level: 2/3rd can experience AH during labor.
Prevalence
• 48–90% of patients with SCI at or above the T6 level
• Males:females 4:1
Morbidity
Primarily due to uncontrolled hypertension leading to myocardial infarction, cerebral
hemorrhage, seizures
Mortality
Rare as a direct result of AH
Any stimulation below the level of SCI. Most commonly:
• Bladder distension
• Bowel distension
• Surgery
• Pressure sores
• Urinary tract infection (UTI)
• Cholelithiasis
• Sexual intercourse
• AH can be seen after the initial spinal shock phase of SCI, when autonomic reflexes return.
• Injury at or above the T6 level is above major splanchnic sympathetic outflow (T6 to L2).
• Sensory input below the level of injury is transmitted via peripheral nerves to the
spinothalamic tract and posterior columns of the spinal cord, and activates sympathetic
neurons.
• However, normal, descending inhibitory outflow is blocked at the level of injury; this leads
to unopposed and abnormal sympathetic discharge and elevated blood pressure (due to
unopposed vasoconstriction).
• Brainstem and carotid baroreceptor reflexes above the level of injury attempt to compensate
for the elevation in blood pressure (below the level of injury) by increasing parasympathetic
discharge to the heart via the vagus nerve; this leads to bradycardia and compensatory
vasodilation above the level of injury.
• Despite the possible loss of sensation, anesthesia for procedures below the level of SCI is
advisable to prevent AH.
– General anesthesia and spinal anesthesia are preferred methods.
– Epidural anesthesia may also be beneficial, but to a lesser extent due to reduced block
density and sacral nerve sparing.
• Be prepared to treat manifestations of AH (e.g., with short-acting and direct-acting
antihypertensives).
SYMPTOMS
Headache, blurred vision, nasal congestion, chest pain, anxiety
History
• Ascertain the level, age, completeness, and stability of the SCI.
• In cervical injury, assess if spinal fixation has been performed.
• Frequency and inciting events for AH (e.g., urinary catheterization, bowel distension, etc.)
Signs/Physical Exam
• Asymptomatic in between episodes of AH
• During an episode of AH:
– Below the level of SCI: Elevated blood pressure, cool to touch, piloerection
– Above the level of SCI: Flushing and sweating, bradycardia, cardiac arrhythmias (atrial
fibrillation, premature ventricular contractions, AV conduction abnormalities)
TREATMENT HISTORY
• Prophylactic efforts include the removal of inciting stimulus:
– Bladder catheterization, fecal disimpaction, etc.
• Sitting patient up from the supine position, legs down
MEDICATIONS
No specific routine medications
Labs/Studies
Depend upon the surgical procedure and other patient comorbid conditions
• Decubitus ulcers
• Contractures and deconditioning
• Frequent UTIs
• Pulmonary impairment
• Acute episodes of AH should trigger a search for, and removal of, inciting stimulus, and/or
postponement of nonemergent surgical interventions.
• Emergent surgical intervention during an AH episode should be performed under spinal or
general anesthesia.
CLASSIFICATIONS
None
TREATMENT
Premedications
• Anxiolytics as appropriate
• Vasodilators if acutely hypertensive
• Cases planned to involve sedation should include the caveat that a spinal or general
anesthetic may be used to treat an acute AH episode.
• Morbidity of an acute AH episode should be reviewed, especially for lower body surgery.
INTRAOPERATIVE CARE
• Spinal anesthesia may be preferred since it blocks descending spinal cord reflexes directly
(1)[C].
• General anesthesia, at adequate levels, can inhibit reflex spinal sympathetic discharge.
• Epidural anesthesia may be used but could be less effective in severe AH cases.
Monitors
• Consider an arterial line if the patient is at high risk (e.g., lower body surgery, prolonged
surgery) for, or has had a confirmed AH episode.
• Awake fiberoptic intubation or other alternative airway devices may be preferred in patients
with previous cervical fusion and limited neck mobility, or in those patients with an
unstable cervical spine.
• Induction drugs should not aggravate pre-existing hypertension, nor should they cause
excessive hypotension, since vascular tone below the level of SCI is lower at baseline (but
higher during an acute AH episode).
• Avoid succinylcholine; a proliferation of extrajunctional receptors due to disuse can result in
massive amounts of potassium extravasating from the muscle with the use of a depolarizing
muscle relaxant.
Maintenance
• General anesthesia should be maintained at adequate levels to inhibit reflex sympathetic
discharge.
• Epidural catheters should be appropriately redosed with local anesthetics or have an
infusion started in order to maintain adequate block density.
• An AH episode should be immediately treated with:
– Direct-acting vasodilators: Calcium channel blockers, nitrates, hydralazine
– Beta-blockers are second-line because of their potential to cause unopposed alpha-related
vasoconstriction.
– Central-acting vasodilators (e.g., clonidine) may be less effective.
• Short-acting antihypertensives should be immediately available to treat emergence-related
hypertension.
• Extubation of patients with cervical fusion should be performed when the patient is
oxygenating and ventilating independently and following commands.
FOLLOW-UP
BED ACUITY
Following an episode of AH, monitor blood pressure and heart rate in a monitored setting for
at least 2 hours.
• If the patient had an intraoperative episode of AH, antihypertensives should be continued,
as appropriate
• If myocardial ischemia is suspected:
– Electrocardiogram
– Troponin levels
– Opioids, nitrates, oxygen, vasopressors, as needed
– Cardiology consultation
COMPLICATIONS
Profound sympathetic discharge can result in (2):
• Cardiac ischemia
• Cerebral edema
• Cerebral hemorrhage
• Renal failure
• Ophthalmic/retinal disease
• Pulmonary edema
REFERENCES
1. Khastgir J, Drake MJ, Abrams P. Recognition and effective management of autonomic
dysreflexia in spinal cord injuries. Expert Opin Pharmacother. 2007;8(7):945–956.
2. Kirshblum SC, Priebe MM, Ho CH, et al. Spinal cord injury medicine: Rehabilitation phase
after acute spinal cord injury. Arch Phys Med Rehabil. 2007;88(3 Suppl 1):S62–S70.
ADDITIONAL READING
• Mallory B.Autonomic dysfunction in spinal cord disease. In: Lin VW, Cardenas DD, Cutter
NC, et al., eds. Spinal cord medicine: Principles and practice, 1st ed. New York: Demos,
2003.
• Spinal shock
• Autonomic nervous system
CODES
ICD9
337.3 Autonomic dysreflexia
ICD10
G90.4 Autonomic dysreflexia
CLINICAL PEARLS
• Autonomic hyperreflexia (AH) is a syndrome characterized by profound and imbalanced
reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) at or above
the T6 level.
• An AH episode is characterized by any of the following: Headache, blurred vision, nasal
congestion, chest pain, anxiety, elevated blood pressure, bradycardia, flushing and sweating
above level of SCI, piloerection, or cardiac arrhythmias.
• Treatment of an AH episode involves the administration of antihypertensives, removal of the
inciting stimulus (bladder catheterization, fecal disimpaction, etc.), sitting the patient up
from the supine position, placing the legs down, and loosening of any tight clothing.
• For all lower body surgeries, even in the absence of sensation, the provision of an anesthetic
should be considered.
AUTONOMIC NERVOUS SYSTEM
Anthony H. Guarino, MD
BASICS
DESCRIPTION
• The autonomic nervous system (ANS) regulates individual organ function and homeostasis
and, unlike the somatic nervous system, is not under voluntary control. It comprises the:
– Sympathetic system
– Parasympathetic system
– Enteric nervous system: Not frequently discussed; a meshwork of nerve fibers that
innervate the GI tract, pancreas, and gallbladder.
• The sympathetic nervous system can be therapeutically blocked via neuraxial techniques
(spinal and epidural), localized paravertebral ganglia blocks, and regional IV sympatholytic
injections.
• Sympathetic nervous system (SNS): The SNS is continuously maintaining homeostasis in the
body. When stress is encountered there is increased activity resulting in the increased
release of catecholamines (“fight or flight”).
– Preganglionic neurons originate in the thoracic and lumbar spinal cord. Their axons
project to a paravertebral sympathetic trunk (or chain) that extends from C2 to the
coccyx. Most preganglionic neurons synapse with postganglionic neurons within the
trunk. Some preganglionic neurons travel to other ganglia outside of the sympathetic
chain and synapse there.
– Postganglionic neurons from the sympathetic trunk (as well as outside ganglia) travel to
the target organ.
– Neurotransmitters:
Preganglion and postganglion synapses: Acetylcholine
Postganglion and target organ: Norepinephrine. An exception is sweat glands that utilize
acetylcholine.
– Effects on organs:
Eyes: Dilates pupils
Heart: Tachycardia and increased force of contractions (increases systolic blood pressure)
Vasculature: Increases the tone (vasoconstriction) and hence diastolic blood pressure
Pulmonary: Dilates bronchioles
Gastrointestinal: Inhibits peristalsis
Renal: Increases renin secretion which retains sodium and water
Penis: Promotes ejaculation
• Parasympathetic nervous system (PNS): The PNS works complementary to the ANS in
maintaining homeostasis in the body. It is generally thought to guide vegetative functions
(“rest and digest”).
– Preganglion neurons originate in the medulla (cranial nerves III, VII, IX, and X) as well as
the cervical and sacral spinal cord. Their axons project to ganglia close to the target organ
where they synapse with postganglionic neurons; they have a longer course compared to
preganglionic sympathetic neurons. Of note, ∼75% of the parasympathetics travel with
the vagus nerve.
– Postganglionic neurons have a short distance that they travel to the target organ.
– Neurotransmitters:
Preganglion to postganglion synapses: Acetylcholine
Postganglion to target organ synapses: Acetylcholine
– Effects on organs:
Eyes: Constricts pupils
Heart: Decreases the heart rate
Vasculature: Decreases tone (vasodilation)
Pulmonary: Constricts bronchioles
Gastrointestinal: Promotes peristalsis
Penis: Promotes erections
• Adrenal medulla: Develops tandemly in utero with the SNS and acts as a modified
sympathetic ganglion. Synapses occur between preganglionic and postganglionic neurons
within it, but the postganglionic neurons do not leave the medulla; instead they directly
release norepinephrine and epinephrine into the blood.
• Complex regional pain syndrome I and II is a chronic neuropathic pain disorder. Although
the exact pathophysiology remains unknown, manifestations are secondary to ANS
dysfunction. CRPS I and II are characterized by pain in a nondermatomal pattern. Signs and
symptoms of neuropathic pain include intense burning pain, hyperalgesia, allodynia, local
edema, sweating, skin color changes, and temperature disturbances in the affected
extremity.
• Peripheral vascular disease refers to arterial obstruction outside the heart. It can cause
ischemia and is believed to be associated with dysfunction of the ANS.
• Raynaud’s disease is an exaggerated and reversible vasospasm of digital arteries in response
to cold or stress. The etiology is believed to be secondary to ANS dysfunction.
• Propofol, at clinically relevant concentrations for sedation, does not alter central
sympathetic outflow at the spinal cord level. However, at deeper levels of sedation and
induction doses, it can depress central sympathetic activity and is likely to lead to
hypotension (decreases preload, afterload, and contractility).
• Ketamine causes direct, dose-dependent stimulation of the CNS that leads to increased SNS
outflow. Consequently, cardiovascular effects resemble SNS stimulation: Increases in
systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and
myocardial oxygen requirements. Systemic vascular resistance and LV end diastolic pressure
are normally unchanged. In the critically ill, it has a negative inotropic effect.
• Etomidate maintains hemodynamic stability through preservation of both sympathetic
outflow and autonomic reflexes.
• Opioids generally have a dose-dependent sympatholytic effect.
• Benzodiazepines can influence autonomic neurocardiac regulation, probably through their
interaction with the gamma-aminobutyric acid A-receptor (GABAA) chloride ion channel
complex. They act in a biphasic manner: Initially causing a reduction in central vagal tone
followed by decreasing the cardiac pacemaker directly. Induction doses can reduce blood
pressure but not to the same degree as propofol.
• Anticholinesterases enhance PNS activity and will cause bradycardia, hypotension,
hypersecretion, bronchoconstriction, GI tract hypermotility, and decrease intraocular
pressure.
• Anticholinergics inhibit parasympathetic nerve impulses by selectively blocking
acetylcholine receptor binding at nerve junctions.
• Inhaled volatile anesthetics generally suppress the ANS components in a dose-dependent
manner.
• Neuraxial blocks: Local anesthetics injected into the epidural or intrathecal space produce a
differential blockade. Nerve fibers have different sensitivities due to their location in the
spinal cord, diameter, and the presence or absence of myelin. Sympathetic nerve fibers are
blocked first, and are usually followed by pain, sensory, and motor nerves.
• Sympathetic blocks: Performed to interrupt nociceptive pathways as well as vasomotor,
sudomotor, and visceromotor nerves. Low concentrations of local anesthetics block small
myelinated A-delta and unmyelinated C fibers with a minimal effect on other parts of the
peripheral nerves. They may be performed as a diagnostic tool to determine if sympathetic
input is a contributor to the pain state. Thus, they help guide decisions on whether a more
permanent intervention would be helpful (e.g., neurolysis or surgery).
• Horner syndrome is seen with interscalene brachial plexus blocks, due to the nerve’s
proximity. Manifests as ptosis, miosis, enophthalmos, conjunctival injection, nasal
congestion, and facial anhidrosis.
GRAPHS/FIGURES
FIGURE 1. Sympathetic nervous system. Preganglionic neurons originate in the thoracic and lumbar spinal cord and
synpase with postganglionic neurons in the paravertebral sympathetic trunk.
FIGURE 2. Parasympathetic nervous system. Preganglionic neurons originate in the medulla and cervical and sacral spinal
cord and then synapse with postganglionic neurons near the target organ.
REFERENCES
1. Marx JL. New information about the development of the autonomic system. Science.
1979;206(4417):434–437.
2. Burnstock G. Autonomic innervation and transmission. Br Med Bull. 1979;35(3):255–262.
3. Burnstock G. Review lecture: Neurotransmitters and trophic factors in the autonomic
nervous system. J Physiol. 1981;313:1–35.
4. Burnstock G. The changing face of autonomic neurotransmission. Acta Physiol Scand.
1986;126(1):67–91.
5. Hirst GD, Choate JK, Cousins HM, et al. Transmission by post-ganglionic axons of the
autonomic nervous system: The importance of the specialized neuroeffector junction.
Neuroscience. 1996;73(1):7–23.
ADDITIONAL READING
• http://www.sciencedaily.com/articles/s/sympathetic_nervous_system.htm
• http://www.ehs.net/2231/pdf/autonomic.pdf
• Complex regional pain syndrome I
• Complex regional pain syndrome II
• Epidural
• Raynaud phenomenon
CLINICAL PEARLS
• Sympathetic blocks can aid an anesthetic as well as reduce pain during postoperative care.
• Autonomics affect every organ system in some manner or form.
AWAKE CRANIOTOMY
BASICS
DESCRIPTION
General
• Evidence of trephinated skulls dates back to prehistoric times. The modern era of awake
craniotomies began with cocaine local anesthesia in 1886; sedation was added in the 1930s.
• Today, awake craniotomies are performed when patients have tumors or epileptic foci near
eloquent areas of the brain (Broca, Wernicke).
• Variations in anesthetic technique depend upon the patient as well as the surgeon’s
preference. During cognitive testing and tumor resection, the patient must be awake.
However, line and block placement, craniotomy, bone flap removal, as well as dural closure
can be performed with an adequate level of sedation versus general anesthesia (“asleep-
awake-asleep” technique).
Position
• In “asleep-awake-asleep” techniques, the patient is positioned after induction, whereas with
sedation the patient’s comfort is assessed before deeper levels are administered.
• Supine, with a bump under the left side so that the patient is facing the anesthesiologist.
• The patient’s left arm is folded over the patient and the right arm is abducted out. Pressure
points are padded.
• The patient is placed in a Mayfield frame. In sedated patients, the scalp block is first tested
and additional local anesthetic is added at pin sites.
• The patient is draped such that there is a window for the patient to communicate with the
anesthesiologist. This also allows emergent access to the airway.
• For the rare right-sided awake craniotomy, the above positioning is reversed.
Incision
Temporal incision: Temporalis flap, Burr hole, bone flap and then excision of the dura
Approximate Time
3–5 hours. The anesthesia and surgical preparatory time is longer than it is for a standard
craniotomy.
EBL Expected
300–500 mL. More bleeding can occur, so adequate venous access and blood products should
be available.
Hospital Stay
3–5 days for uncomplicated surgeries
• Mayfield frame
• Stealth/MRI
• Surgical microscope
• Special surgical drape for access to the patient
• Speech mapping electrodes and neuromonitoring personnel
• Ice cold saline in case of seizure
EPIDEMIOLOGY
Incidence
• The incidence of these lesions being removed under awake craniotomy is neurosurgeon- and
institution-driven, and therefore varies from center to center.
• Improvements in anesthetic techniques have resulted in an increased incidence of awake
craniotomies being performed.
Prevalence
• Dependent on type of lesion and location
• Most epileptic syndromes are treated medically. The prevalence of operable epilepsy is
institutionally dependent.
Morbidity
Low. Patient selection for awake craniotomies provides a healthier cohort. Tumors are also
usually smaller but in strategic brain tissue.
Mortality
Low
• The choice of sedation and analgesic drugs may vary by institution; the ideal drug for the
procedure should be quick in onset, short in duration, and easy to titrate.
• The choice between deep sedation versus “asleep-awake-asleep” technique depends upon the
patient’s, as well as the surgeon’s preference. Sedation is possible because a scalp block is
capable of providing adequate anesthesia for scalp incision/craniotomy and the brain has no
intrinsic nociception. Oversedation can lead to obstruction, apnea, loss of airway, or
hypoventilation with resultant increases in CBF and/or ICP.
• Personal reassurance and communication are powerful tools in keeping patients calm.
Consider meeting the patient in a preoperative visit, the night before, or having a phone
discussion prior to the day of surgery.
• Seizure, stroke, and oversedation can occur quickly. Emergency airway drugs and
equipment must be readily available.
SYMPTOMS
Cognitive speech dysfunction, either expressive (Broca) or receptive (Wernicke)
History
• History of cognitive speech dysfunction, seizures.
• The tumor may be an incidental finding on brain imaging for an unrelated complaint.
• Mental capacity, claustrophobia, anxiety, drug and alcohol abuse, sleep apnea, acid reflux,
and BMI need to be assessed.
Signs/Physical Exam
• Full neurologic exam including speech
• Auscultation of heart and lungs
• Airway exam
MEDICATIONS
• Dexamethasone decreases vasogenic tumor edema.
• Anticonvulsants (phenytoin, levetiracetam)
Labs/Studies
• CBC, Type and Screen
• Chemistry panel, coagulation panel
• Head CT, MRI, functional MRI (fMRI)
Most patients are relatively healthy from a cardiovascular profile. Most complain of
headaches, seizures, or cognitive speech dysfunction.
TREATMENT
Premedications
• A dexmedetomidine bolus should be followed by an infusion.
• When sedation is utilized, a small dose of midazolam may be considered prior to line and
Foley catheter placement. Low-dose remifentanil infusion may be started prior to the scalp
block.
• Antiemetic prophylaxis should be administered with non-sedating drugs such as 5-HT3A and
dexamethasone (also given to treat cerebral edema). Dexamethasone should be slowly
infused in awake patients as it can cause severe rectal itching and burning.
• Antiepileptic loading
• Anticholinergics should be avoided unless necessary. Patients may complain of dry mouth
during cognitive testing if used.
• The patient must be counseled that they will be awake during significant parts of the
surgery. Emphasize that open communication with the anesthesiologist is always possible.
• Risk of seizure and intubation is possible.
• Blood consents for possible transfusion are needed.
Gram-positive coverage for skin flora (cephalosporin, vancomycin for allergies)
INTRAOPERATIVE CARE
• Sedation involves the administration of IV sedative and analgesic medications (most
commonly dexmedetomidine, remifentanil, and propofol). Propofol and remifentanil alone
can be used, but are associated with deeper sedation, hypercarbia, and airway problems.
Neuroleptic analgesia with droperidol and an opioid has been associated with dysphoria,
oversedation, and hypotension.
• “Asleep-awake-asleep" is often performed with a combination of dexmedetomidine,
remifentanil, and propofol at higher doses than sedation and then resumed after tumor
excision.
Monitors
• Arterial line for beat-to-beat monitoring, labs
• 2 large-bore IVs (14–18) for rapid resuscitation and blood transfusion
• Central venous access is only necessary in patients with poor venous access. Awake
placement can be stressful for the patient.
• Foley catheter with urometer. In awake patients, especially in males, urethral lidocaine can
ease discomfort of placement and maintenance.
• Bispectral analysis can help guide the depth of anesthesia during GA or deep sedation.
• Neuromonitoring with speech mapping electrodes and appropriate personnel
• Scalp block: Usually done while the patient is lightly sedated (and before the patient is
induced for the “asleep-awake-asleep”) to monitor for local anesthetic toxicity. Often
performed with 0.5% bupivacaine or ropivacaine. The surgeon can infiltrate pin sites,
incision sites, and dura with 1% lidocaine.
• Sedation: Oxygen delivery via nasal cannula, facemask, or non-rebreather facemask
• “Asleep-awake-asleep": An LMA is often placed with either spontaneous ventilation or
controlled ventilation. Controlled ventilation is associated with lower CO2 levels.
Alternatively, a sphenopalatine block with bilateral placement of nasal trumpets can allow
spontaneous ventilation and a lighter depth of anesthesia than an LMA. The nasal trumpets
can be left in place, allowing the patient to phonate during testing. Obstruction is still
possible.
Maintenance
• Sedation: Dexmedetomidine 1 mcg/kg over 10 minutes followed by an infusion of 0.2–0.5
mcg/kg/hr. Remifentanil 0.01–0.05 mcg/kg/min. For sedation only, propofol should be
used sparingly if at all. Patients may find manipulation of the dura, in particular traction,
painful.
• “Asleep-awake-asleep": Dexmedetomidine 1 mcg/kg over 10 minutes followed by an
infusion of 0.2–0.5 mcg/kg/hr. Remifentanil 0.01–0.05 mcg/kg/min and propofol at 40–80
mcg/kg/min. Titrate to respiratory rate, and ETCO2. If using an LMA, control CO2 with
pressure support ventilation. Turn propofol off for emergence to “awake” portion.
• Brain relaxation: Mannitol and/or loop diuretic for diuresis. Diuresis can offset reductions in
brain relaxation that can result form higher CO2 tensions.
• Cognitive testing: The patient is awake, responsive, and able to participate in testing. If the
patient is under general anesthesia with an LMA or ETT, a smooth emergence should be the
goal to avoid coughing, laryngospasm, bucking, or delirium. Testing consists of a series of
neurologic tests: Counting, ABC’s, names, word association, pictures, and simple motor
commands. During these simple tests, the neurosurgeon electrically stimulates portions of
the brain to determine if it is safe to excise.
• Tumor excision: After testing, the patient remains conversant as the tumor is excised to
assure that eloquent tissue is not removed.
• Seizure precautions: Because the brain is being directly stimulated, the risk of seizure is
significant. Anticonvulsants should be loaded at the beginning of the case. Ice cold saline
should be available to the surgeon to flood the field. Emergency airway drugs and
equipment should be immediately available.
• After tumor removal, the patient can be placed under heavy sedation or GA until the end of
the procedure with appropriate airway protection in place.
• “Asleep-awake-asleep": Medications should be discontinued and the LMA removed when the
patient is breathing and following commands. Patients with nasal airways can have them
removed when they are awake.
• Neurologic exam should be performed to confirm that no changes in neurocognitive
function occurred during closure.
POSTOPERATIVE CARE
BED ACUITY
ICU: Quick discharge if the patient has no neurologic changes
ANALGESIA
• Pain is typically mild since the residual scalp block and dexmedetomidine can provide relief.
• Short-acting IV opioids and oral opioids
• Oral, rectal, and IV acetaminophen
COMPLICATIONS
• Cerebral edema can occur postoperatively. Any changes in neurologic exam need to be
examined and the patient should be sent to neuroimaging.
• Postoperative seizures (1–11% incidence) can be treated with appropriate anticonvulsants.
Continue the patient’s regular medication regimen.
• Postoperative nausea and vomiting should be treated with non-sedating antiemetics.
PROGNOSIS
Good: Residual seizure activity or regrowth of tumor may require additional surgery.
REFERENCES
1. Bonhomme V, Franssen C, Hans P, et al. Awake craniotomy. Eur J Anesthesiol.
2009;26(11):906–912.
2. Bulsara KR, Johnson J, Villavicencio AT, et al. Improvements in brain tumor surgery: The
modern history of awake craniotomies. Neurosurg Focus. 2005;18(4):e5.
3. Mack PF, Perrine K, Kobylarz E, et al. Dexmeditomidine and neurocognitive testing. J
Neurosurg Anesthesiol. 2004;16:20–25.
4. Sarang A, Dinsmore J. Anaesthesia for awake craniotomy—evolution of a technique that
facilitates awake neurological testing. BJA. 2003;90:161–165.
• Seizure disorder
CLINICAL PEARLS
• Patient refusal is a contraindication to an awake craniotomy. Patients with drug or alcohol
abuse, obesity, mental retardation, anxiety, claustrophobia, sleep apnea, and
gastroesophageal reflux should be scrutinized.
• Communication and reassurance are paramount in keeping the patient calm and
cooperative.
• Adequate scalp block and additional local anesthetic in the field can improve success.
• Alpha-2 agonists (dexmedetomidine) have been shown to improve sedation with less
respiratory depression.
• Seizure and loss of airway are a constant risk. Have airway drugs and equipment
immediately available.
AWARENESS UNDER ANESTHESIA
Dave Nisha Davendra, PharmD, DO
BASICS
DESCRIPTION
• The term “awareness” during anesthesia implies that during a period of intended general
anesthesia, the brain is aroused by stimuli that are stored in memory for future explicit
recall.
• The term “awake paralysis” is also included as an anesthesia awareness claim and refers to
errors in the administration of neuromuscular blocking agents, resulting in paralysis of the
unanesthetized patient.
• Despite the infrequent occurrence, awareness is of significant concern to patients and is
associated with significant adverse psychological sequelae.
– Closed Claims Data identified 2 main causes of awareness:
– Light anesthesia (“not enough")
– Anesthetic delivery problems
EPIDEMIOLOGY
Prevalence
• Awareness during anesthesia may affect as many as 60,000 adults each year in the US.
• Explicit recall is estimated to occur in 0.13% of patients (2).
• Awareness with surgical procedures:
– Trauma surgeries: 11–43%
– Cardiac surgeries: 1.5%
– Obstetric emergencies: 0.4%
• Children have an increased incidence of 0.6–2.7%.
• Awareness accounts for 2% of all claims in the Closed Claims database.
Prevalence
The majority of patients in the Closed Claims database are female, ASA class I–II, <60 years
of age, and had elective surgery.
Morbidity
• Postoperative sequelae that may persist for varying durations (33–69%):
– Sleep disturbances including nightmares
– Prone to daytime anxiety and panic attacks, and in the worst case, post-traumatic stress
disorder (PTSD). 10–25% of patients who experience PTSD will not recover and will
require treatment.
– Avoidance of future medical care including any future anesthetic exposure
• Patients, who experience the inability to move or feelings such as helplessness, have a
significant increase in the persistence of late psychological sequelae such as PTSD.
• Light anesthesia increases the risk for awareness. However, in certain patient populations,
the administration of even small doses of anesthetic agents can result in deleterious
hemodynamic consequences.
– Limited cardiac reserve: Cardiac tamponade, coronary artery disease
– Hypovolemia: Sepsis, trauma
– Cesarean sections: Attempts to reduce uterine relaxation, fetal hazard, and hypotension
can result in the administration of low concentrations of volatile anesthetics and the
avoidance of benzodiazepines.
– Cardiopulmonary bypass: Low concentrations of volatile agents and high-dose opioids are
often administered to preserve hemodynamics. Because hypothermia while on pump can
“provide MAC,” volatile anesthetics may be discontinued.
• Anesthetic delivery problems.
– Malfunctioning machines will disrupt the administration of anesthesia. Vaporizer and
circuit leaks prevent administration of full doses of anesthetic agents to the patient.
– Drug administration errors increase the risk of awareness. Accidental administration of
muscle relaxant to an awake/conscious patient will cause awareness.
• Reliance of nitrous, opioids, or muscle relaxants for anesthesia increases the risk of
awareness. Volatile anesthetics are markedly more effective in producing amnesia. Use of
neuromuscular blocking agents will mask physical signs of light anesthesia.
• Premature discontinuation of anesthetics in attempts to awaken the patient more quickly
increases the risk of awareness at the end of the surgical case.
• Difficult intubations may entail repeated attempts to secure the airway, and supplemental
agents may not have been administered.
• Populations with increased anesthetic requirements may be underdosed when normal
concentrations of anesthetic agents are administered. They include:
– Pediatric patients
– Chronic alcohol abusers
– Opioid and cocaine abusers
– Polypharmacy: Cytochrome P450 induction will enhance drug metabolism.
• Patients on beta-blockers and calcium channel blockers can have their physiologic response
to inadequate anesthesia masked.
• Previous history of awareness under anesthesia can be an indication of increased risk for
future awareness.
• Interactions between analgesics and hypnotics are fundamental in the depth of anesthesia
and physiology of awareness.
– Hypnotic drugs are capable of producing CNS depression.
– The net effect of analgesics and hypnotics is to increase the depth of anesthesia and
decrease the probability of responsiveness.
– The use of systemic analgesics and local anesthetics attenuates surgical stimulation before
reaching the cortical level and causing awareness.
• Awareness is the postoperative recall of events occurring during general anesthesia. A
spectrum of cognitive activity, including awareness with, or without, explicit memory, and
unconscious awareness with implicit memory have been reported during the administration
of drugs that are intended to induce and maintain general anesthesia.
– Explicit memory is the conscious recollection of previous experiences.
– Implicit memory is changes in performance or behavior that are produced by previous
experiences but without any conscious recollection of those experiences.
• Perceptions of awareness are variable:
– Most common: Sounds, conversations, sensation of paralysis, anxiety, helplessness, pain,
and panic
– Least common: Visual perception, intubation, and feeling the operation without pain
• Physical and physiologic responses have been reported that may indicate perception of
painful stimulation whether conscious or unconscious.
– Purposeful movement indicates motor response to awareness and surgical stimuli.
– Rate and volume of ventilation in spontaneously breathing subjects, as well as heart rate
and blood pressure, will increase indicating a physiologic response to awareness.
• The incidence of awareness has decreased substantially over recent decades with improved
appreciation of the complications and its morbidity as well as understanding of risk factors
and causes.
• Preoperative measures include patient and equipment assessment:
– Review patient medical records for previous occurrences of awareness or potential risk
factors.
– Interview the patient to assess the level of anxiety and previous experience with
anesthesia.
– Inform high-risk patient of the possibility of intraoperative awareness, consent, and
reassure the patient, as appropriate.
– Conduct a preoperative checklist-based anesthesia machine and equipment check to
ensure that the desired anesthetic drugs and dosages will be delivered. These procedures
should be extended to include proper functioning of intravenous access, infusion pumps,
and their connections.
• Intraoperative measures include the adequate use of medications and monitors.
– Amnestic agents should be strongly considered in anticipation or the possibility of a
patient in whom light anesthesia is required (benzodiazepines, scopolamine).
– Adequate doses of induction agents should be administered (also allow an adequate
amount of time for onset). In rapid-sequence intubations, consider more than just a “sleep
dose” of intravenous induction agents.
– Difficult intubation (anticipated or unexpected) can require supplemental doses of an
induction agent.
– Volatile agents should be maintained at least at 0.8–1.0 MAC; monitor the end-tidal
concentrations.
– Muscle relaxant use should be minimized if not necessary for the surgical procedure since
movement is the best indicator of light anesthesia.
– Nitrous oxide and opioid anesthesia should be supplemented with a potent volatile agent
to decrease the high incidence of awareness.
– Suspected inadequate anesthesia should be immediately addressed with deepening of the
anesthetic and a benzodiazepine.
– A bispectral index (BIS) is a processed electroencephalogram that provides a single
dimensionless number, which ranges from 0 (equivalent to EEG silence) to 100
(equivalent to fully awake and alert). Values of 65–85 have been advocated as a measure
of sedation, whereas values of 40–65 have been recommended for general anesthesia. The
FDA states that the use of BIS monitoring to guide anesthetic administration may be
associated with a reduction in the incidence of awareness with recall in adults during
general anesthesia and sedation. However, studies have shown that awareness can occur
at a BIS value <65, so the standard of care of this monitoring technique is equivocal.
– Modulate operating room behavior. Patients tend to remember auditory perceptions.
Conduct a postoperative interview with the modified Brice Questionnaire.
• What was the last thing you remembered before going to sleep?
• What was the last thing you remembered on waking?
• Do you remember anything between going to sleep and waking?
• While you were sleeping during the operation, did you dream?
TREATMENT
• A discussion with the patient should take place to obtain a detailed account of the patient’s
experience.
• An occurrence report regarding the event should be completed for the purpose of quality
management.
• Apologize to the patient, and offer counseling or psychological support to the patient.
• Notify the patient’s surgeon, nurse, and other key personnel about the incident and
interview.
• Patient should be informed of the Anesthesia Awareness Registry and encouraged to join the
registry by calling (206) 616-2669 and request a paper enrollment packet. Eligibility
includes the following:
– Surgery must be under general anesthesia.
– Patient must be 13 years or older.
– Patient must have the ability to read and understand English.
– Awareness of recall of events or sensations during surgery when you should have been
asleep and unaware.
FOLLOW-UP
CLOSED CLAIMS DATA

• Awareness claims accounted for 79 (1.9%) of 4,183 claims in the database.
• There were 18 claims for awake paralysis, most of which represented substandard care
involving errors in labeling and administration.
• There were 61 claims for recall during general anesthesia, most of which were likely in
women with nitrous–narcotic–relaxant techniques.
REFERENCES
1. merican Society of Anesthesiologists Task Force on Intraoperative Awareness. Practice
advisory for intraoperative awareness and brain function monitoring. Anesthesiology.
2006;104:847–864.
2. Sebel PS, Bowdle TA, Ghoneim MM, et al. The incidence of awareness during anesthesia: A
multicenter United States study. Anesth Analg. 2004;99(3):833–839.
3. Sandin RH, Enlund G, Samuelsson P, et al. Awareness during anesthesia: A prospective case
study. Lancet. 2000;355:707–711.
4. Domino KB, Posner KL, Caplan RA, et al. Awareness during anesthesia: A closed claims
analysis. Anesthesiology. 1999;90:1053–1061.
5. Spitellie PH, Holmes MA, Domino KB. Awareness during anesthesia. Anesthesiology Clin N
Am. 2002;20:555–570.
6. Mashour GA, Wang LY, Turner CR, et al. A retrospective study of intraoperative awareness
with methodological implications. Anesth Analg. 2009;108:521–526.
ADDITIONAL READING
• Myles P, Leslie K, McNeil J, et al. A randomised controlled trial of BIS monitoring to prevent
awareness during anaesthesia: The B-Aware Trial. Lancet. 2004;363:1757–1763.
• Webb RK, Currie M, Morgan CA, et al. The Australian Incident Monitoring Study: An
analysis of 2000 incident forms. Anaesth Intens Care. 1993;21:520–528.
CLINICAL PEARLS
• Awareness during general anesthesia is unintentional consciousness or awareness of events
happening during an operation either with or without pain sensations. It is a frightening
experience that can lead to debilitating emotional injury and even post-traumatic stress
disorder.
• ASA guidelines suggest considering premedication with amnestics, particularly when light
anesthesia is anticipated, administering more than a “sleep dose” of induction agent, and
avoiding muscle paralysis unless necessary.
• Light anesthesia is the most common cause of awareness.
BARIATRIC SURGERY
John D. Kot, MD
BASICS
DESCRIPTION
General
• Bariatric surgery includes a variety of surgical weight loss procedures indicated in the
treatment of morbid obesity (defined as an absolute BMI ≥40 kg/m2 or BMI ≥35 kg/m2
combined with obesity-related comorbidities). Surgical intervention for less obese
individuals who do not meet these criteria is controversial.
• Bariatric surgery may be classified as malabsorptive, restrictive, or mixed.
– Malabsorptive procedures, such as biliopancreatic bypass, are rare due to problems
associated with severe malabsorption.
– Restrictive procedures diminish gastric volume and include gastric banding and sleeve
gastrectomy.
– Roux-en-Y gastric bypass (RYGB) has become the “gold standard,” and combine gastric
restriction with minimal malabsorption.
• Laparoscopy is the preferred and more common approach due to a significant reduction in
postoperative complications and length of hospital stay as compared to an open procedure.
• Medical problems associated with obesity may include hypertension, heart disease, stroke,
type 2 diabetes, metabolic syndrome, obstructive sleep apnea (OSA), respiratory
insufficiency, pulmonary hypertension, thromboembolism, hepatic steatosis, certain cancers,
osteoarthritis, and depression.
• Eligible patients usually have failed supervised medical treatment, have undergone
psychological screening, and have demonstrated lifestyle changes for a specified length of
time in order to optimize surgical benefit.
Position
• Reverse Trendelenburg position (RTP) with back extension for laparoscopic surgery
• Supine for open procedures
• Adequate patient straps and padding of pressure points due to increased risk of slipping and
neuropathy
Incision
• 4–6 port sites for laparoscopy
• Midline for open
Approximate Time
2–4 hours
EBL Expected
25–100 mL
Hospital Stay
2–3 days
• Large OR table with an optional inflatable mat in place to facilitate patient movement after
surgery
• Laparoscopic equipment (including adequately long instruments) or large retractors
• Orogastric (OG) tube with inflatable gastric balloon
EPIDEMIOLOGY
Prevalence
Laparoscopic RYGB is currently the most common bariatric procedure.
Prevalence
In the US in 2008, it is estimated that >200,000 total bariatric procedures were performed
(and has been increasing yearly).
Morbidity
• Wound infection: 10% with open versus 1% with laparoscopic
• Hernia: 8% with open versus <1% with laparoscopic
Mortality
• Overall risk is <1%.
• Mortality risk factors include age >45 years, hypertension, male sex, risk factors for PE, and
BMI >50 kg/m2.
– 4 or more risk factors increase mortality risk to 2.4%.
• Patient population with significant comorbidities
• Preoperative airway examination is critical, and additional airway equipment should be
readily available.
• High risk for DVT/PE, thus preoperative heparin SC and/or an IVC filter are essential. IVC
filters are typically reserved for patients with a history of DVT, PE, or BMI near 60 kg/m2.
• Except for succinylcholine, drug dosing should be based upon lean body mass (LBM).
• Special attention should be made to patient positioning and padding of pressure points to
mitigate nerve injury.
• Avoid endogastric tubes, other than the intragastric balloon tube that may be placed at the
surgeon’s request; this includes esophageal temperature probes.
• Judicious use of sedatives and analgesics to minimize respiratory impairment
SYMPTOMS
As related to comorbidities: Chest pain, dyspnea, somnolence, GERD
History
• Careful assessment of comorbidities especially cardiopulmonary
• Known difficult airway
• Previous bariatric surgery
• History of DVT or PE
Signs/Physical Exam
• Thorough airway examination
• Any evidence of cardiac failure: Pulmonary rales, additional heart sounds, increased JVD
MEDICATIONS
• Weight loss medications: Sibutramine may worsen hypertension, and orlistat may lead to
deficiencies in fat-soluble vitamins (A, D, E, K).
• Consider holding diuretics and ACE inhibitors given bowel prep and the potential for
hypotension especially if the procedure is in the reverse Trendelenburg position.
• Hold oral diabetic medications on the morning of surgery.
Labs/Studies
• Check blood glucose
• Electrolytes if renal insufficiency
• PT/PTT, INR if taking orlistat or previous bariatric surgery given potential for chronic
vitamin K deficiency
• Consider liver function tests
• Consider baseline ABG if respiratory impairment is significant
• EKG, further cardiac testing (Echo, Stress) as indicated
• Consider CXR as indicated
• Neurologic: Cerebrovascular disease
• Cardiac disease: Hypertension, coronary artery disease
• Respiratory impairment: Restrictive disease, OSA with possible pulmonary hypertension
(chronic hypoxia)
• Hepatic steatosis
• Metabolic: Diabetes, hypercholesterolemia
TREATMENT
Premedications
• Heparin SC to decrease risk of DVT
• Antacid as indicated
• Judicious use of anxiolytics
• Potential to convert to open
• Potential for postoperative intubation
Cefoxitin unless precluded by drug allergies
INTRAOPERATIVE CARE
• Epidural for postoperative analgesia if an open procedure is planned
Monitors
• May need to place a NIBP cuff on the wrist or ankle given body habitus
• Avoid esophageal temperature monitoring since the probe may become inadvertently
entrapped
• Invasive monitors only as indicated and central venous catheter if peripheral access proves
difficult
• Foley catheter to monitor urine output for adequate volume resuscitation
• Pre-oxygenation in RTP to maximize FRC. Some anaesthetists administer CPAP for several
minutes prior to induction, as this may decrease atelectasis after the induction of anesthesia.
• Awake fiberoptic intubation if warranted
• Rapid-sequence intubation if indicated
• Proper patient positioning is crucial to facilitate direct laryngoscopy. The upper thorax is
“ramped” with either blankets or by elevating the back of the table 30–40° and extending
the head until the external auditory meatus is level with the sternal notch.
• Additional difficult airway equipment should be readily accessible.
• Drug dosing should be based on LBM, rather than ideal or total body weight (IBW, TBW);
LBM is calculated by adding approximately 20–50% of the difference between TBW and
IBW to IBW.
• Only succinylcholine is dosed based on TBW as pseudocholinesterase levels increase
proportionate to body weight.
Maintenance
• Any anesthetic technique is acceptable although desflurane may improve recovery time.
• Ventilation.
– An FiO2 of 0.5 may decrease atelectasis (the nitrogen in air prevents absorption
atelectasis; it is poorly soluble in blood and thus serves as a “filler" within alveoli, hence
keeping them open).
– PEEP is often administered to decrease atelectasis; increased values may be needed but
must be balanced with decreasing venous return to the heart.
– Recruitment maneuvers may be necessary to address atelectasis.
– Adjust ventilation accordingly to maintain normocapnia during laparoscopic CO2
insufflation.
• Avoid N2O due to the possibility of bowel distention, high oxygen demands of the obese,
and worsening of any underlying pulmonary hypertension.
• Muscle relaxation is required to facilitate surgery and ventilation.
• The surgical team will request the placement of oral intragastric tubes to help size the
gastric pouch, as well as perform leak tests with methylene blue. Lubrication, neck flexion,
and the use of a laryngoscope may be appropriate. No other tubes should be in the
esophagus/stomach.
• Narcotics should be judiciously administered to avoid postoperative respiratory
complications; remifentanil may be preferable intraoperatively.
• Fluids. Address NPO and bowel prep, as well as increased maintenance fluid requirements to
prevent postoperative ATN.
• Full reversal of neuromuscular blockade is essential.
• Place the patient in RTP to maximize FRC and minimize work of breathing.
• Antiemetics to mitigate PONV risk
• Consider the placement of an airway exchange catheter if airway management was difficult.
FOLLOW-UP
BED ACUITY
• Need for mechanical ventilation and/or ICU care is rare but more common after an open
procedure.
• Patients with known or suspected OSA will require a monitored bed. CPAP and BiPAP have
been shown to be safe although there is theoretical concern of anastomotic injury due to the
pressurized air.
ANALGESIA
• Pain is typically mild with laparoscopic procedures.
• Local anesthetic infiltration at incision sites may be helpful initially.
• If the procedure was open, an epidural catheter or dexmedetomidine may be preferable to
limit respiratory depression.
• Avoid NSAIDs given the risk for gastric ulceration.
COMPLICATIONS
• Anastomotic leak (2%) and stricture (10%)
• Respiratory complications (most common)
• Venous thromboembolism
• Laparoscopy related: Gas embolism, pneumothorax, pneumomediastinum
• Stricture or obstruction
• Wound infection (increased with open)
• Incisional hernia (increased with open)
• Dumping syndrome and malnutrition with bypass procedures
PROGNOSIS
• RYGB yields an average loss of 50–60% excess body weight and BMI decrease of 10 kg/m2
within the first 12–24 months.
• Majority experience resolution of other comorbidities: Diabetes (90%), hypertension and
hyperlipidemia (70%), and OSA.
• Overall, significantly reduced long-term mortality
REFERENCES
1. Bguyen NT, Goldman C, Rosenquist CJ, et al. Laparoscopic versus open bypass: A
randomized study of outcomes, quality of life, and costs. Ann Surg. 2001;234:279–291.
2. Demaria EJ, Murr M, Byrne TK, et al. Validation of the obesity surgery mortality risk score
in a multicenter study proves it stratifies mortality risk in patients undergoing gastric
bypass for morbid obesity. Ann Surg. 2007;246(4):578–582.
3. Huerta S, DeShields S, Shipner R, et al. Safety and efficacy of postoperative continuous
positive airway pressure to prevent pulmonary complications after Roux-en-Y gastric
bypass. J Gastrointest Surg. 2002;6:354–358.
4. Larson CP, Dutson E. The bariatric challenge. Curr Rev Clin Anesth. 2010;30:207–214.
5. NIH conference: Gastrointestinal surgery for severe obesity—Consensus Development
Conference Panel. Ann Intern Med. 1991;115:956–961.
6. Ogunnaike BO, Jones SB, Jones DB, et al. Anesthetic considerations for bariatric surgery.
Anesth Analg. 2002;95:1793–1805.
• Continuous positive airway pressure (CPAP)
• Laparoscopy
• Laryngoscopy positioning
CODES
ICD9
• 278.01 Morbid obesity
• V45.86 Bariatric surgery status
ICD10
• E66.01 Morbid (severe) obesity due to excess calories
• Z98.84 Bariatric surgery status
CLINICAL PEARLS
• Patient population with significant comorbidities, including cardiovascular disease
• Preoperative airway examination is critical; additional airway equipment should be readily
available.
• High risk for DVT/PE; preoperative heparin SC and/or IVC filter are essential.
• Judicious use of sedatives and analgesics to minimize respiratory impairment
• Laparoscopy is the preferred and more common approach due to a significant reduction in
postoperative complications and hospital stay as compared to an open procedure.
Laparoscopic RYGB is the “gold standard” bariatric procedure.
BIER BLOCK
Angela T. Hsu, MD
BASICS
DESCRIPTION
• Intravenous regional anesthesia (IVRA) involves the administration of local anesthetic distal
to a tourniquet. It is a simple, safe, and reliable technique to provide anesthesia for
extremity surgery.
• The technique is also known as a Bier block, named after the German surgeon August Bier,
who first described the technique in 1908.
• Benefits of this technique:
– Easy to perform; it requires only the ability to perform venipuncture.
– Low failure rate
– Fast and reliable onset within 5 minutes
– Provides muscle relaxation for a surgical procedure
– Rapid recovery
• Limitations of this technique:
– Anesthesia is limited to the area distal to the tourniquet.
– The maximum duration of anesthesia is usually limited to 1 hour, secondary to the onset
of tourniquet pain.
– There is a concern for systemic toxicity if inadequate tourniquet inflation, early deflation,
or inadvertent deflation occurs.
– Lack of postoperative pain relief
• The mechanism whereby IVRA provides anesthesia is controversial.
• Via studies using radioisotope-labeled local anesthetic, the following mechanism has been
proposed:
– Initially, the local anesthetic works on free nerve endings by binding to intracellular
sodium channels and inhibiting the initiation and propagation of nerve impulses.
– This is later followed by blockade of proximal nerve trunks, as the local anesthetic travels
from superficial veins to deep venules of nerve trunks. The theory of nerve trunk site of
action has been further supported because distal extremity anesthesia is achieved despite
application of an additional distal tourniquet that would inhibit medication distribution to
these tissues.
• Ischemia and compression of nerve trunks have been proposed as a late mechanism of
anesthesia and paralysis.
ANATOMY
• Bier block can be performed for upper extremity surgery below the elbow, or lower
extremity surgery below the knee.
– This technique is particularly suitable for surgery of distal extremities: hand, forearm,
foot, and ankle.
• Local anesthetic systemic toxicity can result from early tourniquet deflation, inadequate
inflation, or inadvertent premature deflation.
– After tourniquet release, patients may complain of dizziness, tinnitus, and perioral
numbness.
– Tourniquet malfunction may lead to the premature release of local anesthetic to the
systemic circulation, resulting in severe local anesthetic toxicity with seizures and
cardiovascular instability.
• IVRA is ideal for outpatient surgical procedures of the distal extremity. It provides a
bloodless surgical field and anesthesia that is reliable in onset and offset. In comparison to
general anesthesia, patients may be discharged earlier and have a decreased incidence of
postoperative nausea and vomiting.
• Patient selection:
– Patients with significant anxiety are unlikely to tolerate tourniquet-related pain.
Administering IV anxiolytic may help, but this may negate the benefits in discharge time
and cost.
– Procedure duration: Procedures longer than 60–90 minutes are not well tolerated
secondary to tourniquet pain.
– Avoid this technique in patients who cannot tolerate extremity ischemia from the
tourniquet.
Raynaud’s disease
Homozygous sickle cell disease (usually tolerated in heterozygous sickle cell disease)
Caution in crush injuries (viable tissues will be subjected to further ischemia)
• Medication selection:
– Prilocaine and lidocaine are commonly used due to their high therapeutic index.
– Prilocaine:
Usual adult dose is 40 mL of 0.5% prilocaine.
Recommended maximum dose is 6 mg/kg.
Because of concerns with methemoglobinemia, prilocaine is not as popular as lidocaine
in clinical practice. However, methemoglobinemia is usually not a concern until
prilocaine levels reach 10 mg/kg.
– Lidocaine:
Usual adult dose is also 40 mL of 0.5% lidocaine.
Recommended maximum dose is 5 mg/kg.
– Bupivacaine is not recommended secondary to its cardiotoxic potential, and reports of
several deaths.
– Ensure that the local anesthetic is preservative-free and does not contain epinephrine.
– Several adjuvants (e.g., clonidine, narcotics, neostigmine, muscle relaxants, ketorolac)
have been studied to improve block quality, tourniquet pain, or postoperative analgesia.
• Technique:
– Prepare equipment: Test the double-lumen tourniquet and ensure that resuscitative
equipment is nearby.
– In the extremity being operated on, place a 20–22 g IV in a vein distal to the surgical site.
– Place a 2nd IV in another limb for administration of fluids or other IV medications that
will be used during the procedure.
– Place a double-lumen tourniquet on the upper arm or thigh; do not inflate. Avoid
tourniquet placement on the forearm or lower leg since arterial compression is inadequate
at these locations.
– The extremity is then elevated and exsanguinated beginning distally via an Esmarch or
rubber bandage. Ensure that even the digits are exsanguinated.
– The proximal tourniquet is inflated to 100 mm Hg above pulse-occlusion pressure. The
pulse-occlusion pressure is best determined by loss of the pulse oximeter signal on the
finger or toe.
– Remove the Esmarch or rubber bandage. Confirm the absence of the radial or dorsalis
pedis pulse.
– Inject local anesthetic slowly (in the distal IV catheter of the operative extremity). Remove
the IV catheter and hold pressure at the IV site.
– The patient should be ready for surgical incision within a few minutes.
– When the patient complains of tourniquet pain, the distal cuff is inflated. The proximal
cuff is released after distal cuff inflation.
– After the surgery is completed, gradual release of the distal lumen is advised. The
minimum recommended time before the tourniquet can be deflated is 20 minutes to avoid
local anesthetic toxicity.
REFERENCES
1. Blackburn EW, Shafritz AB. Why do Bier blocks work for hand surgery… most of the time?
J Hand Surg Am. 2010;35(6):1022–1024.
2. Brown EM, McGriff JT, Malinowski RW. Intravenous regional anaesthesia (Bier block):
Review of 20 years’ experience. Can J Anaesth. 1989;36(3):307–310.
3. Rawal N. Intravenous regional anesthesia. Tech Reg Anesth Pain Manage. 2000;4(1):51–53.
• Local anesthetic systemic toxicity
• Methemoglobinemia
CLINICAL PEARLS
• Bandage wrapping during exsanguination can cause significant pain in a fractured
extremity. An alternative is to elevate the extremity for 30 seconds while applying firm
pressure to occlude the brachial or femoral artery. The tourniquet is then inflated after this
method of extremity exsanguination.
• Typically for upper extremity block, 40 mL of 0.5% lidocaine or prilocaine is used. For
larger or muscular patients, the dose can be increased to 50 mL. For small or frail patients,
the volume can be decreased to 30 mL.
• For the lower extremity, usually a larger volume is utilized to assure adequate distribution
of drug. One technique is 150 mL of 0.25% lidocaine.
• Make sure the local anesthetic contains no epinephrine. It is also recommended to have
preservative-free local anesthetic, although a review of 1,906 cases using local anesthetic
with preservative did not reveal ill-effects.
• Inform the patient that with this regional technique, the extremity may feel warm, numb, or
tingly. The skin will also appear mottled. This is normal.
• Maximum continuous tourniquet inflation time should be limited to 90 minutes secondary
to concern of extremity ischemia.
• Procedures longer than 90 minutes using Bier block as anesthesia are possible with a short
period of tourniquet release. In these cases, the IV cannula is kept in place during surgery.
After 1 hour, the tourniquet is deflated for 5 minutes. The surgeon elevates the arm and
applies a sterile Esmarch bandage, reinflates the tourniquet, and administers 50% of initial
local anesthetic dose. This may be repeated if necessary.
BLALOCK-TAUSSIG (BT) SHUNT
BASICS
DESCRIPTION
General
• Surgeon Alfred Blalock and cardiologist Helen Taussig developed the procedure after noting
that cyanotic children with a patent ductus arteriosus (PDA) did better than those without a
PDA. The first Blalock–Taussig (BT) shunt was performed in 1944 on a human with
Tetralogy of Fallot (TOF).
• The BT shunt is a palliative surgery for cyanotic heart defects with limited pulmonary blood
flow/ductal dependant lesions.
– Single ventricle physiology (most common indication)
– Tetralogy of Fallot
– Tricuspid atresia
– Ebstein anomaly
– Small pulmonary arteries
– Pulmonary stenosis
• The shunt connects the right subclavian artery to the right pulmonary artery (PA); the left
PA can be used as well. This increases the amount of deoxygenated blood directed to the
lungs.
– Classic BT shunt: The subclavian or carotid artery is anastomosed directly to the PA.
– Modified BT shunt uses artificial material (GORTEX) 4–5 mm in diameter to make the
aorticopulmonary connection.
Position
Supine, fully prepped from neck to groin for cardiopulmonary bypass (CPB) or extracorporeal
membrane oxygenation (ECMO) access if needed
Incision
• Historically, the procedure was performed via a lateral thoracotomy at the level of the 4th
intercostal space. However, this approach had limited access to small neonatal anatomy,
commits the surgeon to the side of entry, makes it difficult to ligate the PDA if done via a
right thoracotomy, and has a risk of flail scapula from an incision through the latissimus
dorsi muscle.
• Most institutions now use a median sternotomy; this approach allows for improved access,
easier conversion to CPB, augmentation for diminutive PAs, and less distortion of vascular
anatomy.
Approximate Time
Dependent on the surgeon’s experience; approximately 2–3 hours
EBL Expected
• Surgeon dependant
• Typically minimal (∼50 mL) when only a BT shunt is being performed
• May need to transfuse blood to maintain euvolemia
Hospital Stay
• Highly dependant on the underlying congenital heart disease that necessitated the shunt
• If the shunt remains patent and there are no complications, discharge to home is usually
between 8 and 15 days.
• Most surgeons require the patient to stay reasonably close to the hospital for the first few
weeks due to the risk of shunt occlusion.
• CPB machine should be in the room, prepped, and ready to use.
• ECMO back-up/capability
EPIDEMIOLOGY
Incidence
• Unknown number worldwide
• All congenital heart disease (CHD) = 8/1,000
• Cyanotic CHD is estimated at 25% of all CHD; corresponds to 2/1,000.
• Most registry data (Canada and Europe) quote an annual incidence of 1.5/1,000 live births.
Prevalence
Overall prevalence is increasing as therapies improve.
Morbidity
• Morbidity is largely related to the experience of both the surgeon and anesthesiologist as
well as the postoperative care (ICU).
• Risk of neurologic sequelae from surgery
Mortality
• Dependant on the complexity of the underlying heart defect/comorbidities
• Highest mortality of the 3 stages of the Fontan procedures
• Increased when performed in neonates compared to older children
• Patients have “duct-dependent” lesions; therefore, pulmonary blood flow can be tenuous.
Prevent any condition that would increase pulmonary vascular resistance (PVR), such as
hypothermia, acidosis, hypercapnia, or hypoxia.
• The maintenance of adequate pressures is necessary to prevent shunt occlusion. This is
accomplished via adequate blood volume as well as vasopressors if necessary.
SYMPTOMS
Because CHD presents in the neonatal period, feeding intolerance is a common symptom
reflecting decreased exercise tolerance.
History
• With improvements in fetal ultrasound technology, many lesions are now detected in utero.
• Those who are postnatally diagnosed are often cyanotic at birth, or when the PDA closes.
Signs/Physical Exam
• Murmur—with a diastolic component
• PaO2 <150 mm Hg on 100% FiO2
• Tachypnea, diaphoresis, central cyanosis
• Hepatomegaly
MEDICATIONS
Patients arrive on prostaglandins to maintain PDA patency. Most cyanotic heart disease is due
to inadequate blood flow to the lungs; If the ductus closes, pulmonary blood flow will be
inadequate and cardiopulmonary collapse will occur.
Labs/Studies
• Chest radiograph: Look for signs of heart failure and lung congestion/fluid accumulation
• Echocardiogram: To determine the exact cardiac anatomy and nature of the lesion causing
the cyanosis
• CBC, chemistry, coagulation panel
• Cardiac MRI now gaining popularity
• Heart failure
• Acidosis from malperfusion/hypoxemia
TREATMENT
Premedications
• Anxiolytics are not usually necessary due to the young age of the patient. If the patient is
older, midazolam or pentobarbital may be considered.
• Maintain the prostaglandin infusion
Parents should be made aware of the risk of complications/death.
• Important in the modified BT shunt due to placement of the indwelling gortex graft
• Skin flora
INTRAOPERATIVE CARE
General endotracheal anesthesia
Monitors
• Arterial line on the contralateral side of the shunt can be placed postinduction.
• 2 well-functioning IVs; if performed in the immediate postnatal period, an umbilical vein
line allows for the measurement of venous pressures.
• Surgeon may place right atrial lines prior to chest closure for right-sided pressures.
• Urine Foley catheter
• Bag mask ventilation and intubation should avoid hypercapnia, hypoxia, or coughing and
bucking as these derangement increase the pulmonary vascular resistance.
• Aggressive hydration is not usually needed as TOF repair is most commonly done as a
single-stage operation and does not undergo BT shunts anymore. In the TOF subset, there is
concern for RVOT obstruction in the face of inadequate intravascular volume. Adequate, but
not overaggressive, hydration is required to prevent this.
Maintenance
• Gas (isoflurane usually) with fentanyl or other short-acting opioids
• Standard paralysis doses of pancuronium or vecuronium as most of these patients are
extubated at the conclusion of surgery.
• Hypotension is often caused by surgical manipulation of great vessels.
• Neuromonitoring is not currently used, but is an evolving area of research.
• On clamping of the PA, some patients (in particular neonates) may develop profound
desaturation due to increases in dead space. This can also cause increases in the PaCO2,
causing the PVR to rise even further and reversing flow through the PDA (ceases pulmonary
blood flow). This will require going on CPB for the completion of surgery.
• Good surgical technique will minimize the effect of traction on the lung.
• In classical BT shunt, arterial flow to the ipsilateral arm is often compromised and can result
in ischemia. Modified BT shunt decreases this risk by maintaining flow to the arm.
• Ionotropes (such as epinephrine) are often utilized when weaning from CPB, until the blood
pressure is stabilized.
• Heparin is utilized to prevent clot formation during clamping of arteries; this can increase
the patient’s risk of bleeding.
• If the shunt is too large, overcirculation of the pulmonary vasculature can occur, resulting in
pulmonary edema and desaturation.
• Depending on the underlying heart defect, most can be extubated immediately after surgery.
• Patient must be strong, awake, and able to protect their airway in order to be extubated.
Hemodynamics should also be stable, with minimal ionotropic support. ABG results should
not reveal acidosis, which could reflect underperfusion of tissues.
FOLLOW-UP
BED ACUITY
Cardiac ICU
ANALGESIA
• IV opioids: morphine is often administered (easy to titrate); however other opioids are
acceptable and based upon practitioner and institution preferences. If the patient is older
(mental capacity >7 years of age), PCA may be considered.
• No current studies in the pediatric population for regional techniques
COMPLICATIONS
• Shunt occlusion—surgical emergency
• Pseudoaneurysm—can compress mediastinal structures
• Excessive pulmonary blood flow leading to pleural effusions
• Decreased diastolic pressures
• Distortion of vascular anatomy
• Pulmonary artery hypoplasia
• Phrenic/vagus/recurrent laryngeal nerve injury
• Arrhythmias
PROGNOSIS
• Dependant on the complexity of the underlying heart defect
• It is considered a palliative procedure, not curative; if done for single ventricle pathology,
this is the first of 3 steps to a Fontan completion.
REFERENCES
1. Kandakure PR, Dharmapuram AK, Ramadoss N, et al. Sternotomy approach for the
modified Blalock-Taussig Shunt: Is it a safe option? Asian Cardiovasc Thorac Ann.
2010;18(4):368–372.
2. Mavroudis C, Backer C. Pediatric cardiac surgery. Philadelphia: Mosby, 2003.Van Arsdell
GS, Maharaj GS, Tom J, et al. What is the optimal age for repair of tetralogy of Fallot?
Circulation. 2000;102(19 Suppl 3):III123–III129.Alkhulaifi AM, Lacour-Gayet F, Serraf A,
et al. Systemic pulmonary shunts in neonates: Early clinical outcome and choice of surgical
approach. Ann Thorac Surg. 2000;69(5):1499–1504.
3. Pearl JM, Nelson DP, Schwartz SM, et al. First-stage palliation for hypoplastic left heart
syndrome in the twenty-first century. Ann Thorac Surg. 2002;73(1):331–339; discussion
339–340.
• Fetal cardiovascular physiology
• Extracorporeal membrane oxygenator
CODES
ICD9
746.89 Other specified congenital anomalies of heart.
ICD10
Q24.8 Other specified congenital malformations of heart
CLINICAL PEARLS
• It is critical to maintain patency of the shunt in the postoperative period. Maintain adequate
blood pressure and volume. Shunt occlusion is a life-threatening surgical emergency.
• Patients may become severely hypoxic upon clamping of the PA. CPB must be on standby
and ready to cannulate.
• An A-line should be placed on the opposite side of the shunt. Otherwise when the artery is
clamped, the arterial line will be useless.
BLOOD COAGULATION PHYSIOLOGY IN PREGNANCY
Andrew Geller, MD
Mark Zakowski, MD
BASICS
DESCRIPTION
• Normal pregnancy becomes a hypercoagulable state at 6–8 weeks of gestation and returns to
the pre-pregnancy state in the 1st month after delivery (1).
• Hypercoagulability during pregnancy minimizes blood loss during delivery and in the
postpartum period (2).
• Hypercoagulability during pregnancy is achieved via several mechanisms:
– Increased levels of procoagulants: Factors V, VII, VIII, IX, X, and XII; vWF; fibrinogen;
prothrombin.
– Decreased levels of anticoagulants: Factors XI and XIII; protein S.
– Decreased fibrinolysis is caused by increased concentrations of plasminogen activator
inhibitors 1 and 2 (1,3).
• Thromboembolism: Deep venous thrombosis (DVT) and pulmonary embolism (PE) are the
greatest cause of morbidity and mortality in the parturient, occurring in 1 in 1,600
pregnancies.
– Contributing factors include: Hypercoagulable state, increased venous distention and
obstruction due to compression of the inferior vena cava by the gravid uterus.
– Thrombus primarily occurs in the venous system of the legs or, less commonly, in the
pelvic veins.
– Diagnostic tests include ultrasound imaging of the deep venous system of the lower
extremities and D-dimer levels. If PE is suspected, V/Q scan, MRI/MRA, or CT angiogram
is indicated.
– Prophylaxis is recommended for women at high risk for thromboembolism (e.g., bed rest,
postsurgical procedure, or pre-existing hypercoagulable disease state).
Thromboprophylaxis is accomplished with heparin SQ q12h (adjusted to the mid-range
of therapeutic PTT), dalteparin 200 U/kg SQ q24h, or enoxaparin 1 mg/kg q12h.
Thromboprophylaxis is discontinued at the time of delivery.
• Gestational thrombocytopenia: Platelet counts 70,000–150,000/μL.
– Occurs in ∼10% of pregnancies, usually in the third trimester.
– Proposed etiology includes increased plasma volume (dilutional) and increased platelet
clearance.
– Condition usually does not require treatment.
• Idiopathic thrombocytopenia purpura (ITP)
– Occurs in ∼3% of pregnancies, usually manifests in the first or second trimester.
– Treatment is with corticosteroids and/or intravenous IgG.
• Hemolysis, Elevated Liver enzymes, Low Platelet counts (HELLP) Syndrome
– Form of severe preeclampsia that can start after 20 weeks of gestation and up to 2 days
post-delivery.
– Thrombocytopenia results from increased anti-platelet IgG levels, activation of the
coagulation cascade (platelet consumption), and platelet sequestration in the spleen (4,5).
– Mortality results from liver rupture, disseminated intravascular coagulation (DIC), acute
renal failure, acute respiratory distress syndrome (ARDS), shock, and stroke.
– Management is supportive care.
Seizure prophylaxis with intravenous magnesium sulfate.
Blood pressure control for systolic pressure >160 mm Hg or diastolic pressure >90
mm Hg.
– Definitive treatment is delivery of the fetus and placenta.
• Thrombotic thrombocytopenia purpura (TTP)
– Thrombocytopenia is a result of platelet aggregation due to impaired vWF protease.
– Occurs anytime during pregnancy (first trimester through postpartum period).
– Severe cases can be treated with plasmapheresis.
• Hemolytic uremic syndrome (HUS)
– Microangiopathic hemolytic anemia from microvascular injury (6).
– 90% of cases occur postpartum with a mean onset of 26 days postdelivery (7).
– May require plasmapheresis
• Hypercoagulable states increase the risk of thromboembolism.
– Complications include uteroplacental thrombosis, fetal loss, DVT, PE, CVA, and cortical
venous thrombosis.
– Prophylaxis against thromboembolism (following surgical procedures and Cesarean
section) include: Graduated compression stockings, sequential leg compression devices,
early ambulation, and thromboprophylaxis.
• Some inherited congenital coagulopathies may improve or worsen depending on whether
the given factor increases or decreases with pregnancy.
– Hypofibrinogenemia and von Willebrand disease may improve.
– Factor XI deficiency may worsen.
• Hypocoagulable states may cause:
– Increased risk of postpartum hemorrhage
– Increased risk of placental abruption
– Increased risk of non-reassuring fetal status during labor
– A contraindication to neuraxial anesthesia due to increased risk of bleeding and epidural
hematoma formation.
Generally a stable platelet count >80,000/mL is sufficient for neuraxial anesthesia.
ALERT
• Management of anticoagulation pre-delivery
– Low molecular weight heparin (LMWH) should be switched to SQ or IV unfractionated
heparin 36 hours before elective induction or C-section.
– Many prefer to switch to unfractionated heparin at 36 weeks, to avoid going into labor on
LMWH, which might delay or preclude epidural placement.
– IV heparin should be turned off 4–6 hours before anticipated delivery.
• Management of anticoagulation prior to neuraxial block
– SQ heparin is not a contraindication for neuroaxial anesthesia if the total daily dose is
<10,000 U divided q12h.
– Conventional doses of fractionated LMWH require waiting at least 12 hours after the last
dose to perform a regional block; if higher doses are used, wait 24 hours.
– IV heparin can be administered 1 hour after a neuraxial block is in place.
– Removal of epidural catheters should occur at least 2–4 hours after the last heparin dose
(PTT measurement may be warranted).
– Restart fractionated or unfractionated (regular) heparin (for DVT prophylaxis) at least 2
hours after removal of the epidural catheter. Doses of heparin (5,000 U SQ q12h) and
LMWH (e.g., enoxaparin 1 mg/kg SQ q24h) should not increase the risk of hematoma
formation with neuraxial blockade after delivery if guidelines are strictly observed.
• Postoperative anticoagulation guidelines:
– Prophylaxis: Wait 12 hours after vaginal delivery to restart heparin and 24 hours after
Cesarean delivery for LMWH.
– Therapeutic: Wait 24 hours after delivery (8).
REFERENCES
1. Brenner B. Haemostatic changes in pregnancy. Thromb Res. 2004;114:409–414.
2. Crowley JP. Coagulopathy and bleeding in the parturient patient: Recent information has
helped in the identification of individuals at special risk. R I Med J. 1989;72:135–143.
3. Cerneca F, Ricci G, Simeone R, et al. Coagulation and fibrinolysis changes in normal
pregnancy: Increased levels of procoagulants and reduced levels of inhibitors during
pregnancy induce a hypercoagulable state, combined with a reactive fibrinolysis. Eur J
Obstet Gynecol Reprod Biol. 1997;73:31–36.
4. Leduc L, Wheeler JM, Kirshon B, et al. Coagulation profile in severe preeclampsia. Obstet
Gynecol. 1992;79:14–18.
5. Burrows RF, Hunter DJ, Andrew M, et al. A prospective study investigating the mechanism
of thrombocytopenia in preeclampsia. Obstet Gynecol. 1987;70:334–338.
6. McCrae KR, Cines DB. Thrombotic microangiopathy during pregnancy. Semin Hematol.
1997;34:148–158.
7. Esplin MS, Branch DW. Diagnosis and management of thrombotic microangiopathies
during pregnancy. Clin Obstet Gynecol. 1999;42:360–367.
8. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving
antithrombotic or thrombolytic therapy. American Society of Regional Anesthesia and Pain
Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med. 2010;35:64–
101.
ADDITIONAL READING
• Chestnut D, Polley L, Tsen L, et al. Chestnut’s obstetric anesthesia, 4th ed., 2009, chap. 43.
• Hoffman R, Benz EJ, Shattil SJ, et al. Hematology: Basic principles and practice, 5th ed.
Churchill Livingstone, chap. 161.
• Preeclampsia
• Thrombocytopenia
CLINICAL PEARLS
• Patients with a history of an early pregnancy loss need to be worked up for genetic disorders
of coagulation.
• Hypercoagulable states are a leading cause of maternal mortality in the world because of the
risk of PE.
• Symptoms of DVT, PE, and cortical vein thrombosis need to be evaluated and have a low
threshold for workup.
• DIC in pregnancy is associated with dead fetus syndrome, preeclampsia, HELLP syndrome,
placental abruption, massive transfusion, uterine rupture, and amniotic fluid embolism.
• Pregnant women on anticoagulants need coordination and correct timing of medication,
regional anesthesia, and delivery per guidelines.
BLOOD FLOW RESISTANCE
BASICS
DESCRIPTION
• Blood flow resistance (BFR) is the impedance offered by the blood vessels and its
interactions with the flowing blood. Conductance is the reciprocal of BFR.
• The basics of BFR are adapted from Ohm’s impedance law in electricity: R = V/I where R is
resistance, V is voltage, and I is current. Extrapolation of these factors and concepts to the
vascular system is as follows:
– Resistance (R): Equivalent to the vascular resistance and measured in dynes ×
seconds/cm5 (or Woods units)
– Voltage (V): Equivalent to the pressure difference across the area being discussed and
referred to as the ΔP
– Current (I): Equivalent to the cardiac output and measured as liters/minute
– R = ΔP/CO
• Resistance to flow can also include additional elements; for example, when expressed across
a valve it will be related to the valve size as well.
• BFR is expressed as the ratio between the pressure gradient (arterial and venous pressure
difference) and the flow of blood. Factors affecting vascular resistance are arteriole radius,
viscosity, and length.
• Arteriole radius: Resistance is inversely proportional to the fourth power of the radius (r4).
Radius is affected by:
– Autonomic control
– Hormones: Angiotensin II, norepinephrine, and epinephrine
– Metabolites:
Adenosine
Serotonin
Endothelium-derived relaxing factor (EDRF)
Prostacyclin
Nitric oxide (NO)
– Autoregulation is present in critical organs including the cerebral, myocardial, hepatic,
and renal circulations to maintain a constant (and adequate) blood flow and delivery of
oxygen and glucose across a range of mean arterial pressures. Increased flow elicits
vasoconstriction and decreases blood flow, whereas decreased flow results in vasodilation
to increase blood flow.
• Viscosity describes the tendency of a fluid to resist flow. It is affected by the hematocrit,
temperature, and flow state.
• Length: Does not appreciably change in vivo; this is more applicable to airflow.
• Blood flow patterns and resistance:
– Laminar flow describes low-resistance, straight-line flow. Under ideal laminar flow
conditions, resistance is mostly dependent on the radius. Poiseuille’s law can be applied to
measure the resistance: R = (8 × L × n)/r4, where L is length, n is viscosity, and r is
radius.
– Turbulent flow describes high-resistance, high-velocity flow that creates eddy currents
(whirls of blood); overall flow is decreased at any given perfusion pressure compared to
laminar flow.
ANATOMY
• Vessel diameter has a direct effect on the resistance of the vessel.
• Arteries have 3 layers:
– Intima is a smooth layer that essentially helps lower BFR (low friction).
– Media has 2 components: An elastic component that is predominant in the large arteries
and is responsible for the stretch-recoil vessel properties, and a muscular component
predominantly present in medium-size arteries and arterioles which is responsible for
changing the vessel size.
– Adventitia bestows a protective and tissue-securing role; it thereby plays no role in BFR.
• Chronic hypertension: In primary hypertension, the cardiac output increases initially, while
the systemic vascular resistance (SVR) remains normal. Eventually, the cardiac output
returns to normal and the SVR remains elevated.
• Pulmonary hypertension: Results from an imbalance in vasoactive peptides (prostacyclin,
endothelin 1, NO), which initiates smooth muscle proliferation followed by vasoconstriction
and right heart pressure overload.
• Temperature: Hypothermia increases blood viscosity and decreases vessel radius via
vasoconstriction (in order to preserve warmth).
• Hematocrit: Hemoconcentration and polycythemia vera increase blood viscosity. Anemic
patients, conversely, have a decrease in blood viscosity with a consequent decrease in
resistance; transfusion can, in addition to increasing oxygen-carrying capacity, increase
resistance and improve blood pressure in hypotensive patients.
• Prosthetic valves: As the cross-sectional area of the valve decreases from stenosis or
prosthetic valve housing, BFR increases, velocity increases, and pressure decreases across
the valve. This translates into a need for a large systolic pressure to drive blood forward.
A1V1 = A2V2, where A = cross-sectional area and V = velocity across the valve.
• Sepsis and anaphylaxis: Vasodilation decreases the BFR.
• BFR is often considered and discussed in regard to:
– SVR: Represents the change in pressure after being ejected from the left ventricle to the
pressure upon returning to the right atrium. SVR = (MAP – CVP)/CO, where MAP is
mean arterial pressure, CVP is central venous pressure, and CO is cardiac output. Normal
values range from 1,200 to 1,500 dynes × seconds/cm5.
– Pulmonary vascular resistance (PVR): Represents the change in pressure from the
beginning (pulmonary arteries) to the end (left atrium) of the pulmonary circulation. PVR
= (PAP – LAP)/CO, where PAP is the mean pulmonary artery pressure, LAP is left atrial
pressure, and CO is cardiac output. Normal values range from 100 to 300 dynes ×
seconds/cm5.
– Across heart valves: Stenotic valves and prosthetic heart valves can impose increased
resistance to flow. Transvalvular gradients can be measured via cardiac catheterization or
estimated/calculated with echocardiogram.
• Vasopressors and inotropes
– Phenylephrine: A synthetic, selective, and pure alpha-1 agonist. Receptor binding
increases the release of calcium from the sarcoplasmic reticulum and causes contraction of
vascular smooth muscle. This results in increased preload from venoconstriction and
afterload from vasoconstriction.
– Norepinephrine: Endogenously, it is released by the postsynaptic terminal of the
sympathetic nervous system. When exogenously administered, it has strong alpha-1
receptor agonism at veins and arteries, resulting in increased preload and afterload.
Coronary blood flow increases due to the increase in diastolic blood pressure. Side effects
include an increase in PVR, mesenteric ischemia, renal failure, decreased hepatic blood
flow, and peripheral hypoperfusion (digit necrosis).
– Dopamine: When exogenously administered, it causes alpha-1 agonism at higher dosages
(>10 mcg/kg/min). Initially, the vasoconstricting effects predominate in the skeletal
muscle vascular beds; with increasing doses, circulation in the limbs may become
compromised.
– Epinephrine: When exogenously administered, it causes alpha-1 agonism at higher
dosages.
– Vasopressin: V1 receptor agonism functions to increase sarcoplasmic release of calcium
and vascular smooth muscle constriction, primarily in capillaries and small arterioles. This
functions to shift blood flow away from splanchnic, muscle, fat and skin tissues to vital
organs.
– Phosphodiesterase inhibitors block enzymatic breakdown of cAMP to cGMP. In the
myocardium, this results in increased intracellular calcium with resultant enhanced
inotropy. However, in vascular smooth muscle, increased cAMP results in vasodilation.
• Vasodilators
– Nitrovasodilators: Nitroglycerin breaks down into NO, which consequently causes calcium
sequestration within vascular smooth muscle. At lower doses, venous and coronary
arteries are primarily affected; at higher doses, arterial dilation occurs. Nitroprusside
similarly breaks down into NO, but has a greater effect on arterial smooth muscle.
– Angiotensin-converting enzyme inhibitors (ACE I) block the conversion of angiotensin I to
angiotensin II. Angiotensin II is a potent endogenous vasoconstrictor.
– Angiotensin II receptor blockers (ARBs) competitively antagonize angiotensin II binding to
receptors on blood vessels.
– Calcium channel blockers (CCB) block voltage-gated calcium channels in the sarcoplasmic
reticulum, resulting in decreased intracellular calcium and decreased vasomotor tone.
– Hydralazine is a direct vasodilator. It increases cGMP levels with resultant decreases in
calcium release from the endoplasmic reticulum causing arterial vessel dilation (diastolic
pressure is decreased to a greater extent than systolic blood pressure) and venodilation.
• Anesthetic medications with vasodilatory properties:
– Propofol
– Volatile agents
– Lidocaine
• Resistance to blood flow also provides the basis for calculations obtained from pulmonary
artery catheter data.
EQUATIONS
• Ohm’s law: R = V/I, where R is resistance, V is voltage, and I is current
• Fluid dynamics extrapolation: R = ΔP/CO, where R is resistance, ΔP is change in pressure,
and CO is cardiac output
• Poiseuille’s law: R = (8 × L × n)/r4, where R is resistance, L is length, n is viscosity, and r
is radius
REFERENCES
1. Khalafbeigui F, Suga H, Sagawa K. Left ventricular systolic pressure-volume area correlates
with oxygen consumption. Am J Physiol. 1979;237:H566–H569.
2. Maughan WL, Sunagawa K, Burkhoff D, et al. Effect of arterial impedance changes on the
end-systolic pressure-volume relation. Circ Res. 1984;54:595–602. [A]
3. Rose WC, Shoukas AA. Two-port analysis of systematic of systemic venous and arterial
impedances. Am J Physiol. 1993;265:H1577–H1587. [C]
4. Sasse SA, Chen PA, Mahutte CK. Relationship of changes in cardiac output to changes in
heart rate in medical ICU patients. Intens Care Med. 1996;22:409–414.
5. Suga H. Total mechanical energy of a ventricle model and cardiac oxygen consumption.
Am J Physiol. 1979;236:H498–H505.
6. Sunagawa K, Sagawa K. Models of ventricular contraction based on time-varying elastance.
Crit Rev Biomed Eng. 1982;6:193–228.
7. Wallace A, Lam HW, Mangano DT. Linearity, load dependence, hysteresis, and clinical
association of systolic and diastolic indices of left ventricular function in man. Multicenter
Study of Perioperative Ischemia (McSPI) Research Group. J Card Surg. 1995;10:460–467.
[B]
• Laminar flow
• Cardiac output
• Cerebral blood flow
• Septic shock
• Anaphylactic shock
CLINICAL PEARLS
• Circulation is influenced by the resistance of the vascular bed against which the heart is
pumping. Cardiac output is directly influenced by BFR.
• The most important determinant of BFR is vessel radius, which is regulated by the
sympathetic nervous system (SNS), hormones, metabolites, and autoregulation. The SNS can
increase the blood pressure 3-fold via increasing the heart rate, inotropy, and both arterial
and venous resistances.
• Therapy for arterial blood pressure management is aimed at changing the BFR (changing the
vessel radius or blood flow viscosity).
• Pulmonary artery catheter data and its calculations, as well as echocardiography imaging,
aid with clinical decision-making and guidance of therapy.
• Several anesthetic medications cause vasodilation, with resultant decreases in BFR.
BLOOD OXYGEN CARRYING CAPACITY
Onyi Onuoha, MD, MPH
BASICS
DESCRIPTION
• The blood oxygen-carrying capacity is the milliliters of oxygen present in 1 deciliter of
blood.
• In blood, oxygen can exist in 2 forms: Dissolved and attached to hemoglobin. Hemoglobin is
the primary transporter of oxygen in mammals.
• In the event of decreased oxygen delivery, the blood provides a limited cushion against
hypoxia.
• Oxygen is necessary for aerobic metabolism and cell integrity. However, despite its absolute
necessity, the body only has minimal storage capacity (unlike glucose). When apneic,
oxygen stores are limited to the oxygen in the lungs (FRC) and the blood; both of which are
unable to sustain life beyond a few minutes.
• In a healthy adult at rest, oxygen consumption is ∼200–250 mL O2/min and oxygen
delivery is ∼950–1,150 mL O2/min. Thus, ∼25% of the arterial oxygen is used every
minute, and the deoxygenated blood returning to the lungs has ∼75% saturation (mixed
venous oxygen saturation) (1).
• Hemoglobin provides the most efficient means of carrying and transporting blood. At full
oxygen saturation, 1 g of hemoglobin in 1 dL of blood is capable of carrying 1.34 mL of O2.
Thus, Hgb × 1.34 × SaO2 determines the milliliters of oxygen bound to hemoglobin in 1
dL of blood. Oxygen bound to hemoglobin does not exert partial pressure.
• Oxygen is poorly soluble in blood with a coefficient of 0.003 milliliters of oxygen per
deciliter of plasma per millimeter of mercury oxygen. Hence, a patient breathing room air
with an approximate PaO2 of 100 mm Hg has 0.3 mL of oxygen dissolved in 1 dL of blood.
• Oxygen–hemoglobin (O2–Hgb) dissociation curve: PaO2 on the x-axis, and SaO2 on the y-
axis. As PaO2 increases, SaO2 increases. The curve is not linear, but sigmoid in shape. This
represents hemoglobin’s desire to be fully bound or fully dissociated from oxygen; it is
unstable in intermediate states. This characteristic facilitates its physiologic function; at the
lungs, hemoglobin will fully saturate and at the tissue level, it will easily dissociate and
unload to oxygenate the tissues.
• Assuming normal hemoglobin moieties and conditions, the PaO2 is in equilibrium with
oxyhemoglobin and dissolved oxygen. For example, a PaO2 of 100 mm Hg has an SpO2 of
98% and 0.3 mL O2/dL of blood. A PaO2 of 500 mm Hg has an SpO2 of 100% and 1.5 mL
O2/dL of blood.
ANATOMY
• Hemoglobin is an iron-containing protein that is composed of 4 polypeptide chains or
subunits. The iron-containing heme group of each polypeptide reversibly binds up to 4
molecules of oxygen (2).
• The adult hemoglobin (HbA) molecule is made of 2α globin and 2β globin subunits.
• The binding of the first oxygen molecule to hemoglobin induces conformational changes in
the structure of the hemoglobin that allows the binding of other molecules of oxygen more
readily. At normal resting conditions, 25% of the oxygen bound to hemoglobin is extracted
by the tissues (equivalent to a partial pressure of 40 mm Hg).
• Fetal hemoglobin (HbF), on the other hand, has 2α and 2γ subunits that possess a strong
affinity for oxygen. The fetus is exposed to much lower oxygen pressures from the placenta;
∼21% of the level found in the adult lung (1).
• Low oxygen-carrying capacity is the result of a low PaO2, low hemoglobin, impaired
oxygen-to-hemoglobin binding, or an increased oxygen demand/consumption.
– Low PaO2: Hypoxic mixture (low inspired oxygen), hypoventilation, V/Q mismatching,
shunting, impaired diffusion
– Low hemoglobin: Chronic or acute anemia
– Impaired oxygen-to-hemoglobin binding: Abnormal hemoglobins (fetal, thalassemia, sickle
cell disease), carboxyhemoglobin, cyanhemoglobin, methemoglobin, sulfhemoglobin
– Increased oxygen demand/consumption: Hyperthermia, hyperthyroidism, sepsis,
pregnancy, vigorous exercise
• Acute anemia: The initial hemodynamic response is a fall in systemic vascular resistance
(SVR) that is partly due to the decrease in blood viscosity and in part, the result of nitric
oxide-mediated vasodilation. The decrease in SVR reduces blood pressure and causes a
baroreceptor-mediated neurohormonal activation, identical to that seen in patients with
severe low-output heart failure. Eventually, sympathetic and renin–angiotensin–aldosterone
activity cause peripheral vasoconstriction and decrease in renal blood flow and glomerular
filtration rate. Kidneys retain salt and water (3).
• Chronic anemia results in hemodynamic and non-hemodynamic (erythropoiesis)
compensatory responses to enhance oxygen-carrying capacity (2,4).
– Hemodynamic responses are complex and involve a vasodilation-mediated high-output
state with neurohormonal activation (as described above in acute anemia). The high-
output state initially helps to increase oxygen transport. However, compensatory
mechanisms have deleterious long-term consequences and could contribute to anemia’s
role as an independent risk factor for adverse outcomes.
– Non hemodynamic responses: Increased levels of 2,3-diphosphoglycerate (2,3-DPG) shift
the O2–Hgb dissociation curve to the right. This is the least energy-consuming mechanism
to support increased oxygen delivery to the tissues (lacks significant increase in cardiac
output). Erythropoiesis also serves to increase red blood cell production.
• In elevated altitudes, ventilation and heart rate are elevated with a minimum reduction in
stroke volume. In addition, plasma volume is reduced over 24–48 hours to improve the
oxygen-carrying capacity of the blood. Prolonged sojourn at altitudes is compensated for
with enhanced erythropoiesis and a larger hemoglobin mass, allowing for a partial or full
restoration of the blood volume and arterial oxygen content.
• General anesthesia causes a 15% reduction in metabolic rate and a subsequent decrease in
oxygen requirement. Artificial ventilation further decreases the oxygen requirement by 6%
with the removal of the work of breathing. Anesthetic agents, however, do not affect the
transport of oxygen by hemoglobin or its solubility in blood.
• The increased utilization of oxygen when metabolic rate is increased (postoperative
shivering, malignant hyperthermia, etc.) leads to a decrease in PaO2 which activates normal
protective responses to hypoxia (aortic and carotid chemoreceptors, sympathetic nervous
system) to increase cardiac output. However, these protective responses are usually reduced
by anesthetic drugs intraoperatively, and can extend into the postoperative period.
• Blood transfusion: It remains the clinician’s responsibility to determine the transfusion
“trigger” for an individual patient based on multiple elements that determine the demand
for the delivery of oxygen and the physiological reserve. The decision should be based on
the premise that the oxygen-carrying capacity is increased to prevent oxygen consumption
from exceeding oxygen delivery. Additionally, the following should be considered:
– Theoretically, the oxygen-carrying benefit of red blood cells should hasten recovery from
respiratory failure, and transfusion would therefore be expected to shorten the duration of
mechanical ventilation. However, evidence to the contrary has been reported.
– Storage of packed red blood cells (pRBCs) is associated with a decline in 2,3-DPG that
leads to a subsequent left shift of the O2–Hgb dissociation curve. Therefore, while
transfusion increases the patient’s hemoglobin, it results in a less efficient oxygen delivery
when compared to the native hemoglobin at that same hematocrit. 2,3-DPG levels return
to normal over 12–24 hours.
– The need to restore blood viscosity may precede the need to restore oxygen-carrying
capacity during hemodilution or anemic conditions. A minimum level of blood viscosity
appears to be necessary for generating shear stress and stimulating the release of
vasoregulatory factors such as nitric oxide and prostacyclin (3).
– Studies in subpopulations (renal failure, Jehovah’s Witnesses, military casualties) have
shown that considerably greater amounts of anemia than was previously believed can be
well tolerated.
– Patients that are unable to increase their cardiac output (coronary artery disease,
prior/acute myocardial infarction, beta-adrenergic blockade, decreased SVR such as sepsis
or post-cardiopulmonary bypass) or have impaired oxygenation (pulmonary disease, high
altitude) have limited compensatory responses to hypoxia.
• Isovolemic hemodilution to hemoglobin levels of 5 g/dL in normal volunteers is well
tolerated. A robust cardiovascular response manifested by increases in heart rate and stroke
volume leads to compensation.
• Blood substitutes are being investigated to increase oxygen-carrying capacity. At this time,
there are no available products for clinical use.
EQUATIONS
• Oxygen content = [(Hgb × 1.39 × SaO2) + (PaO2 × 0.003)]. Units are as follows: Hgb is
in g/dL; 1.39 is mLO2/dL; SaO2 is % (0.01) but no units (5).
• Oxygen arterial content (CaO2) = [(Hgb × 1.39 × SaO2) + (PaO2 × 0.003)] (5).
• Oxygen venous content (CvO2) = [(Hgb × 1.39 × SvO2) + (PvO2 × 0.003)]. If obtained
at the pulmonary artery (PAC), it is a representation of the true mixed venous oxygen (5).
• Oxygen delivery (DO2) (mL/min) = cardiac output (CO) × blood oxygen content
GRAPHS/ FIGURES
Oxygen–hemoglobin dissociation curve
REFERENCES
1. aw R, Biukwirwa H. The physiology of oxygen delivery. Update Anaesth. 1999;10(3):1–2.
2. reacher DF, Leach RM. Oxygen transport. BMJ. 1998;317(7168):1302–1306.
3. abrales P, Martini J, Intaglietta M, et al. Blood viscosity maintains microvascular
conditions during normovolemic anemia independent of blood oxygen-carrying capacity.
Am J Physiol Heart Circ Physiol. 2006;291(2):H581–H590. Anand IS. Heart failure and
anemia: Mechanisms and pathophysiology. Heart Fail Rev. 2008;13:379–386.
4. Martin L. The four most important equations in clinical practice. Available at:
http://www.globalrph.com/martin_4_most2.html
ADDITIONAL READING
• Bartsch P, Saltin B. General introduction to altitude adaptation and motion sickness. Scand J
Med Sci Sports. 2008;18(Suppl 1):1–10.
• Henig NR, Pierson DJ. Mechanism of hypoxemia. Respir Care Clin N Am. 2000;6(4):501–
521.
• Ouellette DR. The impact of anemia in patients with respiratory failure. Chest. 2005;128(5
Suppl 2):576S–582S.
• Isovolemic hemodilution
CLINICAL PEARLS
• Pulse oximetry is not a reliable monitoring modality in the presence of dyshemoglobins
(hemoglobin that is unable to bind to oxygen). The 2 major dyshemoglobins seen in clinical
practice are carboxyhemoglobin (COHb) and methemoglobin (MetHb). Co-oximeters are
able to separate out oxyhemoglobin from MetHb and COHb and are therefore more accurate
for quantifying oxygen-carrying capacity/content.
• Blood substitutes: Include hemoglobin-based oxygen carriers (HBOCs) which transport
oxygen when introduced intravenously. Synthetic analogs, such as perfluorocarbon
emulsions (PFCs), have also been used as substitutes. These chemicals are able to dissolve
large amount of gases such as oxygen. Unlike blood, PFCs exhibit a linear oxygen
dissociation curve with an increase in PaO2 enhancing oxygen transport by these molecules
and increasing the driving pressure of diffusion of oxygen into tissues. With a linear
relationship however, the need for oxygen remains greater since most of the oxygen is
released prior to the arrival of the oxygen-laden molecule to the capillary network where
the partial pressure of oxygen is low. These also require high FiO2 to dissolve adequate
amounts of oxygen. However, optimal oxygen transport still remains difficult to reproduce
and continues to differentiate real blood from blood substitutes and volume expanders.
BLOOD PRESSURE
Mitesh Patel, MD
BASICS
DESCRIPTION
• Blood pressure (BP) is the pressure exerted by circulating blood upon the walls of blood
vessels and is one of the principal vital signs.
• During each heartbeat, BP varies between a maximum (systolic) and a minimum (diastolic)
pressure.
• The mean BP is a function of pumping by the heart and resistance to flow in blood vessels; it
decreases as the circulating blood moves away from the heart through arteries (1,2).
• Mean arterial pressure (MAP) is the average pressure over a cardiac cycle and is determined
by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure
(CVP); it can be calculated by the equation MAP = (CO × SVR) + CVP.
• Pulse pressure (PP) is the difference between systolic and diastolic BP which results from the
pulsatile nature of cardiac output. PP = SBP − DBP.
• BP regulation is modulated by several reflexes on a minute-to-minute basis.
– Arterial baroreflex is mediated by stretch-sensitive sensory nerve endings located in the
carotid sinuses and the aortic arch. The rate of firing of these baroreceptors increases with
arterial pressure, and the net effect is a decreased sympathetic outflow, resulting in
decreased arterial pressure and heart rate.
– The renin–angiotensin–aldosterone system contributes to the regulation of arterial
pressure primarily via the vasoconstrictor properties of angiotensin II and the sodium-
retaining properties of aldosterone (3).
– Chemoreceptors located in the carotid and aortic bodies regulate BP by monitoring blood
pO2, pCO2, and pH.
• Diastolic BP plays an important role in coronary perfusion pressure. Coronary perfusion
pressure (CPP) is the difference between the aortic diastolic pressure and left ventricular
end-diastolic pressure (LVEDP). CPP = DBP − LVEDP.
• Manual intermittent measurement techniques: Auscultation remains the most widely used
and was originally described by Nikolai Korotkoff in 1905. A sphygmomanometer, cuff, and
stethoscope measure BP by auscultating sounds generated by turbulent arterial flow beyond
the partially occluding cuff. The first sound is heard at the systolic pressure (phase I). Its
character progressively changes (phases II and III), becomes muffled (phase IV), and is
finally absent (phase V). Diastolic pressure is recorded at phase IV or V.
• Automated intermittent measurement techniques: Most automated noninvasive BP devices
are based on oscillometry, where variations in cuff pressure resulting from arterial
pulsations during cuff deflation are sensed. The pressure at which the peak amplitude of
arterial pulsations occurs corresponds closely to MAP; systolic and diastolic pressures are
derived from proprietary formulas that examine the rate of change of the pressure
pulsations.
• Direct measurement techniques of arterial BP: Arterial cannulation with continuous pressure
transduction and waveform display remains the accepted reference standard for BP
monitoring. It is invasive, more costly, and requires technical expertise to perform (4).
• Acute hypertension is a risk factor for myocardial ischemia, stroke, and bleeding from the
surgical sites.
• Chronic hypertension doubles the risk of cardiovascular disease including coronary heart
disease (CHD), congestive heart failure (CHF), ischemic and hemorrhagic stroke, renal
failure, and peripheral arterial disease. Because most patients with long-standing
hypertension are assumed to have some element of coronary disease and cardiac
hypertrophy, excessive BP elevations are undesirable.
• Uncontrolled hypertension (>180/120 mm Hg) and/or clinical signs and symptoms of
hypertensive emergency warrant cancellation of elective surgery until the BP is optimized.
Patients should receive emergency medical care and not simply be sent home. Warning
signs and symptoms of hypertensive emergency include:
– Headache
– Confusion
– Visual changes
– Seizures
– Focal neurologic changes
– Nausea and vomiting
– Papilledema
– Exudative hemorrhages
– Shortness of breath
– Chest pain
– Azotemia, oliguria, and proteinuria
• In the operative setting, systolic and diastolic pressures should generally be kept within 10–
30% of preoperative levels (5).
• The systolic BP (generated from myocardial ventricular contraction) helps estimate the risk
for a heart attack or stroke according to the Framingham study. Intraoperatively, systolic BP
correlates with the amount of surgical bleeding.
• MAP is commonly referred to during cardiac surgery (particularly during bypass) and is a
determinant of cerebral perfusion pressure (CPP = MAP – ICP). Cerebral blood flow is
autoregulated between MAPs of 60 and 180 mm Hg; should the MAP fall below 60 mm Hg,
the cerebral blood flow becomes severely decreased. In hypertensive patients, the
autoregulation curve is shifted to the right (6).
• Severe intraoperative hypotension is an anesthetic emergency, and treatment is vital to
ensure adequate organ blood flow, particularly to the brain, heart, kidneys, and the placenta
in pregnancy. Consequences of hypotension can include stroke, myocardial infarction, acute
tubular necrosis, fetal compromise, acidosis, and death. Because hypotension can be
harmful, this symptom is often treated before the cause has been ascertained. Hypotension
can result from abnormalities in preload, contractility, afterload, heart rate, cardiac rhythm,
intravascular volume, or SVR. Common causes of hypotension include:
– Hypovolemia can reduce preload and may be due to hemorrhage, vomiting, diarrhea,
burns, or sepsis.
– Increased intrathoracic pressure, as seen with positive pressure ventilation and tension
pneumothorax, can reduce preload.
– Spinal and epidural anesthesia cause vasodilatation and decreased preload due to
sympathetic block; if the block is above T4, it may also result in decreased myocardial
contractility and bradycardia.
– Excessive anesthesia: General anesthetics (both inhalation and intravenous) may cause
hypotension by reducing CO and SVR.
– Obstruction of major vessels can increase afterload and cause pump failure. Causes include
pulmonary embolism or aortocaval compression by tumor or pregnancy.
– Decreased myocardial contractility, as from beta-blockers, cardiac arrhythmias, cardiac
tamponade, and myocardial infarction
– Bradycardia, as from heart block or vagal overtone
– Shock, as from spinal, cardiogenic, or anaphylaxis shock or sepsis
• Treatment of intraoperative hypotension often precedes treating the cause:
– Optimize preload: Administer an intravenous fluid bolus.
– Elevate legs or head down tilt to improve venous return.
– Reduce anesthetic agent if appropriate.
– Use sympathomimetic drugs.
• Causes of intraoperative hypertension include:
– “Light” anesthesia or pain
– Hypercarbia
– Medication error (inadvertent administration of pressors)
– Preeclampsia/eclampsia
– Acute increase in intracranial pressure
– Volume overload
– Full bladder
– Pheochromocytoma
– Autonomic hyperreflexia
– Decreased vascular compliance (arteriosclerosis)
– Disorders with increased cardiac output (aortic regurgitation, thyrotoxicosis)
– Renal parenchymal diseases
– Aortic coarctation
– Medications (such as monamine oxidase inhibitors, cocaine, or methamphetamine)
• Autonomic hyperreflexia or dysreflexia (AD) is a life-threatening condition which occurs
most often in individuals with spinal lesions above the T6 spinal cord level. At this level, the
lesion is cephalad to the sympathetic cell bodies in the spinal cord and is believed to disrupt
descending CNS impulses that normally regulate sympathetic outflow. AD is a reaction of
the autonomic (involuntary) nervous system to overstimulation which is characterized by
severe hypertension, (reflex) bradycardia, profuse sweating, vasodilation above the level of
the lesion (including flushing of the skin, nasal stuffiness, severe headaches), apprehension,
anxiety, and occasionally cognitive impairment. AD is believed to be triggered by afferent
stimuli originating below the level of the lesion, which increase BP via sympathetically
mediated vasoconstriction in muscle, skin, and splanchnic vascular beds (7). The stimuli
that trigger AD often result from the distension of a viscous such as the bladder or intestine.
GRAPHS/FIGURES
See Table
See Table
REFERENCES
1. Health and Life. Normal blood pressure range adults. Available at:
http://healthlifeandstuff.com/2010/06/normal-blood-pressure-range-adults/
2. labunde R. Cardiovascular physiology concepts. Lippincott Williams & Wilkins, 2005.
3. Klabunde RE. Cardiovascular physiology concepts: Mean arterial pressure. Available at:
http://www.cvphysiology.com/Blood%20Pressure/BP006.htm [Accessed September 29,
2008; Archived version October 3, 2009.
4. Karlsson AK. Autonomic dysreflexia. Spinal Cord. 1999;37:383–391.
5. Rohrig R, Junger A, Hartmann B, et al. The incidence and prediction of automatically
detected intraoperative cardiovascular events in noncardiac surgery. Anesth Analg.
2004;98(3):569–577.
ADDITIONAL READING
• Morgan GE, Mikhail MS, Murray MJ. Anesthesia for patients with cardiovascular diseases.
In: Clinical Anesthesiology, 4th ed., McGraw Hill, 2005, chapter 20.
• Autonomic hyperreflexia
• Controlled hypotension
• Arterial waveform
• Perioperative hypertension
• Mean arterial pressure
CLINICAL PEARLS
• Maintaining an adequate BP is essential to maintain perfusion to vital organs. BP should be
maintained within 10–30% of the patient’s baseline.
• The consequences of hypotension are sufficiently serious to potentially warrant treatment
even before the cause of the hypotension is ascertained. Intraoperative hypotension most
commonly reflects “deep” anesthesia, hypovolemia, or the use of specific drugs or anesthetic
techniques.
• Uncontrolled hypertension is associated with an increase in perioperative morbidity and
mortality. Elective cases should be cancelled when a patient demonstrates signs of a
hypertensive emergency. Anesthesiologists are often faced with the decision to cancel or
proceed with uncontrolled BPs exceeding 180/110 mm Hg.
• Titrating therapies to traditional endpoints such as blood pressure does not ensure that the
microvascular bed is being adequately perfused. For example, a normal or high blood
pressure may be a vasoconstrictive response to a low cardiac output state.
BLOOD SUBSTITUTES
Jonathan S. Jahr, MD
Dayna Zimmerman, BS
BASICS
DESCRIPTION
• “Blood substitutes” have been studied for >50 years and are either derivatives of
hemoglobin or perfluorocarbons; they are designed to carry and offload oxygen to tissues.
– Hemoglobin-based oxygen carriers are termed (HBOCs); attained from human or bovine
sources.
– Perfluorocarbon-based oxygen carriers are termed (PFBOCs).
• No products discussed are FDA approved for human use. One product (Hemopure®, OPK
Biotech, Cambridge, MA) has been approved in South Africa and Russia. Another product
(Oxyglobin®, OPK Biotech) is FDA and European Union approved for canine anemia.
• Blood substitutes have been designed to carry oxygen to ischemic tissue as well as tested as
a resuscitation fluid.
• HBOCs are:
– Synthesized from human or bovine blood cells in a process that removes the red cell
membrane, purifies and deactivates pathogens (prions), and re-polymerizes the purified
hemoglobin (via glutaraldehyde pegylation, encapsulation, or zero-link polymerization).
– Prepared as a bag of solution around 250–500 mL, or the equivalent amount of
hemoglobin as a unit of packed red blood cells. Some of the HBOCs offload oxygen more
easily and may be more efficient than banked blood.
– Newer generations have attempted to link oxygen carrying with diminished extravasation
from the vascular compartment, block nitric oxide scavenging, and serve as anti-
inflammatory agents to diminish the deleterious effects of ischemia.
• “First-generation” HBOCs are designed to have a normal hemoglobin (10–13 g/dL), normal
viscosity, elevated colloid oncotic pressure, shift the oxyhemoglobin dissociation curve to
the right, and a normal Hill coefficient.
– They include α-α cross-linked hemoglobin, 2,3 diaspirin cross-linked hemoglobin
(HemAssist®, Baxter, Deerfield, IL), and hemoglobin raffimer (Hemolink™, Hemosol,
Toronto, ON).
• “Second-generation” HBOCs are designed with the same goals as first-generation HBOCs but
with fewer side effects. They too have a normal hemoglobin (10–13 g/dL), normal viscosity,
elevated colloid oncotic pressure, shift the oxyhemoglobin dissociation curve to the right,
and a normal Hill coefficient. To date, they remain the most successful HBOCs.
– Human polyhemoglobin (PolyHeme®, Northfield, Evanston, IL) and hemoglobin glutamer
(bovine) 200 and 250 (Hemopure® and Oxyglobin®, OPK Biotech) have completed FDA
Phase III testing but were not approved in the US.
• “Third-generation” HBOCs have a low hemoglobin (5–6 g/dL), normal to high viscosity,
lower colloid oncotic pressure, shift the oxyhemoglobin dissociation curve to the left, and a
normal Hill coefficient.
– There are a number of “third-generation” HBOCs currently undergoing preclinical and
clinical testing (Maleimide-Polyethylene Glyco-modified Hemoglobin [MP4], Hemospan®,
Sangart, San Diego, CA; Zero-linked Hemoglobin Polymer Oxyvita®, OXYVITA, New
Windsor, NY).
• “First-generation” HBOCs had serious complications including renal failure and increased
mortality in trauma trials (HemAssist®).
• “Second-generation” HBOCs cause increased systemic and pulmonary blood pressure,
increased lipase without clinical signs or symptoms of pancreatitis, and transient jaundice,
secondary to breakdown of the hemoglobin by the reticuloendothelial system.
• “Third-generation” HBOCs may avoid the hypertension, but may still have other
complications.
• In one study, elderly patients tended to have worse outcomes with the particular blood
substitute, suggesting that patients with pre-existing hypertension, cardiac, renal, and
cerebrovascular disease may be susceptible to the hypertensive effects.
• The concept of blood substitutes is attractive in that they are:
– Stable at room temperature
– Do not require cross-matching and are immediately available
– Do not carry infectious disease risk
– Not dependent on a limited donor supply
• Possible indications for blood substitutes include:
– Shock
– Organ ischemia
– Red blood cell incompatibility
– Acute lung injury
– Transplant organ preservation
– Cardioplegia
– Sickle cell anemia
– Tumor therapy
– Air embolism
– Anemia refractory to allogenic blood transfusion
– Emergency civilian or military setting of severe trauma or perioperative bleeding
• Allogenic blood transfusions have multiple risks, including infectious, immunologic,
metabolic, and critical illnesses.
– Screening of blood has reduced the incidence of HIV and Hepatitis C; however, new
infections take time to be detected and removed from the donor supply.
– Immunomodulation can result in increased surgical wound infection and recurrence of
cancer (especially colon cancer) as well as decreased graft survival of transplanted organs.
– Transfusion-related acute lung injury (TRALI) can occur in 1:5,000 transfusions and
carries a high mortality ranging from 6% to 9%.
– Transfusion reactions from laboratory or transfusion error can result in serious morbidity
and mortality.
– Metabolic derangements include hypothermia, hyperkalemia, and decreased 2,3-DPG.
– Transfusion-associated circulatory overload (TACO) is due to rapid transfusion of a large
volume of blood and can cause dyspnea, orthopnea, peripheral edema, and rapid increases
in blood pressure. It carries an incidence of 1:100–10,000.
– However, even if a blood substitute is developed and has minimal complications, blood
donation cannot be replaced; donor blood is fractionated to multiple products including
platelets, fresh frozen plasma, and cryoprecipitate.
GRAPHS/FIGURES
Hypothesized Mechanism of Action
Nitric Oxide (NO) Scavenging of Hemoglobin
REFERENCES
1. Jahr JS, Walker V, Manoochehri K. Blood substitutes as pharmacotherapies in clinical
practice. Curr Opin Anaesthesiol. 2007;20:325–330.
2. ahr JS, Moallempour M, Ellis JE. Transfusion update—triggers, targets, and will we ever
have a blood substitute? Curr Rev Clin Anesth. 2008;28(21):249–260.
3. Jahr JS, Moallempour M, Lim JC. HBOC-201, Hemoglobin glutamer 250 (bovine),
Hemopure® (Biopure Corporation, Cambridge, MA). Expert Opin Biol Ther.
2008;8(9):1425–1433.
4. Jahr JS, Mackenzie C, Pearce B, et al. HBOC-201 as an alternative to blood transfusion:
Efficacy and safety evaluation in a multicenter phase III trial in elective orthopedic
surgery. J Trauma Injury Infect Crit Care. 2008;64(6):1484–1497.
http://www.nhlbi.nih.gov/health/dci/Diseases/bt/btrisk.html
• Jahr JS, Sadighi Akha A, Doherty L, et al. Hemoglobin-based oxygen carriers: History, limits,
brief summary of the state of the art, including clinical trials. In: Mozzarelli A, Bettati S.
Chemistry and biochemistry of oxygen therapeutics: From transfusion to artificial blood.
London: John Wiley and Sons Ltd, 2011, chap. 22.
• Blood transfusion
• Blood transfusion infectious risks
CLINICAL PEARLS
• Ideally, blood substitutes could benefit patients who refuse allogenic blood transfusions,
trauma patients (military or civilian) for whom blood is not easily available, patients who
are unable to receive allogenic blood for immunologic reasons (hemolytic anemia), and to
augment acute normovolemic hemodilution.
• Side effects of blood substitutes that limit their use include:
• Vasoactivity
• Nephrotoxicity
• Interference with complement
• Mononuclear phagocytic system activation
• Histamine release
• Antigenicity
• Oxidation in storage
• Activation of kinin and coagulation
• Iron deposition
• Lack hemoglobin’s ability to scavenge nitric oxide
• At this time, there are no FDA-approved products available for human use.
BONE MARROW TRANSPLANT (HARVEST PROCEDURE)
Lori Dangler, MD, MBA
BASICS
DESCRIPTION
General
• Bone marrow transplants (BMT) are used to help patients with various kinds of serious
illnesses:
– Marrow failure (aplastic anemia)
– Hematologic malignancy (AML, ALL, CML, CLL, myeloma)
– Selected chemotherapy-responsive solid tumors (lymphoma, Hodgkin’s, non-Hodgkin’s)
– Immunodeficiency syndromes
– Other genetic disorders
• Bone marrow harvesting and transplantation procedures were first developed in the 1950s
and the first successful bone marrow transplantation occurred in 1968.
• Spaces in the bone marrow hold both blood and stem cells. Stem cells are multipotent
hematopoietic cells that have the ability to grow into various types of future blood cells.
• During a harvest, a small portion of marrow is collected to be used for transplantation.
Multiple large-bore needle aspirations of marrow are taken from the posterior iliac crests. At
the end of the procedure, aspiration sites are cleaned and covered with pressure dressings.
• Transplantation terms:
– Autologous BMT is when one has marrow harvested and frozen for future use.
– Allogenic BMT is when marrow is harvested for a relative.
– Syngeneic BMT is harvested for an identical twin.
– Unrelated BMT is when there is a donation through the registry.
• Marrow donor patient types:
– Autologous: Patients with malignancies who respond to chemotherapy (should be free of
active disease and have functioning bone marrow)
– Allogenic: HLA-matched healthy donors (often related) for recipient with malignancy or
marrow failure
Position
• Supine for intubation, then prone
• Prep around iliac crests
Incision
• Operating physician is often a hematologist.
• Large-bore needle insertion into the posterior iliac crests (other sites less common)
Approximate Time
1–2 hours
EBL Expected
• 1–2 quarts of bone marrow are commonly collected from adults.
• Cell count of marrow determines volume needed (1–4 × 108 cells/kg recipient body
weight).
Hospital Stay
• Outpatient to overnight maximum (healthy donors)
• Prolonged hospitalization for autologous donors/future recipients with anticipated support
for anemia, thrombocytopenia, neutropenia, and graft versus host issues
• Bone marrow aspiration needles
• Collection bags
• Padding/chest rolls/head support for prone positioning
• Pathologist on standby to determine the cell count
EPIDEMIOLOGY
Incidence
• 950 transplants were performed using bone marrow during 2010.
– Children (0–17 years) received 21% of transplants.
– Adults 18–50 years received 38% of transplants.
– Adults >50 years received 41% of transplants.
Prevalence
15,000 people in the US are diagnosed with life-threatening illnesses yearly where a BMT or
cord blood transplant from a matched donor is their best treatment option.
Morbidity
• Autologous donor: Postoperative morbidity ranges from moderate to high secondary to
underlying malignancy.
• Allogenic: Life-threatening complications are extremely rare (0.27%) for healthy donors.
Mortality
• Rare
• Between 1993 and 2005, there were 27,770 first BMTs, with only 1 fatal event (pulmonary
embolism) reported and 12 serious adverse events were observed. The most frequent
adverse events were cardiac (European Group for Blood and Marrow Transplantation
analysis).
• Familiarity with the patient’s specific chemotherapy. Avoid unnecessary oxygen enrichment
if the patient had Bleomycin.
• Avoid nitrous oxide since it inhibits methionine synthetase.
• Volume status and blood loss assessment; replacement with crystalloids, albumin, and
irradiated products
• Prior steroid therapy usage can lower adrenal reserves.
• Careful positioning to avoid prone position-related injuries
SYMPTOMS
• Healthy donor may be asymptomatic.
• Assessment points apply primarily to autologous donors.
– GI: Vomiting, diarrhea, melena
History
When autologous harvesting, attain a thorough history of underlying disease, complications
of chemotherapy (e.g., pericardial effusion, impaired cardiac function), and presence of
infection.
Signs/Physical Exam
• CV: Focused exam to assess for congestive heart failure (jugular venous distention, pitting
edema, murmurs, rales or crackles)
• Peripheral: Edema, orthostasis
• Heme: Ecchymosis, petechiae
MEDICATIONS
• Iron supplementation
• Erythropoietin
• Granulocyte colony stimulating factor (Filgrastim, Pegfilgrastim)
• Chemotherapy; last dosage
Labs/Studies
• Urinalysis to rule out urinary tract infections
• Electrolytes if recent chemotherapy
• CBC for platelets, hemoglobin (baseline)
• Coagulation profile if bleeding history
• ECG, echocardiogram, and/or stress testing if there is a concern for cardiac dysfunction
• Type and cross for 2 units irradiated blood if autologous donation was not performed
Autologous donors: Prior chemoradiation treatments resulting in temporary/permanent organ
dysfunction
TREATMENT
Premedications
• Benzodiazepines
• Opioids
• Steroid coverage
Blood transfusion highly probable
INTRAOPERATIVE CARE
• General endotracheal most common used for prone positioning
• Neuraxial block with a spinal or epidural may be appropriate if the patient is hydrated and
without coagulopathies
Monitors
• Minimum of 2 large-bore IVs; central line access may be considered if venous access is
difficult.
• Foley catheter if large fluid shifts and replacement are anticipated
• Arterial access may be useful if the BP is labile.
• Monitor ETCO2 closely; an acute drop may indicate marrow embolism (dead space
pathophysiology).
• Consider lower doses of induction agent when there is a history of orthostasis and
cardiotoxic chemotherapy use.
• Endotracheal tube provides a secure airway.
Maintenance
• After induction of anesthesia, establish prone positioning and careful padding of pressure
points.
• Heparin is administered pre-harvest.
• The total volume of marrow harvested is dependent on the body mass of the recipient as
well as the cellularity of the donor marrow. The target number of donor stem cells for
allogenic engraftment of unmanipulated marrow is 2–3 × 108 nucleated marrow cells/kg.
• If the patient requires a pRBC transfusion, irradiated units should be administered to avoid
potential engraftment of random donor nucleated cells.
Return to supine position for extubation
POSTOPERATIVE CARE
BED ACUITY
• Often performed on an outpatient basis
• Most donors are admitted to a same-day surgical unit on the morning of donation (volume
status changes).
• PACU monitoring is typically for 1–2 hours.
• Check pressure dressing on back
• May need transfusion; most donors will store 1–2 units of autologous blood.
ANALGESIA
• Local anesthetic at harvest puncture sites
• Tylenol with codeine
• Consider NSAIDs such as ketorolac if the patient is not coagulopathic.
COMPLICATIONS
• Pain is the most common complication of bone marrow harvesting and results from trauma
of the iliac bones and overlying soft tissue.
• Anemia
• Transfusion-related complications
• Fever
• Orthostasis
• Vomiting
• Bleeding/hematoma
• Infection
• Compressive neuropathies (should resolve with reabsorption of the hematoma)
• Anesthesia-related complications
REFERENCES
1. Bolwell BJ, Maurer W, Anderson J, et al. Outpatient bone marrow harvest: The Cleveland
Clinic experience. Bone Marrow Transplant. 1995;16(5):703–705.
2. Borton MM, Buckner CD. Major complications of marrow harvesting for transplantation.
Exp Hematol. 1983;11:916–921.
3. Bosi A, Bartolozzi B. Safety of bone marrow stem cell donation: A review. Transplant Proc.
2010;42(6):2192–2194.
4. Buckner CD, Clift RA, Sanders JE, et al. Marrow harvesting from normal donors. Blood.
1984;64:630–634.
5. Burmeister MA, Standl T, Brauer P, et al. Safety and efficacy of spinal vs. general
anaesthesia in bone marrow harvesting. Bone Marrow Transplant. 1998;21(11):1145–
1148.
6. Chern B, McCarthy N, Hutchins C, et al. Analgesic infiltration at the site of bone marrow
harvest significantly reduces donor morbidity. Bone Marrow Transplant. 1999;23:947–949.
7. Filshie J, Pollock AN, Hughes RG, et al. The anaesthetic management of bone marrow
harvest for transplantation. Anaesthesia. 1984;39(5):480–484.
8. Jin NR, Hill RS, Petersen FB, et al. Marrow harvesting for autologous marrow
transplantation. Exp Hematol. 1985;13(9):879–884.
9. Knudsen LM, Johnsen HE, Gaarsdal E, et al. Spinal versus general anaesthesia for bone
marrow harvesting. Bone Marrow Transplant. 1995;15(3):486–487.
10. Lederhaas G, Brock-Utne JG, Negrin RS, et al. Is nitrous oxide safe for bone marrow
harvest? Anesth Analg. 1995;80(4):770–772.
11. Machaczka M, Kalaitzakis E, Eleborg L, et al. Comparison of general vs. regional
anaesthesia for BM harvesting: A retrospective study of anaesthesia-related complications.
Bone Marrow Transplant. 2010;45(1):53–61.
12. Miller JP, Perry EH, Price TH, et al. Recovery and safety profiles of marrow and PBSC
donors: Experience of the National Marrow Donor Program. Biol Blood Marrow Transplant.
2008;14(9 Suppl):29–36.
13. Stein RA Jr, Messino MJ, Hessel EA 2nd. Anaesthetic implications for bone marrow
transplant recipients. Can J Anaesth. 1990;37(5):571–578.
14. Stroncek DF, Holland PV, Bartch G, et al. Experiences of the first 493 unrelated marrow
donors in the National Marrow Donor Program. Blood. 1993;81:1940–1946.
15. Thorne AC, Malbin KF, Jain M, et al. Autologous bone marrow harvesting in outpatients.
J Clin Anesth. 1996;8(7):551–556.
16. Thorne AC, Stewart M, Gulati SC. Harvesting bone marrow in an outpatient setting using
newer anesthetic agents. J Clin Oncol. 1993;11(2):320–323.
17. Vanhelleputte P, Nijs K, Delforge M, et al. Pain during bone marrow aspiration:
Prevalence and prevention. J Pain Symptom Manage. 2003;26(3):860–866.
CODES
ICD9
• V42.81 Bone marrow replaced by transplant
• V59.3 Bone marrow donors
ICD10
• Z52.3 Bone marrow donor
• Z94.81 Bone marrow transplant status
CLINICAL PEARLS
• Patients should hold aspirin or aspirin-containing compounds for 10 days prior to the
procedure; ibuprofen and ibuprofen-containing compounds should be held for 3 days prior.
• The procedure is performed under sterile conditions to avoid infection; autologous harvests
may involve immunocompromised patients.
BOWEL RESECTION/COLECTOMY
BASICS
DESCRIPTION
General
• Small bowel and colon resections are performed for elective and acute abdominal conditions
and may be performed either open or laparoscopically.
– Elective indications include tumors, diverticulitis or diverticulosis, Crohn’s disease,
ulcerative colitis, angiodysplasia, familial adenomatous polyposis, radiation enteritis, and
intestinal fistula.
– Acute conditions include bowel or colon obstruction or perforation, mesenteric infarction,
bleeding, volvulus, intussusception, and trauma.
– Laparoscopy has the advantage of decreased pain, earlier return of GI functions, and
quicker discharge from the hospital. However, it can be technically challenging, or may
not be appropriate in coagulopathic or acute abdomens.
• Bowel resections involve identifying, mobilizing, and confining the affected bowel. Bowel
clamps are applied proximally and distally to the site and then resected.
– Re-anastomosis is performed by one of the following techniques: Open end-to-end, closed-
end-to-end, stapled, or functional end-to-end.
– Stomas are created when inflammation is present to allow time to heal.
– Colon resection procedures include right or left hemicolectomies, sigmoid colectomies,
and total colectomies.
– Malignant disease processes can involve the removal of lymph nodes or mesentery.
Incision
Vertical or transverse depending on the procedure
Approximate Time
Variable—may increase with adhesions, obesity, or “re-do” abdomen
EBL Expected
Variable—may increase with proximity to vascular structure, vascularity of malignancy, or
inadvertent vessel penetration
Hospital Stay
2–5 days; based upon return of bowel function, perioperative complications, and
comorbidities
Laparoscopic equipment as appropriate
EPIDEMIOLOGY
Prevalence
Acute abdomen: Bowel obstruction 0.13%; mesenteric infarction 0.3–8.5%; bowel/colon
perforation 1.8–4.1%
Prevalence
Increases with age and a family history
Morbidity
Complications associated with resection: Ileus <10%; atelectasis 10%; anastomosis
insufficiency of the small bowel <3%, colon 2–4%; wound infection small bowel repair
<5%, colon repair 4–10%; splenic injury following colon resection 1%; and bleeding 1%
Mortality
• Major cause is anastomosis insufficiency with subsequent sepsis.
• Small bowel resections 1–5%; colon resection 0.5–2%
• Acute conditions >20%
• Gangrenous mesenteric infarction 60–70%
• Fluid and electrolyte deficits can be dramatic; aggressive hydration and replacement of
electrolytes need to take place while concurrently reassessing the patient’s volume status.
• Increased intra-abdominal pressures from the underlying disease process, surgical retractors
and packing, or Trendelenburg position result in decreased FRC and lung compliance. High
PIP and PEEP can be necessary.
• Hemodynamic instability may occur with exposure, manipulation of the bowel, onset of
sepsis, or hypovolemia.
SYMPTOMS
• Dependent upon the location of bowel disease
• Pain
• Nausea and vomiting
• Diarrhea or constipation
History
• Bowel prep
• Recent weight loss
• Anticoagulants that would preclude epidural placement
Signs/Physical Exam
• Signs of dehydration: Vital signs; decreased skin turgor, capillary refill, or urinary output
• Signs of electrolyte abnormalities: ECG changes or muscle weakness
• Signs of sepsis: Fever, tachycardia, or hypotension
MEDICATIONS
• H2 blockers or proton pump inhibitors
• Stool softeners
• Anti-inflammatories, steroids
• Chemotherapy
• Acute abdomen: Intravenous fluids, vasopressors, antibiotics, and electrolyte replacement
Labs/Studies
• CBC to assess for anemia, infection, thrombocytopenia, or thrombocytosis (acute phase
reactant)
• Coagulation profile
• Electrolytes
• Chest radiograph may be indicated when pulmonary comorbidities exist.
• Abdominal radiograph for the evaluation of free air under the diaphragm
Age-related diseases
TREATMENT
Premedications
• Metoclopramide, antacids, H2 blockers prior to induction for full stomach. Promotility
agents are contraindicated in bowel obstruction and perforation.
• Nasogastric (NG) tube placement may be indicated.
• Blood transfusion may be considered for anemia.
• Epidural catheter placement for postoperative pain management; the potential benefits
should be discussed.
• Central line access may be needed in acute abdomens.
• Postoperative ventilation, particularly in acute abdomens
• Elective bowel resections:
– Coverage for Gram-positive cocci and Gram-negative coccobacilli: First- and second-
generation cephalosporins; second generation provide better Gram-negative coverage.
• Colorectal procedures:
– Additional coverage of anaerobes: First- and second-generation cephalosporins combined
with metronidazole
– Resistance or allergies, consider gentamicin or imipenem combined with metronidazole
INTRAOPERATIVE CARE
• General endotracheal anesthesia is typically performed for open and laparoscopic
procedures; this allows for a secure airway, as well as the ability to provide positive
pressure ventilation and profound muscle relaxation.
• Epidurals (T8–T10 placement) for postoperative analgesia combined with a general
anesthetic have the potential benefit of reduced blood loss during surgery, lower extremity
venous stasis and thrombosis, atelectasis and hypoxia; improved analgesia; and quicker
return of bowel function and time to ambulation. Epidurals are not typically utilized for
laparoscopic resections; however, if there is a reasonable possibility of converting to an
open procedure, it may be considered. Contraindications include sepsis, coagulopathy, or
acute abdomen.
• Epidural for surgical anesthesia with monitored anesthesia care (MAC) may be considered
when the incision is below the umbilicus. This is not typical, but may be considered when
intubation and mechanical ventilation or general anesthesia could have untoward effects
(i.e., pulmonary cripples, postoperative delirium).
Monitors
• Nerve stimulator
• 2 large-bore IVs; central line access may be warranted in emergent cases for acute
abdomens.
• Invasive monitors (arterial line, central line, pulmonary artery catheter, TEE) are based
upon comorbidities, extent of surgery, and perioperative hemodynamic disturbances.
• Rapid-sequence induction (RSI) may be indicated for bowel obstruction, bowel motility
impairment, or peritoneal irritation.
– If an NG tube is in place, it should be suctioned to reduce the risk, or volume, of
aspiration.
– Induction agents should take into account volume status and comorbidities. Propofol may
cause profound hypotension; etomidate or ketamine may be considered.
– Neuromuscular blocking agents: Succinylcholine 1–1.5 mg/kg or rocuronium bromide
0.6–1.2 mg/kg
– Narcotics may be withheld in patients with a potentially difficult airway or hemodynamic
impairment.
Maintenance
• Balanced anesthetic
– Volatile or total intravenous anesthesia plus epidural anesthesia; minimal to no
intravenous opioids
– Volatile or total intravenous anesthesia combined with intravenous opioids
• Nitrous oxide is typically avoided since it can cause bowel distention.
• Muscle relaxation allows for adequate retraction and prevents bowel extrusion.
• Mechanical ventilation: Patients can have decreased pulmonary compliance and FRC from
the underlying bowel disease, as well as surgical maneuvers (e.g., retractors, packing,
Trendelenburg). Inspiratory flows, I:E ratios, respiratory rate, and ventilation mode
(pressure versus volume control) may need to be adjusted.
• Epidural infusion with a local anesthetic and opioid is commonly utilized in open
procedures.
– Local anesthetics: Bupivacaine (0.125–0.5%) or ropivacaine (0.1–0.2%)
– Opioids: Fentanyl (1–5 mcg/mL) or hydromorphone (10 mcg/mL)
– Infusion rate usually ranges from 4 to 12 mL/hr.
– Boluses often range from 2 to 6 mL.
– Doses and rates should be reduced in hypotension.
• Fluid and blood management
– Crystalloids: In acute cases, the patient may require significant volumes as high as 10–15
mL/kg/hr. Laparoscopic cases have less insensible losses.
– Colloids, such as albumin or hetastarch, may be utilized. Hetastarch may not be
appropriate in patients with known renal disease and/or coagulopathies.
– Blood transfusion may be indicated to increase the oxygen-carrying capacity.
• ABG monitoring: Aids in the diagnosis, assessment of severity, and response to therapy for
metabolic acidosis
• Stress dose steroids should be considered in patients who have taken high-dose steroids for 2
weeks within the past 6–12 months. The administered steroid should have glucocorticoid
and mineralocorticoid activity.
• Avoid hypothermia: Bowel exposure and cold fluid administration can result in radiation
and evaporation of heat to the environment.
– Upper and lower body warming blankets, underbody fluid blanket, and fluid warmers can
reduce heat loss and facilitate warming.
– Hypothermia can result in delayed awakening, arrhythmias, impaired myocardial
contractility (and hypotension), coagulopathy, prolonged ventilation, and postoperative
wound infection.
• DVT prophylaxis includes intermittent pneumatic compression devices, anti-embolism
stockings, low-dose unfractionated heparin, LMWH as per institution protocol.
• Antiemetic prophylaxis: Abdominal procedures may have an increased incidence of
postoperative nausea and vomiting.
• Muscle relaxation is often needed to facilitate closure; careful titration and twitch
monitoring can help achieve this effect without compromising the ability to reverse the
patient at the end of the case.
• Extubation criteria are the same for elective and acute surgery. However, in acute surgery,
the patient may be less capable of meeting the criteria.
– Ensure adequate reversal of muscle relaxants
– Carefully assess for extubation criteria in acute abdomens; consider performing an ABG.
Additionally, take into account other organ systems and the potential to return to the
operating room in the near future.
FOLLOW-UP
BED ACUITY
• Elective cases can often be discharged to the floor; comorbidities or intraoperative events
may require increased acuity.
• The ICU is often appropriate for acute procedures.
ANALGESIA
Epidural analgesia: Continue infusion with a long-acting local anesthetic combined with an
opioid, blood pressure permitting.
COMPLICATIONS
• Anastomosis insufficiency, infections, ileus
• Hemodynamic instability, thrombosis/embolic events
• Atelectasis, hypoxemia
• Hemorrhage
• Postoperative nausea and vomiting
• Rare complications: Postoperative bleeding and surgical site infection after laparoscopic
surgery, fistulas, strictures, short bowel syndrome, urethral injures, bladder injures, sexual
dysfunction, trapped ovary syndrome
PROGNOSIS
Depends on underlying condition
REFERENCES
1. itkenheadAR. Anesthesia and bowel surgery. Br JAnesth.1984;56:95–101.
2. Lund C. Anaesthesia for minimally invasive gastric and bowel surgery. Best Pract Res Clin
Anaesthesiol. 2002;16(1):21–33.
ADDITIONAL READING
• Ogunnaike BO, Whitten CW. Gastrointestinal disorders. In:Barash PG, CullenBF, Stoelting
RK, etal., eds. Clinical anesthesia. Philadelphia:Wolters Kluwer Lippincott Williams &
Wilkins, 2009.
• Crohn disease/ulcerative colitis
• Colorectal surgery
• Fluid management
CLINICAL PEARLS
• Patients presenting for bowel resections can have a myriad of indications.
• Emergent procedures for acute processes can be associated with significant fluid and
electrolyte imbalances, multiple-organ insults, as well as mortality.
• Minimally invasive surgical procedures are increasing in scope.
BRACHIAL PLEXUS ANATOMY
Mandip S. Kalsi, MD
BASICS
DESCRIPTION
• The brachial plexus is composed of the anterior primary divisions (ventral rami) of the C5,
C6, C7, C8, and T1 nerve roots.
• As the plexus travels through the neck into the upper extremity, it divides into roots, trunks,
divisions, cords, and branches. There are 5 “terminal” branches and other “collateral”
branches that leave the plexus at various points along its length.
• An understanding of brachial plexus anatomy is essential for successful placement of
regional nerve blocks of the upper extremities, as well as recognizing and minimizing
complications, should they occur.
• The building units of peripheral nerves are the “nerve fascicles.” Each fascicle contains
numerous nerve fibers and blood vessels within loose connective tissue called the
endoneurium. Each bundle of fascicles is separated from one another by a multilayer
epithelial sheath (perineurium). The fascicles are held together by an outer connective
tissue sheath (epineurium).
• Peripheral nerves are mixed nerves; different types of nerve fibers exist within the same
nerve and serve different functions (motor, sensory, autonomic).
• Each nerve fiber can be classified by size and whether or not it is myelinated.
• The ratio of connective tissue to neuronal tissue increases from proximal to more distal
locations.
• The brachial plexus provides the somatic sensory and motor nerve supply to most of the
upper extremity.
– Radial nerve (posterior cord)
Motor: Extensors of the elbow, wrist, and fingers
Sensory: Lateral 3 and ½ fingers on the dorsal side (thumb, index, middle finger, and ½
of the ring finger) minus the proper palmar digital area (finger tips)
– Median nerve (both the lateral and medial cords)
Motor: Flexors of the forearm and intrinsic muscles of the thumb (thenar muscles)
Sensory: Lateral 3 and ½ fingers on the palmar side (thumb, index and middle finger,
and ½ of the ring finger) and proper palmar digital on the dorsum (finger tips)
– Ulnar nerve (medial cord)
Motor: Intrinsic muscles of the hand
Sensory: Medial 1 and ½ digits (pinkie, and ½ of the ring finger) dorsal and palmar side
– Musculocutaneous nerve (lateral cord)
Motor: Flexors of the arm
Sensory: Lateral side of the forearm
ANATOMY
• The nerve fibers leave the intervertebral foramina and join together to form 5 nerve roots
that subsequently form 3 trunks, followed by divisions, cords, and several terminal nerves.
• Each trunk has 2 divisions that eventually rearrange into 3 cords and several terminal
branches. This most common representation occurs only in about 65% of people. There are
approximately 39 other variations.
• Roots: The ventral rami of the spinal nerves of C5–8 and T1 form the 5 roots of the brachial
plexus. The roots emerge from the vertebral foramina between the anterior and posterior
tubercle of the transverse process, pass between the anterior and middle scalene muscles,
and converge into the 3 trunks. Of note, the transverse process of C7 is characterized by its
lack of an anterior tubercle. This feature can be very helpful to distinguish the nerve roots
at different levels during ultrasound imaging of the brachial plexus.
• Trunks and divisions: The 3 trunks termed superior, middle, and inferior, due to their
vertical arrangement in relation to one another, are formed between the anterior and
middle scalene muscles. The superior trunk is derived from the C5–6 roots, the middle trunk
from the C7 root, and the inferior trunk from the C8–T1 roots. The phrenic nerve lies close
to the brachial plexus as it passes over the anterior scalene muscle. As the trunks continue
over the first rib and below the mid-portion of the clavicle, each trunk divides into the
anterior and posterior divisions.
• Cords and branches: As the divisions emerge below the clavicle, the fibers arrange again to
form the lateral, medial, and posterior cords that are so named according to their
relationship to the axillary artery. The lateral cord is formed from the superior divisions of
the superior and middle trunks, the medial cord is a continuation of the anterior division of
the inferior trunk, and the posterior cord is formed from the inferior divisions from all 3
trunks. The 3 cords then divide into, and ultimately form, the peripheral nerves of the upper
extremity. The lateral cord divides into the lateral head of the median nerve and terminates
as the musculocutaneous nerve. The medial cord divides into the medial head of the median
nerve, the medial antebrachial, the medial brachial cutaneous, and terminates as the ulnar
nerve. Finally, the posterior cord gives rise to the axillary nerve and terminates as the radial
nerve.
• Brachial plexus injury can result from excessive stretching or avulsion injury during labor
due to shoulder dystocia. Other causes for brachial plexus injury may include shoulder
trauma, excessive stretching, and radiation to the neck. The severity of injury depends on
the extent of the nerve damage. It ranges from neurapraxia, where there is no interruption
of nerve conduction, to complete disruption of the nerve fiber.
• Nerve injury during placement of a brachial plexus block may be safeguarded against by:
– Having an awake patient who can communicate the sensation of pain and paraesthesia on
intraneural injection
– Not injecting against high resistance. This may be a sign of intraneural injection.
– Utilizing ultrasound imaging. Theoretically, it can decrease the incidence of nerve injury,
but this has yet to be demonstrated in the setting of large clinical trials.
– Not injecting local anesthetic at a neurostimulator current intensity of 0.2 mA or less
• Systemic toxicity of local anesthetic: All measures should be taken to avoid intravascular
injection of local anesthetic.
– In an awake patient, monitor for signs/symptoms of toxicity.
– Monitor vital signs and EKG.
– Intermittently aspirate during injection of the local anesthetic.
• Pneumothorax: The proximity of the pleura to the brachial plexus makes this a possibility.
Ultrasound techniques have helped revive some of the blocks that were falling out of favor
(e.g., supraclavicular block).
• Blocks above the clavicle (mainly the interscalene block and, to a lesser extent, the
supraclavicular block) may miss the lower trunk (ulnar nerve distribution) of the plexus.
• The musculocutaneous nerve is a terminal branch of the lateral cord of the brachial plexus.
It takes off from the brachial plexus sheath into the body of the coracobrachialis muscle. It
needs to be blocked separately when performing the axillary nerve block.
• The intercostobrachial nerve (T2) branch needs to be blocked separately if planning to cover
a small area in the antero-medial aspect of the arm. It is often referred to as a tourniquet
block.
• Do not perform blocks on branches that are located in tight anatomical compartments (e.g.,
ulnar nerve blocks at the sulcus ulnaris).
• The phrenic nerve proximity to the plexus explains its vulnerability to blockade during
interscalene block. Blocking unilateral diaphragmatic movement can result in significant
dyspnea in pulmonary cripples.
GRAPHS/FIGURES
FIGURE 1. Peripheral nerve anatomy. (Reused from www.asra.com/image-library-public.php)
See Table
FIGURE 2. Approaches to the brachial plexus block. (Reused from www.asra.com/image-library-public.php)
REFERENCES
1. Partridge BL, Katz J, Benirschke K, et al. Functional anatomy of the brachial plexus sheath:
Implications for anesthesia. Anesthesiology. 1987;66:743–747.
2. Thompson GE, Rorie DK. Functional anatomy of the brachial plexus sheaths. Anesthesiology.
1983;59:117–122.
• Pneumothorax
• Rotator cuff repair
CLINICAL PEARLS
• History of any neurologic injury and assessment of the extent of the nerve damage should be
documented before performing a brachial plexus block.
• Identify the distribution of nerve supply to the area involved in the surgical procedure and
apply your knowledge of anatomy of the brachial plexus when planning your regional
anesthetic.
BRADYCARDIA
BASICS
DESCRIPTION
• Bradycardia is defined as a heart rate of <60 beats per minute (bpm). It can be secondary
to:
– Organic disease
– Medications
– Vagal tone
– Healthy, well-conditioned heart
• Perioperatively, treatment may consist of a temporary or permanent pacemaker for organic
disease, or medications for other causes. Treatment is only indicated when the heart rate is
affecting the cardiac output.
EPIDEMIOLOGY
Prevalence
Third-degree atrioventricular (AV) block is highest in people >70 years of age
(approximately 5–10% of patients with heart disease).
Prevalence
• At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5–2% of healthy people. At
age 60 years, >5% of healthy individuals have PR intervals exceeding 0.20 seconds.
• Approximately 5% of patients with heart disease have first-degree AV block, and about 2%
have second-degree AV block.
Morbidity
Low heart rate observed in third-degree or Mobitz II AV block may lead to syncopal episodes
with major injuries (e.g., head trauma, hip fracture), exacerbation of congestive heart failure,
or exacerbation of ischemic heart disease symptoms due to low cardiac output.
Mortality
The mortality of patients with sick sinus syndrome is significant and not always due to
cardiac causes.
• Intrinsic causes:
– Sinus node disease
– AV node disease
– Idiopathic degeneration (aging)
– Infarction or ischemia (coronary artery disease and/or myocardial infarction [MI])
– Hypertension
– Hypoxemia
– Obstructive sleep apnea
– Myxedema
– Infiltrative diseases
– Surgical trauma
– Heart transplantation
• Extrinsic causes:
– Autonomically mediated syndromes
– Vasovagal syncope
– Pressure on the carotid sinus or carotid sinus sensitivity
– Vomiting or coughing
– Bezold–Jarisch reflex
– Hypothermia
– Increased intracranial pressure (Cushing reflex)
– Electrolyte imbalance (hypokalemia, hyperkalemia)
• Drugs:
– Sympatholytic drugs: Beta-blockers, clonidine, neostigmine
– Digoxin
– Non-dihydropyridine calcium channel blockers
– Antiarrhythmic agents (amiodarone, propafenone)
– Lithium
– Anesthetic drug overdose: succinylcholine, induction agents, neostigmine, opioids.
• Sinus bradycardia is defined as a sinus rhythm with a rate <60 bpm. It is caused by an
increase in vagal tone or a reduction in sympathetic tone. It is seen in:
– The absence of heart disease and can occur in 25–35% of asymptomatic individuals <25
years of age as well as well-conditioned athletes and some elderly patients.
– Sleep: In young and healthy patients, rates of 30 bpm and pauses of up to 2 seconds are
not uncommon.
• Sick sinus syndrome is chronic sinoatrial (SA) nodal dysfunction that can result from a
variety of causes. It is characterized by chronic, inappropriate, and often severe
bradycardia, sinus pauses, arrest, and exit block with or without appropriate atrial and
junctional escape rhythms. The failure of escape pacemakers may lead to symptomatic
bradycardia. Additionally, atrial tachyarrhythmias have been seen in >50% of cases.
– Sinus node fibrosis: The replacement of sinus node tissue by fibrous tissue may be
accompanied by degeneration and fibrosis of other parts of the conduction system
including the AV node.
– SA nodal artery disease: The artery may be narrowed by atherosclerosis, inflammatory
processes, or emboli.
– Tachycardia–bradycardia syndrome: Atrial fibrillation (AF) is the most common atrial
tachyarrhythmia, and prolonged symptomatic pauses can occur after termination of AF
that may result from tachycardia-mediated remodeling of the sinus node.
– Infiltrative diseases: The SA node may be affected by amyloidosis, scleroderma,
hemochromatosis, and rarely tumor.
– Epicardial and pericardial disease: The SA node is located near the epicardium. As a
result, diseases that involve the epicardium or pericardium (such as pericarditis and
tumors) may affect the SA nodal function.
– Inflammatory diseases: Rheumatic fever, pericarditis, diphtheria, Chagas disease, Lyme
disease, and other disorders may depress SA nodal function.
– Trauma: Cardiac trauma may affect either the SA node directly or its blood supply.
• AV blocks describe a delay or interruption in the transmission of an impulse from the atria
to the ventricles due to an anatomic or functional impairment in the conduction system. The
conduction disturbance can be transient or permanent; conduction can be delayed,
intermittent, or absent.
– First-degree AV block is slowed conduction without missed beats and results from a PR
interval >200 ms (>210 ms at slow heart rates).
– Second-degree AV block is divided into 2 types:
Mobitz type I: The block is within the AV node and there is progressive PR interval
prolongation, preceded by a nonconducted P wave. It is often transient and
asymptomatic.
Mobitz type II: The block is usually below the AV node, within the His-Purkinje system.
During normal conduction, the PR interval remains unchanged prior to the P wave.
However, there is paroxysmal failed conduction to the ventricles. This block is often
symptomatic, with the potential to progress to complete (third-degree) AV block.
– Third-degree or complete AV block may occur at the AV node, bundle of His, or bundle
branches. When third-degree AV block is present, no impulses pass between the atria and
ventricles.
– Idiopathic progressive cardiac conduction disease (i.e., fibrosis and sclerosis of the
conduction system) accounts for approximately 50% of AV blocks.
– Ischemic heart disease accounts for about 40% of cases of AV block.
– Cardiomyopathy and myocarditis can result from hypertrophic obstructive
cardiomyopathy and infiltrative processes such as amyloidosis and sarcoidosis. Causes of
myopathy include: rheumatic fever, Lyme disease, diphtheria, viruses, systemic lupus
erythematosus, toxoplasmosis, bacterial endocarditis, and syphilis.
– Congenital heart disease
– Iatrogenic AV block
Drugs: Digitalis, calcium channel blockers (especially verapamil and to a lesser extent
diltiazem), amiodarone, adenosine, and beta-blockers
Cardiac surgery
Transcatheter closure of VSD
Alcohol (ethanol) septal ablation
• Palpate the patient’s pulse, assess EKG and pulse oximetry (strength of pulse)
• Assess EKG to determine if sinus bradycardia (P wave preceded QRS complex) is present.
• Review recent events: Vagal stimulation, medications, ischemic insult, hypoxemia,
hypothermia
• Consider checking labs:
– Electrolyte levels, magnesium, calcium
– Glucose level
EKG interference
TREATMENT
• Bradycardia may be well tolerated if it develops slowly or is >50 bpm. Acute onset of
bradycardia is more likely to be symptomatic.
• Treatment should be instituted independently of the heart rate when bradycardia becomes
symptomatic. In most cases the treatment threshold lies between 30 and 40 bpm.
• Cease vagal stimulation
– Oculocardiac reflex
– Carotid sinus stimulation
– Laparoscopic insufflation of the abdomen
– Bladder catheterization
– Electroconvulsive therapy (ECT)
• Medications should be implemented when bradycardia is persistent and affecting the cardiac
output.
– Atropine is the drug of choice irrespective of the etiology
Recommended dosing: 0.5 mg IV q 3–5 minutes to a maximum of 3 mg.
Paradoxical slowing of the heart rate may be seen with doses <0.5 mg
Paradoxical AV block may occur in patients s/p heart transplantation
Should not delay implementation of external pacing for patients with poor perfusion
Use cautiously in the presence of acute coronary ischemia or MI (increased myocardial
oxygen demand)
– Glycopyrrolate
– Ephedrine
– Dopamine, epinephrine, isoproterenol
– Catecholamine infusion is an alternative for bradycardia treatment when a
bradyarrhythmia is unresponsive to or inappropriate for treatment with atropine, or while
awaiting pacemaker placement.
• Transcutaneous (TCP) or transvenous pacing: Immediate pacing might be considered in
unstable patients with high-degree AV block when IV access is not available. Additionally, if
the patient does not respond to drugs or TCP, transvenous pacing is indicated.
FOLLOW-UP
• Bradyarrhythmias that occur in the perioperative period are usually secondary to some
other cause, such as certain medications, an electrolyte disturbance, hypoxemia, vagal
stimulation, or ischemia.
• Indications for permanent pacing, regardless of associated symptoms:
– Sinus bradycardia in which symptoms are clearly related to the bradycardia (usually in
patients with a heart rate <40 bpm or frequent sinus pauses)
– Symptomatic chronotropic incompetence
– Complete (third-degree) AV block
– Advanced second-degree AV block (block of ≥2 consecutive P waves)
– Symptomatic Mobitz I or Mobitz II second-degree AV block
– Mobitz II second-degree AV block with a widened QRS or chronic bifascicular block,
regardless of symptoms
– Intraventricular conduction delays, bifascicular or left bundle-branch block with or
without first-degree AV block in the presence of syncope or a more advanced AV block.
REFERENCES
1. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life support:
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation. 2010;122(Suppl 3):S729–S767.
ADDITIONAL READING
• Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-
Based Therapy of Cardiac Rhythm Abnormalities: A report of the American College of
Cardiology/American Heart Association Task Force on Practice. J Am Coll Cardiol.
2008;51(21):e1–e62.
CODES
ICD9
• 426.0 Atrioventricular block, complete
• 426.11 First degree atrioventricular block
• 427.89 Other specified cardiac dysrhythmias
ICD10
• I44.0 Atrioventricular block, first degree
• I44.2 Atrioventricular block, complete
• R00.1 Bradycardia, unspecified
• Sick sinus syndrome
CLINICAL PEARLS
• Active bradyarrhythmias for which the patient should undergo evaluation and treatment
before noncardiac surgery include:
– High-grade AV block
– Symptomatic bradycardia
– Third-degree AV heart block
– Mobitz II AV block
• High-grade cardiac conduction abnormalities, such as complete AV block, if unanticipated,
can increase operative risk and may necessitate temporary or permanent transvenous
pacing.
• Intraventricular conduction delays, in the presence of a left or right bundle-branch block,
but lacking a history of advanced heart block or symptoms, rarely progress to complete
heart block in the perioperative period.
• Atropine is a drug of choice irrespective of the type of etiology of the bradycardia;
ephedrine and glycopyrrolate are also commonly used.
• Unstable patients require temporary or permanent pacing.
• Severe bradycardia can complicate regional anesthesia (in particular, subarachnoid or
epidural anesthesia, not necessarily with high block). Ensure volume loading, vasopressors
(early epinephrine), airway support, and left uterine displacement (parturients).
BRAIN DEATH
Stephanie Gargani, MD
BASICS
DESCRIPTION
Brain death is defined as the irreversible cessation and complete absence of critical functions
of the whole brain, including the brain stem.
EPIDEMIOLOGY
The Organ Procurement and Transplantation Network identified the following causes of death
for donors from January 1, 1988 to November 30, 2010:
• All causes: 138,321
• Anoxia: 16,578
• CVA/stroke: 45,892
• Head trauma: 44,538
• CNS tumor: 883
• Other: 2,618
• Not reported: 119
• Not collected prior to 4/1/94: 27,693
Can be classified as either primary or secondary (see below)
• The pathogenesis of brain death consists of primary and secondary causes:
– Primary or direct causes destroy neurons. They include severe head injury, expanding
intracranial mass lesions, hemorrhagic or ischemic stroke, and anoxia/asphyxia.
– Secondary or indirect causes add volume to an already enclosed space and further increase
intracranial pressure (ICP). As the pressure increases, it exceeds the mean arterial blood
pressure and intracranial circulation will cease. This further impairs perfusion and
compounds ischemia, neuronal injury, and brain death.
– Several days later, intracranial pressure falls, and this allows for blood flow through the
necrotic brain. Due to the ability to more rapidly diagnose brain death, evidence of frank
necrosis is less often seen (1).
Prevention of the underlying cause of brain injury is the main goal. If injury has occurred,
preventing further increases in ischemia, intracranial pressure, edema, and or bleeding is
critical.
DIAGNOSIS
• The American Academy of Neurology’s criteria for clinical diagnosis of brain death (2)
includes prerequisites, 3 cardinal findings, and an apnea test.
• Prerequisites:
– Clinical or neuroimaging evidence of an acute CNS catastrophe that is compatible with the
clinical diagnosis of brain death
– Exclusion of complicating medical conditions that may confound clinical assessment (no
severe electrolyte, acid–base, or endocrine disturbance)
– No drug intoxication or poisoning
– Core temperature ≥32°C (90°F)
• The 3 cardinal findings in brain death:
– Coma or unresponsiveness: No cerebral motor response to pain in all extremities
– Absence of brainstem reflexes:
Pupils will have no response to bright light; the size ranges from midposition (4 mm) to
dilated (9 mm).
Ocular movement: No oculocephalic reflex (testing should be avoided in patients with
cervical spine fracture or instability) and no deviation of the eyes to irrigation in each
ear with 50 mL of cold water (allow 1 minute after injection and at least 5 minutes
between testing on each side)
Facial sensation and facial motor response: No corneal reflex to touch with a throat
swab, no jaw reflex, no grimacing to deep pressure on nail bed, supraorbital ridge, or
temporomandibular joint
Pharyngeal and tracheal reflexes: No response after stimulation of the posterior pharynx
with tongue blade, and no cough response to bronchial suctioning
• Apnea test:
– Required prior to testing:
Core temperature ≥36.5°C or 97°F
Systolic blood pressure ≥90 mm Hg
Euvolemia (option—positive fluid balance in the previous 6 hours)
Normal PaCO2
Normal PaO2 (option—preoxygenation to obtain an arterial PaO2 of 200 mm Hg)
– Connect a pulse oximeter and disconnect the ventilator.
– Deliver 100% FIO2 at 6 L/min, into the trachea (option—place a cannula at the level of
the carina).
– Look closely for respiratory movements (abdominal or chest excursions with adequate
tidal volumes).
– Measure arterial PaO2, PaCO2, and pH after approximately 8 minutes and reconnect the
ventilator.
– If respiratory movements are absent and the arterial PaCO2 is 60 mm Hg, the apnea test
result is positive; it supports the diagnosis of brain death. An alternate measure is a 20
mm Hg increase in the PaCO2 over a baseline normal PaCO2.
– If respiratory movements are observed, the apnea test result is negative, and the test
should be repeated.
– Reconnect the ventilator if, during testing, the systolic blood pressure drops to 90 mm Hg,
the pulse oximeter indicates significant oxygen desaturation, and/or cardiac arrhythmias
are present. An arterial blood sample should be immediately drawn and analyzed. The test
is positive if the PaCO2 is 60 mm Hg or the PaCO2 increase is 20 mm Hg over baseline
normal PaCO2. The test is negative if the PaCO2 is <60 mm Hg or the PaCO2 increase is
<20 mm Hg over baseline normal PCO2; an additional confirmatory test can be
considered.
• Confirmatory tests (optional in adults, but recommended in individuals <1 year of age) (2).
– Conventional angiography
– Electroencephalography
– Transcranial Doppler
– Ultrasonography
– Technetium-99m scan
– Somatosensory-evoked potentials
• A differential diagnosis, or more so a misdiagnosis, can be possible with other syndromes
that mimic brain death (no evidence of clinical brain function). When making a diagnosis,
one must rule out:
– Drug intoxication
– Hypothermia
– Guillain–Barré syndrome
– Neuromuscular blockade
– Locked-in syndrome
TREATMENT
• There is no treatment for brain death; it is the irreversible loss of brain function.
• The correct diagnosis of brain death is critically important to ensure that:
– Unnecessary treatments and procedures are not performed.
– Families can have closure and are provided the chance to grieve.
– Critical resources are preserved, and organ donation can be planned if those are the
patient’s and family’s wishes (3).
FOLLOW-UP
There are no published reports of recovery from neurologic function after a diagnosis of brain
death using the criteria reviewed in the 1995 American Academy of Neurology practice
parameters (4).
REFERENCES
1. Nathan S, Greer D. Brain death. Semin Anesth Perioper Med Pain. 2006;225–231.
2. American Academy of Neurology. Practice parameters for determining brain death in
adults. Neurology. 1995;45:1012–1014.
3. Wijdicks EF, Varelas PN, Gronseth GS, et al. Determining brain death in adults. Neurology.
2010;74:1911–1918.
ADDITIONAL READING
• The American Academy of Neurology (AAN). www.aan.com
• The Organ Procurement and Transplantation Network. http://optn.transplant.hrsa.gov/
CODES
ICD9
348.82 Brain death
ICD10
G93.82 Brain death
CLINICAL PEARLS
• The determination of brain death is that of a clinical diagnosis.
• Pitfalls in brain death that can interfere with the diagnosis and hence require confirmatory
tests: Severe facial trauma, pre-existing papillary abnormalities, toxic levels of drugs, sleep
apnea, or severe pulmonary disease with retention of CO2.
• When determining brain death, the cause of the neurologic state must be known to be
irreversible (4).
• The majority of organ transplant donors have a diagnosis of brain death. It is possible, with
mechanical ventilation, to perfuse and maintain function of vital organs, despite the lack of
brain activity and legal death. This provides time for harvesting of organs.
BREATHING CIRCUIT
Verghese T. Cherian, MBBS, MD, FFARCSI
BASICS
DESCRIPTION
• The breathing circuit connects components of the anesthesia machine to the patient’s
airway. It maintains a bidirectional flow between the patient’s lungs and the
ventilator/reservoir bag, delivering oxygen and anesthetic agent while carrying exhaled gas
away from the patient.
• The circle system is essentially composed of:
– Fresh gas inlet
– 2 unidirectional valves
– Breathing tubes with a Y-piece
– Reservoir bag
– Canister containing CO2 absorbent
– Adjustable pressure limiting (APL) valve
• It also contains additional components:
– Pressure gauge
– Oxygen analyzer
– Positive end-expiratory pressure (PEEP) valve
– Bacterial filter
• Advantages of a circle system include:
– Relative stability of inspired gas concentration
– Conservation of respiratory moisture and heat (co-axial circuits further improve this)
– Reduction of waste in volatile anesthetics (financial savings and decreased environmental
pollution)
• Circuits are described as open, semi-open, closed, and semi-closed:
– Open circuit systems describe “non-circle” circuits such as the “open drop” technique.
Historically, cloths saturated with volatile anesthetic were applied over a patient’s face
and mouth. This technique provided little control over volatile agent delivery and is not
used today in developed countries.
– Semi-open systems describe “non-circle” circuits such as the Mapleson A, B, C, D, and E
circuits. These systems lack a scavenging system and the ability to absorb CO2; hence they
require high fresh gas flows (FGF) to prevent rebreathing of CO2. Additionally, they
cannot humidify and warm inspired gases (except the Mapleson D/Bain circuit) (1).
– Closed circuit systems are also “circle” circuits, but the FGF and volatile agent delivered
are titrated to match the patient’s consumption or uptake, respectively. CO2 is absorbed
by a CO2 absorbent; however, “extra” fresh gas flows are not scavenged.
– Semi-closed systems are “circle” circuits, have additional components, are today’s modern
circuits on anesthesia machines, and are the focus of the current chapter.
• Fresh gas inlet is positioned between the canister and inspiratory unidirectional valve.
• Unidirectional valves are lightweight discs on an annular seat which ensure movement of
gases in one direction.
• Breathing tubes are attached to the inspiratory and expiratory ports on the canister and at
the patient-end to the Y-piece. They carry gases to and from the patient. A single-limb circle
system is available wherein the inspiratory and the expiratory channels are side-by-side,
within one tube, separated by a partition.
• Reservoir bag is located diagonally across from the patient with the unidirectional valves on
either side. It provides:
– Peak inspiratory flows of ∼60 L/min, which exceeds the FGF
– A means for manual ventilation
– A “reservoir” of volatile agent; at the time of emergence, compressing and emptying the
bag aids with removal of volatile agent that can otherwise slow awakening (“rebreathing”
of agent).
• Canister containing CO2 absorbent is attached to the anesthesia machine and houses the APL
valve, fresh gas inlet, and the unidirectional valves. It is transparent to allow detection in a
change in the color of the absorbent. CO2 absorbents are available in 3 formulations:
– Soda lime: Ca(OH)2 80%, NaOH 4%, KOH 1%, silica, and kieselguhr. It has an absorbent
capacity of 26 L of CO2/100 g.
– Baralyme (discontinued in 2004 due to potential for extreme heat and fires): Ba(OH)2
20%, Ca(OH)2 80%
– Calcium hydroxide lime: Ca(OH)2, CaCl, CaSO4, polyvinylpyrrolidone. It has an absorbent
capacity of 10.2 L of CO2/100 g.
– Indicators are added to signal the exhaustion of the absorptive capacity of the absorbent,
by changing color based on the pH. Ethyl violet is a commonly used indicator which
changes from white to violet.
• APL valve is located between the expiratory unidirectional valve and the canister. Opening
pressure is 1 cm H2O at the “open” position and 60–70 cm H2O at the “closed” position.
During mechanical ventilation, the APL valve is isolated from the circuit.
• 3 essential rules are implemented in any circle system to ensure that the exhaled gases pass
through the canister for CO2 absorbent, before they are rebreathed:
– Unidirectional valves must be located between the patient and the reservoir bag, one on
the inspiratory and the other on the expiratory limb of the circuit.
– The fresh gas inflow should not enter the circuit between the patient and the expiratory
unidirectional valve.
– The APL valve cannot be located between the inspiratory unidirectional valve and the
patient.
• The positions of the other components are arranged to achieve the optimal compromise of
conservation of fresh gas, humidification and warming of inspired gases, economical use of
soda lime, and practicality.
ANATOMY
Components are arranged in a circular manner (as shown in Figure 1).
• Disadvantages of the circle system include:
– Complex design
– Multiple connections that open up the potential for misconnections, disconnections, and
leaks
– Malfunction of unidirectional valves: The open position results in rebreathing, while the
closed position can cause high airway pressure.
• In a single-limb circuit, disruption in the partition between the inspiratory and expiratory
channels will increase the dead space as well as the interaction between anesthetics and
absorbents.
• Compound A from sevoflurane usage:
– Sevoflurane may degrade to form a toxic substance named Compound A (fluoromethyl-
2,2-difluoro-1-trifluoromethyl vinyl ether) when it comes in contact with soda lime.
– This is enhanced with low FGF, increased sevoflurane concentrations, higher absorbent
temperatures, and fresh absorbent.
– In animal studies, Compound A has been shown to cause renal necrosis. However,
histologic evidence and case reports have not demonstrated this in humans. Nonetheless,
to avoid this potential, a minimum of 2 L/min FGF is often utilized.
• Carbon monoxide (CO) formation can result from prolonged contact between absorbent and
anesthetic.
– The amount increases with the use of desiccated absorbent, use of baralyme compared to
soda lime, higher temperature of the absorbent, higher anesthetic concentrations, and low
FGF rates.
– Increased production is also dependent on the type of volatile anesthetic, with desflurane
≥ enflurane > isoflurane > halothane = sevoflurane.
• Fire within the canister can result when sevoflurane is administered with desiccated
baralyme, higher temperature of the absorbent, higher anesthetic concentration, and low
FGF rates. Indicators of a decomposition reaction between sevoflurane and absorbent
include a rapid change in color of the absorbent or a slow rise in inhaled sevoflurane
concentration compared to the vaporizer concentration control dial setting.
• Oxygen
– The oxygen consumption for most patients is 200–250 mL/min; FGF should be adequate
to replace this (in a closed circuit system, the FGF needs to match this).
– Pre-oxygenation is achieved in 3 minutes with an oxygen flow of 5 L/min.
• Fresh gas flow
– High flow >1,000 mL/min
– Low flow <1,000 mL/min
– Minimal flow <500 mL/min
– Metabolic flow = 250 mL/min
– FGF replaces the gases that are taken up by the patient and that which are vented out of
the circuit.
– In a “closed” circle system, the FGF replaces the oxygen and the anesthetics taken up by
the tissues. Initially, the tissue uptake of nitrous oxide and volatile anesthetic gases is high
but decreases with time while the uptake of oxygen is maintained. This can be partially
overcome by providing a higher FGF (3 L/min) for the initial 15 minutes, which
corresponds to the period of peak tissue uptake, before initiating “minimal” flow of
oxygen.
• Carbon dioxide
– In clinical settings, the arterial CO2 is dependent on the minute ventilation rather than the
FGF, unlike in the Mapleson circuit.
– In a circle system, rebreathing is possible if the absorbent is exhausted or if the
unidirectional valve is stuck in the open position. This will appear as “high” inspired CO2
on the ETCO2 monitor.
• The dead space extends from the patient port of the Y-piece to the partition between the
breathing tubes.
• Thus, any gadget (filter, ETCO2 adapter) between the Y-piece and the patient would increase
the dead space, unacceptably, in a small child.
• Calculation of actual minute ventilation may be difficult due to the compression of the gases
within the distensible corrugated tubes. Therefore, in pediatric patients, short, thinner tubes
are used with a standard canister.
• Checking the integrity of the circle system:
– The “leak” test involves closing the APL valve and Y-piece while using the oxygen flush to
pressurize the system to at least 30 cm H2O. If the pressure in the system is maintained for
10 seconds, it can be considered leak-free.
– The “flow” test involves attaching the reservoir bag to the Y-piece and ventilating using
the mechanical ventilator. Cyclical inflation and deflation of the bag ensures a patent
circuit with functioning unidirectional valves.
• The integrity of the circle system is checked during the “self-test” which is incorporated into
newer anesthesia workstations.
• The in-line pressure gauge monitors the pressure in the circuit, and the in-line oxygen
analyzer measures the percentage of oxygen delivered.
GRAPHS/FIGURES
CIRCLESYSTEM
REFERENCES
1. Taha S, El-Khatib M, Siddik-Sayyid S, et al. Preoxygenation with the Mapleson D system
requires higher oxygen flows than Mapleson A or circle systems. Can J Anaesth.
2007;54(2):141–145.
2. Feldman JM. Managing fresh gas flow to reduce environmental contamination. Anesth
Analg. 2012 March 13.
ADDITIONAL READING
• Dorsch JA, Dorsch SE, eds. The circle system. In: Understanding anesthesia equipment, 5th
ed. Philadelphia: Wolters Kluwer, 2008:223.
• Alveoli
• Alveolar
• Dead space
• CO2 transport
• Oxygen analyzers on the anesthesia machine
CLINICAL PEARLS
• There are 3 essential rules to ensure that the exhaled gases pass through the canister for the
CO2 absorbent before they are rebreathed:
– A unidirectional valve must be located between the patient and the reservoir bag, one on
the inspiratory and the other on the expiratory limb of the circuit.
– The fresh gas inflow should not enter the circuit between the patient and the expiratory
unidirectional valve.
– The APL valve cannot be located between the inspiratory unidirectional valve and the
patient.
• In clinical settings, the arterial CO2 is dependent on the minute ventilation rather than the
FGF, unlike in the Mapleson circuits.
• The use of low FGF and closed circuits can decrease the ecotoxicologic effects (ozone
depletion, global warming) of volatile agents and nitrous oxide (2).
BRONCHIECTASIS
BASICS
DESCRIPTION
• The term “bronchiectasis” stems from the Greek words bronchus (windpipe) and ektasis
(stretching).
• It is a disease state of abnormal and irreversible dilation of bronchial tree branches which
results from congenital airway syndromes (e.g., cystic fibrosis) or acquired causes (recurrent
bronchial infections).
• Bronchiectasis is characterized by a chronic neutrophilic inflammation and secretory
response, with excessive and tenacious mucous production leading to an obstructive defect.
• Exacerbations can lead to respiratory failure.
EPIDEMIOLOGY
Incidence
• 1–10 per 100,000 people
• In the pre-antibiotic era, onset was usually in childhood; in modern times, it is more
commonly diagnosed in adults.
Prevalence
• In the US: 100,000–200,000 persons
• It has decreased in modern times with the use of antibiotics, but diagnosis is again
increasing with more frequent use of high-resolution CT imaging (allows for improved
detection).
• Slightly Female > Male.
Morbidity
• Severity and frequency of symptoms is highly variable.
• One large study showed an average of 1.5 exacerbations per year per patient.
Mortality
• In the US: Approximately 1,000 per year
• Mortality rate is similar to that for asthma or chronic obstructive pulmonary disease
(COPD).
• Postinfectious (recurrent or persistent respiratory infections):
– Bacterial
– Viral
– Fungal
• Bronchial obstruction
• Congenital diseases:
– Cystic fibrosis (CF) (most common)
– Kartagener’s syndrome (also known as primary ciliary dyskinesia) can present as
bronchiectasis, situs inversus, and chronic sinusitus.
– Other mucociliary defects
– Alpha-1-antitrypsin deficiency
– Immunodeficiency states
• Chronic aspiration or gastroesophageal reflux
• Idiopathic
• May be a feature of:
– COPD
– Asthma
– Sarcoidosis and other autoimmune diseases
– Bronchiolitis obliterans
PATHOPHYSIOLOGY
• Although there are numerous etiologies, the common pathway is chronic bronchial
inflammation and recurrent cycles of airway infection.
• Persistent inflammatory infiltration of muscle layers and supportive airway cartilage leads to
the replacement of elastic tissue with fibrous tissue, causing irreversible dilation of
bronchial branches. Can be localized or diffuse.
• Chronic inflammation leads to:
– Mucous gland hypertrophy
– Lymphoid hyperplasia
– Impaired ciliary function
– Copious purulent secretions
– Increased vascularity of pulmonary mucosa, with extensive collateral blood flow
• Pulmonary function testing reveals:
– Obstructive airflow defects (due to secretions and lymphadenopathy): Decreased FEV1,
FEV1/FVC, increased residual volume. Progressive pulmonary decline shows an average
FEV1 decrease of 1–3% per year (~50 mL/year in adults).
– Restrictive defects can be seen in advanced cases.
• Generally results in poor pulmonary reserve
• Assess severity of disease and current exacerbations
• Optimize pulmonary function
• Assume poor pulmonary reserve
– Anticipate intraoperative airway secretions, obstruction, possibility of hemoptysis or
pneumothorax, and progressive respiratory compromise
– Anticipate possible postoperative pulmonary complications
SYMPTOMS
• Chronic productive “wet” cough
• Constitutional symptoms:
– Fatigue
– Weight loss
• Hemoptysis
History
• Age of onset
• Underlying etiology
• Frequency of cough
• Daily sputum production
• Frequency of exacerbations
• Hospitalizations
• Hemoptysis
Signs/Physical Exam
• Wet cough
• Sputum production
• Respiratory noises (wheezes, rales)
• Cyanosis
• Clubbing of the digits, if extreme
TREATMENT HISTORY
• Individualized for etiology and course; elucidate treatment history for both chronic course
and exacerbations.
• Pulmonary hygiene to expel mucous and open up airways:
– Chest PT
– Postural drainage
– Cough assistance
• Surgical options:
– Bronchoalveolar lavage
– Resection for failed medical therapy or for uncontrolled hemoptysis
• Lung transplantation
MEDICATIONS
• Antimicrobials, guided by sputum microbiology (1)[A]
• Anti-inflammatory
– Inhaled corticosteroids (2)[B]
– Oral corticosteroids
– Oral macrolides
– Inhaled NSAIDs
• Bronchodilators:
– Beta-agonists
– Anticholinergics
– Theophylline
– Leukotriene antagonists
• Inhaled mucolytics
Labs/Studies
• High-resolution chest CT (gold standard) shows bronchial dilatation, bronchial wall
thickening, “tram lines” or “signet ring” formations.
• CXR may show bronchial dilatation, atelectasis, bronchial wall thickening, hyperinflation,
and cysts.
• Flexible fiberoptic bronchoscopy
• Pulmonary function testing
• Consider ABG (PaO2 and PaCO2)
• Sputum culture
• WBC count (look for current infection)
• Temperature (look for current infection)
• Immunoglobulin levels (look for immunodeficiencies)
• Consider echocardiographic assessment of right heart function
Chronic hypoxemia may lead to pulmonary vasoconstriction, pulmonary hypertension, and
right heart dysfunction, e.g., cor pulmonale.
Postpone elective surgery if acute exacerbation, e.g., active infection, hemoptysis, worsening
productive cough.
CLASSIFICATIONS
Commonly associated with cystic fibrosis, so often designated as “CF” or “non-CF”
bronchiectasis
TREATMENT
Premedications
• Consider avoiding sedatives if moderate-to-severe disease, due to poor pulmonary reserve
• Consider bronchodilators
• Stress dose steroids if recent steroid therapy
INTRAOPERATIVE CARE
• Regional anesthesia as a sole technique, if appropriate, has the benefit of avoiding airway
instrumentation and the need for positive pressure ventilation.
• Regional anesthesia in combination with general anesthesia can decrease the need for
systemic opioids. Neuraxial techniques can improve postoperative deep breathing and
pulmonary mechanics.
• Goal is to maintain optimal pulmonary function in the setting of chronically poor pulmonary
reserve.
Monitors
• Consider arterial line for ABGs
• Vigilance for capnograph changes; sloping in the plateau portion of the waveform suggests
obstruction.
• Caution with nasal intubations due to the possibility of chronic sinusitis
• Achieve deep anesthesia prior to airway instrumentation or surgical stimulation to minimize
coughing and airway reactivity.
– Although ketamine is a potent intravenous bronchodilator, it can increase secretions and is
undesirable.
– Consider mask ventilating with volatile agents to achieve bronchodilation prior to airway
instrumentation.
– Ensure adequate dosing and onset time for neuromuscular blockade.
• For pulmonary surgery, lung isolation is needed to minimize the transfer of infected
secretions from bronchiectatic regions to healthy lung tissue.
Maintenance
• Careful, frequent suctioning due to increased quantity and tenacity of airway secretions
• Humidify inhaled gases to soften secretions
• Vigilance for bronchospasm/obstruction; the capnograph tracing should be closely
monitored. Treat bronchospasm by:
– Deepening the anesthetic with increased volatile agent (potent bronchodilators)
– Deepening the anesthetic with intravenous agents (e.g., propofol)
– Administering inhaled beta-agonists
• Be vigilant for the possibility of hemoptysis due to increased vascularity of bronchiectatic
lung tissue, pneumothorax, and spillage of suppurative secretions from bronchiectatic areas
to healthy pulmonary tissues.
• Usual extubation criteria, with vigilance for secretions and awareness of elevated risk for
postoperative respiratory distress.
• Antimuscarinics may thicken secretions; consider reducing the dose if appropriate.
POSTOPERATIVE CARE
BED ACUITY
• Disposition depends on the patient’s preoperative condition, surgical procedure,
intraoperative course, and airway condition.
• Frequent careful suctioning
• Incentive spirometry
• Supplemental oxygen
• Monitor for respiratory distress
• Consider ABG for PaO2 and PaCO2, as appropriate
• Chest radiography
• Echocardiogram, if concern for right heart failure
COMPLICATIONS
• Fever (e.g., pneumonitis from suppurative secretion, spillage into previously healthy lung
tissue, or bacteremia from airway manipulation)
• Respiratory distress/failure:
– Hypoxemia
– Hypercarbia
– Respiratory acidosis
– Retained secretions
REFERENCES
1. Evans DJ, Bara A, Greenstone M. Prolonged antibiotics for purulent bronchiectasis in
children and adults. Cochrane Database Syst Rev. 2007;2:CD001392.
2. apur N, Bell S, Kolbe J, et al. Inhaled steroids for bronchiectasis. Cochrane Database Syst
Rev. 2009;1:CD000996.
3. O’Donnell AE. Bronchiectasis. Chest. 2008;134:815–823.
4. Redding GJ. Bronchiectasis in children. Pediatr Clin N Am. 2009;56:157–171.
• Asthma
• Cor pulmonale
• Cystic fibrosis
CODES
ICD9
• 494.0 Bronchiectasis without acute exacerbation
• 494.1 Bronchiectasis with acute exacerbation
• 748.61 Congenital bronchiectasis
ICD10
• J47.1 Bronchiectasis with (acute) exacerbation
• J47.9 Bronchiectasis, uncomplicated
• Q33.4 Congenital bronchiectasis
CLINICAL PEARLS
• Clinical presentation is variable; a high-resolution CT is the gold standard for diagnosis.
• Diverse underlying etiologies mean there is no universal treatment. Additionally, there is
sparse, high-quality, randomized controlled trial data available regarding the efficacy of
particular treatment strategies for bronchiectasis, especially in children.
• Avoid elective surgery during exacerbations
• Airway secretions of increased volume and tenacity can complicate the entire perioperative
course.
• Similar to asthma and COPD, bronchiectasis increases the postoperative risk for respiratory
compromise.
BRONCHOSCOPY, FLEXIBLE AND RIGID
BASICS
DESCRIPTION
General
• In the operating room (OR), bronchoscopies are typically performed by interventional
pulmonologists or thoracic surgeons (and by intensivists in the ICU) for a myriad of
indications:
– Visual inspection of the airway to assess for dynamic airflow obstruction, tumor, source of
bleeding, glottic dysfunction or edema, or bronchial disruption (3)
– Biopsy for diagnosis of intrabronchial or peribronchial lesions (via endobronchial
ultrasound)
– Injection of collagen for vocal cord paralysis
– Placement or revision of a stent for airway mass or collapse
– Ablation of airway lesion
– Retrieval of foreign body
– Assessment of airway bleeding
– Emergent airway stenting in acute obstruction (e.g., mediastinal mass)
– As a component of pan-endoscopy surveillance for surgical evaluation of head and neck
cancer for esophagoscopy with dilation of stricture
– Laser ablation of airway papilloma
• An increasingly wide range of procedures can be performed via flexible bronchoscopy. Rigid
bronchoscopy is more invasive and tends to be reserved for more aggressive interventional
procedures such as stent placement.
Incision
None
Approximate Time
15 minutes to 2 hours
EBL Expected
Minimal except in bleeding mass, hemoptysis, or resection
Hospital Stay
Typically outpatient unless coexisting disease or primary illness necessitates otherwise
• Laser in some procedures
• Endobronchial ultrasound equipment
• Pathology/cytology availability
• High-frequency jet ventilator
• Airway catheters and tube exchangers such as Aintree intubation catheter
• Small and large bore endotracheal tubes (4, 5, 6, 9 mm and MLT) depending on surgeon
preference
• Nebulizer
EPIDEMIOLOGY
Prevalence
Majority of procedures are in patients with lung disease, especially lung cancer.
Morbidity
• Sore throat
• Bleeding or hematoma
• Airway swelling
• Severe coughing
• Obstruction
• Aspiration
• Tracheal/bronchial disruption from mucosal tear
Mortality
Rare
• Broad range of anesthetic options. Anesthetic plan should be formulated only after direct
consultation with the surgical team as to type of procedure planned, patient comorbidities,
and risk level for maintaining airway patency.
• Challenging airways with limited pulmonary reserve should be assumed.
• Multiple different airway devices and modalities may be used in a single procedure. Be
prepared for alternative strategies.
SYMPTOMS
• Dysphagia
• Hoarseness
• Dyspnea and positional effects
• Hemoptysis
• GERD
• Asthma
• Cough
History
Underlying disease and prior treatment
Signs/Physical Exam
• Airway exam with history of obstruction
• Clubbing
• Pulse oximetry <92% on room air
• Tachypnea or stridor
• Weak cough
• Inability to lie flat
• Fever (concomitant pneumonia)
MEDICATIONS
• Home oxygen
• Antibiotics for active pneumonia
• Inhalers (beta-agonists, steroids, anticholinergics)
• Systemic steroids
• Surgeon may desire discontinuation of NSAIDs depending on risk factors.
Labs/Studies
• CBC (hemoglobin and white blood count)
• Chemistry panel (assess [HCO3-])
• Flow-volume loops if concern for dynamic obstruction
• Chest radiograph (active infection, pleural or pericardial effusion, pulmonary edema)
• CT scan may be available and can aid with assessing anatomy of lesions or potential
difficulties with ventilation or securing the airway.
• If the underlying pathology is associated with COPD or intrinsic lung disease, the patient
may demonstrate pulmonary hypertension and cardiac dysfunction from chronic
hypoxemia.
• Decreased pulmonary volumes and capacities secondary to prior lung surgery or intrinsic
lung disease
TREATMENT
Premedications
• Consider midazolam (caution in chronic hypoxemia or airway lesion prior to OR)
• Consider glycopyrrolate to diminish secretions (caution for tachycardia)
• Consider nebulized lidocaine (8 mL of 2% solution over 15–20 minutes) in the holding area
• Patients with significant disease, poor functional status, or extensive procedure may require
postoperative intubation and should be counseled.
• If starting the case with sedation, patients should be counseled that amnesia may be
incomplete.
INTRAOPERATIVE CARE
• Flexible bronchoscopy: It is common to start with topicalization with or without sedation for
the initial assessment and progress to general anesthesia, as necessary. The maintenance of
spontaneous ventilation is often advantageous during functional assessment and may be
crucial in patients with severe obstruction.
• Rigid bronchoscopy invariably requires general anesthesia. Muscle relaxation is not
essential, but immobility is imperative to avoid traumatic injury to teeth, glottis, or
tracheobronchial tree.
Monitors
• Consider invasive arterial monitoring for serial ABGs in patients with poor baseline function
undergoing long procedures.
• Processed EEG for high-risk patients (rapid swings in stimulus level) should be considered.
The avoidance of muscle relaxants may further facilitate identification of inadequate depth
of anesthesia.
• During sedation, continuous capnometry should be monitored.
• Strongly consider pre-induction topicalization with nebulized lidocaine and/or targeted
nerve blocks for both awake and asleep procedures. The total dose of lidocaine should be
monitored (doses may need to be decreased in patients with liver disease). The patient
should be monitored for local anesthetic systemic toxicity.
• Most procedures are performed with the bed rotated to 90° away from the anaesthetist;
starting in this position will facilitate immediate intervention by the proceduralist.
• For sedation, agent selection should focus on the goals for the individual patient. Many
approaches will produce suitable results, and the key is to achieve a smooth equilibrium to
avoid bolusing at unfavorable points during the procedure.
– Remifentanil infusion can be considered (0.25–0.5 mcg/kg bolus followed by 0.05
mcg/kg/min) and titrated in increments of 0.02 mcg/kg/min every 3–5 minutes to attain
the desired effect (1)[A]. The key is slow titration to allow CO2 levels to build as the
apneic threshold is raised, provide immobility, and blunt the cough reflex. Chest wall
rigidity or glottic spasm is possible with high doses. The addition of benzodiazepines to
this infusion will have unpredictable effects and may exaggerate sedation levels.
– Dexmedetomidine infusion is very effective for the maintenance of respiratory drive and
following commands (1)[A]. Consider a slow loading dose of 0.5–1.0 mcg/kg over 10
minutes prior to a maintenance dose of 0.3–1.0 mcg/kg/h. Upper airway obstruction can
still be observed, but the patient should remain responsive. Amnesia is unreliable.
– Ketamine (0.5 mg/kg bolus; 3–10 mcg/kg/min) can be combined with dexmedetomidine
for added hypnosis and analgesia with limited respiratory effects for stimulating
procedures (1)[A]. Consider co-administration of an antisialagogue to decrease secretions.
• General anesthesia is typically induced via intravenous medications, unless the goal is to
maintain spontaneous ventilation for any part of the procedure (e.g., foreign body removal,
tracheal stenosis, tracheomalacia, anterior mediastinal mass).
• Airway
– Flexible bronchoscopy: The airway can be readily secured with a disposable, classic LMA.
A bronchoscope adapter should be available to facilitate simultaneous ventilation and
bronchoscopy; supportive struts, if present, should be cut away. Alternatively, a small,
uncuffed (or deflated) endotracheal tube may be placed.
– Rigid bronchoscopy: A small, uncuffed (or deflated) endotracheal tube may be placed and
the rigid scope inserted alongside it. Alternatively, air entrainment or jet ventilation via
the side-port of the rigid bronchoscope may be utilized.
Jet ventilation will deliver more reliable ventilation than standard positive pressure
ventilation via an endotracheal tube in a partially open circuit. Automated jet ventilators
with pressure alarms should be strongly considered to limit the risk of barotrauma (2).
Maintenance
• The procedure necessitates frequent disconnection from the ventilation circuit, repositioning
of airway devices, and introduction of airway instruments. If inhaled anesthesia is used,
delivery will be variable and significant room contamination is unavoidable. To that extent,
intravenous maintenance is strongly preferred unless spontaneous ventilation is desired.
• Avoid long-acting opioids as post-procedure respiratory compromise is to be expected.
• Local anesthetic in the airway will provide adequate pain relief in most cases.
• Consider dexamethasone for dual-agent postoperative nausea/vomiting prophylaxis and
modulation of edema.
• Consider placing a processed EEG if total intravenous maintenance is used with muscle
relaxation.
• After a general anesthetic, the goal is to confirm adequate recovery of respiratory function
prior to extubation of LMA removal.
• Suctioning of the airway should be done before extubation to remove any accumulated
blood.
• In patients who are significantly compromised at baseline or following an extensive
procedure, postoperative intubation should be strongly considered. Communicate with the
surgeon to confirm clinical impressions and the extent of procedure.
POSTOPERATIVE CARE
BED ACUITY
• Continuous pulse oximeter monitoring for patients on chronic oxygen
ANALGESIA
• Acetaminophen
• Short-acting opioids if needed
COMPLICATIONS
• Respiratory failure with hypercarbia, hypoxemia, aspiration
• Bleeding in the airway
• Tracheal or bronchial tear with mediastinal emphysema or crepitus
• Glottic trauma or edema; particularly from rigid scope
• Dislodged airway stent
• Dental injury
REFERENCES
1. Atkins JH, Mirza N. Anesthestic considerations and surgical caveats for upper airway
surgery. Anesthesiol Clin. 2010;28(3):555–575.
2. Hautmann H, Gamarra F, Henke M, et al. High frequency jet ventilation in interventional
fiberoptic bronchoscopy. Anesth Analg. 2000;90(6):1436–1440.
3. Conacher ID. Anaesthesia and tracheobronchial stenting for central airway obstruction in
adults. Br J Anaesth. 2003;90(3):367–374.
ADDITIONAL READING
• Pawlowski J, Pratt SD. Anesthesia for bronchoscopy. In: Ernst A, ed. Introduction to
bronchoscopy. New York, NY: Cambridge University Press, 2009.
• Jet ventilation
CLINICAL PEARLS
• Bronchoscopies are performed for such a wide range of indications and conditions that a
clear appreciation of the goals and needs of the proceduralist must be achieved prior to the
start of anesthesia care.
• There is no substitute for adequate topical anesthesia of the airway when bronchoscopy is
performed under sedation or general anesthesia with spontaneous ventilation.
• Be prepared for departure from the original anesthetic plan as the scope of the procedure
commonly changes as a result of the initial diagnostic assessment (e.g., flexible
bronchoscopy followed by a rigid bronchoscopy with dilation and stenting).
BUFFERING SYSTEMS
Carlee Clark, MD
BASICS
DESCRIPTION
• Biochemical and metabolic functions occur most optimally within a narrow pH range (7.35–
7.45). Acidosis and alkalosis, therefore, have significant physiologic impact such as
neurophysiologic dysfunction as well as decreased inotropy, enzyme activity, cerebral and
myocardial microperfusion, and catecholamine efficacy. Additionally, the oxyhemoglobin
curve shifts and electrolyte abnormalities occur.
• Acid–base buffering systems within the body serve to keep the physiologic concentration of
hydrogen ions (H+) constant; they serve as a reservoir or cushion. There are several systems
that provide overlap and graduated lines of defense against pH disturbances. They include
chemical (bicarbonate, proteins, phosphate), respiratory, renal, liver, and bone buffering
systems.
• Despite their large capacity, when buffering systems fail or are overwhelmed, pH and
physiologic abnormalities manifest. The pH range required for compatibility with life is
between 6.8 and 7.8.
• Acids are compounds that contain hydrogen and release H+ when dissolved in solution;
they are proton producers or “donors.” The terms “strong” and “weak” refer to the donor’s
“willingness” or “ability” to donate the H+. A strong acid readily dissociates its H+ from
the conjugate base (A−; anion). A weak acid does not easily donate its H+ and will exist
mostly in the HA form.
• Bases are compounds that contain hydroxide and release hydroxide ion (OH−) when
dissolved in solution; they are OH− producers, or conversely H+ acceptors. A strong base
readily dissociates its OH− from the conjugate acid (C+; cation). A weak base does not
easily donate its OH− and will exist mostly in its COH form.
• The concentration of H+ in distilled water is very small (0.0000001 mol/L, or 10−7 mol/L).
The concept of pH provides a useful way of describing these small values in a
comprehensible manner; pH is a negative logarithm of the concentration of H+ (equation
1). A decrease in pH signifies an increase of H+ and vice versa.
– pH = log 1/[H+]
– [H+] = 0.0000001 = pH of 7
• Neutralization of acids and bases occur when they bind to a conjugate base or acid,
respectively. An example of this is H+ + OH− → H2O, where the free H+ and OH−
disappear and the pH does not change. This is the concept behind buffering systems.
• Buffering capacity describes the capability of a buffering system to neutralize acid or base.
The capacity increases when there is an increase in the number of buffer molecules ready to
bind additional H+ (or OH−).
• Chemical buffering systems are the body’s first line of defense against acid–base
abnormalities. They act within seconds to minutes, with the purpose of minimizing changes
in pH when an acid or base is added. Buffering solutions comprise either a weak acid and its
conjugate base or a weak base and its conjugate acid.
– Bicarbonate (HCO3−) and carbonic acid (H2CO3) are abundant in the extracellular fluid
(ECF) making this the most important buffer system in the ECF for noncarbonic acids (1).
The CO2/HCO3− buffer ratio is 1:20; however, the ability for CO2 to be eliminated by
ventilation changes it from a “closed” to an “open” system. Alveolar ventilation self-
adjusts to keep the pCO2 constant. Additionally, the renal system is capable of adjusting
the HCO3− concentration.
– Proteins are important buffers of the intracellular space because they contain both acidic
and basic groups to combine with H+ or OH−.
– Hemoglobin molecules buffer H+ from carbonic acids; it has a buffering capacity 5–6
times that of plasma proteins. The hemoglobin molecule can bind either O2
(oxyhemoglobin) or H+ (deoxyhemoglobin) at any given time, but not both; additionally,
binding of one results in release of the other (this exchange/trade is known as the Bohr
effect). This is physiologically advantageous; in the the peripheral circulation where H+ is
increased from tissue metabolism, O2 is unloaded to the tissue.
– Amino groups of intracellular proteins have pK values close to the physiologic pH,
rendering these substances important intracellular buffers.
– Phosphate exists in several compartments: Blood/intravascular, intracellular, and urine.
With a pKa of 6.9, H2PO4− readily binds to H+. Intracellularly, phosphate is present in
high concentrations, and plays an important buffering role. However, in extracellular
compartments, its low concentration relegates it to a more minor role. Phosphates also
contribute to H+ excretion in the renal tubules.
• Respiratory system: During aerobic metabolism, the mitochondria generate ATP while
producing CO2 as a byproduct. CO2 is capable of easily diffusing across lipid cell
membranes into the blood stream and erythrocytes because it is not ionized or charged.
Inside erythrocytes, CO2 is converted into HCO3− via carbonic anhydrase. HCO3− is unable
to diffuse out of the erythrocyte due to its ionization (cannot cross the lipid membrane);
instead it is stored and transported from peripheral tissues to the lungs. When reaching the
lungs, HCO3− within the erythrocyte gets reversed to CO2 and diffuses into the alveolar
space to be exhaled.
– Alveolar ventilation and respiratory drive are adjusted by brainstem centers in response to
changes in pH. Because alveolar ventilation is easily increased and decreased, the range of
shifting the CO2 elimination up and down is large and the response is very fast. In
addition, this is facilitated by the almost linear CO2-binding curve in blood.
• Renal system: Although the kidneys are slower to respond to changes in pH, they have a
tremendous buffering capacity. At the glomerulus and Bowman’s capsule, HCO3− and H+
are filtrated from the blood into the renal tubule.
– In the lumen:
H+ can combine with titratable acids (HPO4−, SO4−, NH3) and be excreted.
H+ can bind to HCO3- via carbonic anhydrase (present in the lumen) to form H2O and
CO2. The CO2 readily diffuses into the renal cells and out to the capillaries (~85% of the
filtrated bicarbonate is reabsorbed in the proximal tubules).
– Aldosterone also stimulates direct H+ excretion in the collecting ducts.
• Liver metabolism: Although hepatic metabolism produces HCO3−, CO2, and NH4+
byproducts, these compounds are consumed and “buffered” during urea synthesis. In the
event of incomplete consumption, NH4+ is released into the circulation, where it is either
consumed during glutamine synthesis (which in turn facilitates renal tubular H+ excretion)
or excreted in the urine. Additionally, the liver eliminates H+ with the cleavage of lactic
acid, acetoacid, and citric acid.
• Bone: Functions as a buffer via ionic exchange (acute) and dissolution of bone crystal
(chronic). Bone “takes up” H+ in exchange for calcium, sodium, and potassium in acidemic
states. In alkalemic states, it releases HCO3−, CO3−, or HPO4−. Ionic exchange does not
involve bone breakdown and deals with acute acidosis. Chronic intracellular acidosis in
osteoclasts causes an intracellular hypocalcemia and osteoclast stimulation. The result is
bone breakdown involving the release of calcium carbonate via direct physiochemical
breakdown of crystal, which is independent of parathyroid hormone.
• GI tract: Small bowel and pancreatic exocrine secretions reverse gastric acids but are of
minor importance for the systemic buffering of the whole body.
ANATOMY
• Changes in pH are communicated between the ICF and the ECF via CO2 transfer across the
cell membrane and proton–cation exchange mechanisms. It should be noted that only the
extracellular space is clinically accessible for monitoring of test parameters.
• Regulatory organs for maintenance of acid–base balance include the:
– Lungs exhaling and excreting CO2 by adapting the alveolar ventilation to normalize PaCO2
– Circulation matching oxygen delivery to oxygen demands
– Kidneys excreting and reabsorbing acid–base relevant substances
– Liver providing metabolism and synthesis of glutamine and proteins
Acid–base imbalances result from the failure of the total of the buffering systems. Depending
on the details of the underlying cause, various outcomes of failure of the buffering system can
be described:
• Metabolic acidosis or alkalosis
• Respiratory acidosis or alkalosis
• Partial metabolically compensated respiratory acidosis or alkalosis
• Partial respiratory compensated metabolic acidosis or alkalosis
• Mixed acid-base abnormalities can involve ≥2 abnormalities.
• Patients commonly present to the operating room with disturbances in their acid–base
equilibrium, or are at-risk for abnormalities that can increase morbidity and mortality such
as:
– Hyperventilation and hypoventilation
– Anemia
– Fluid loss
– Malnutrition with low albumin
– Hyperkalemia and hypokalemia
– Gastric drainage
• Conditions in which the physiologic buffer systems fail can demand therapeutic and
pharmacologic interventions, requiring exact diagnosis of the nature of the acid–base
disturbance. These include the following:
– Blood gas analysis with pH, PCO2, [HCO3−], and base excess (BE). BE is the amount of
acid or base needed to titrate the patient’s blood to a pH of 7.4.
– Anion gap
• THAM (trome thamine) can be used when patients are unable to exhale sufficient amounts
of CO2 either spontaneously or with mechanical ventilation. About 30% of THAM has a pH
= 7.40 and is not ionized, being able to penetrate cells and act intracellularly. THAM
actively binds hydrogen ions (H+) and cations of fixed or metabolic acids and increases
bicarbonate. THAM is not recommended in patients with hyperkalemia or hyponatremia.
• Sodium bicarbonate and THAM are equal in their ability to alkalinize; the latter is shorter
lasting. Treatment of metabolic alkalosis focuses mainly on treating the underlying
pathophysiologic problem.
• Carbonic anhydrase inhibitors, which cause renal excretion of HCO3−, are also an option.
EQUATIONS
• Henderson-Hasselbach equation; rectangular brackets indicate molar concentrations
pH = –log [H+]
pH = pK + log([HCO3−] / [CO2])
• Anion gap (AG): AG = Unmeasured anions – unmeasured cations = ([Na+] + [K+]) – ([Cl
−] + [HCO −])
3
REFERENCES
1. Casey JR. Why bicarbonate? Biochem Cell Biol. 2006;84(6):930–939.
2. Adrogué HJ, Gennari FJ, Galla JH, et al. Assessing acid-base disorders. Kidney Int.
2009;76:1239–1247.
3. Fidkowski C, Helstrom J. Diagnosing metabolic acidosis in the critically ill: Bridging the
anion gap, Stewart, and base excess methods. Can J Anesth. 2009;56:247–256.
ADDITIONAL READING
• Falimirski ME. Civetta, Taylor, and Kirby’s critical care. Philadelphia: Wolters
Kluwer/Lippincott Williams and Wilkins.
• Rose BD, Post TW. Clinical physiology of acid-base and electrolyte disorders. New York:
McGraw-Hill Medical Publishing Division.
• Base excess
CLINICAL PEARLS
• Bicarbonate/CO2 is the most clinically relevant buffer system and is carefully regulated by
the pulmonary and renal systems.
• Perioperatively, diagnosis and monitoring of acid–base excess involves clinical assessment
and is aided by ABG draws (pH, HCO3−, and base excess).
• Treatment is aimed at the underlying cause and may be aided by exogenous bicarbonate or
THAM; however, outcomes studies have not supported this practice.
BURNS
Naola Austin, MD
Andreas Grabinsky, MD
BASICS
DESCRIPTION
• Anesthesia providers are critical members of the multidisciplinary team that is required to
treat patients with severe burn injuries, as well as burn reconstruction procedures.
• Severe burns affect every organ system, present multiple medical and psychological
challenges, and must be treated with prompt and vigilant care.
EPIDEMIOLOGY
Prevalence
In the US: 700,000/year; males: 70%, females: 30%; children <5 years: 17%; patients >60
years: 12%
Prevalence
• Mild burns: 600/100,000 inhabitants
• Severe burns: 5/100,000 inhabitants
Morbidity
Chronic pain, cosmetic consequences, contractures with resultant loss of limb function, long-
term rehabilitation, need for repeat surgeries, and financial impact
Mortality
• Overall mortality is 3.7% and increases with advancing age (age <16 years: 0.3–1.0%; age
>80 years: 27.0%)
• Increases with the total body surface area (%TBSA) affected
• Increases with smoke inhalation injury
• Etiology: Fire/flame (41.6%); scald (31.0%; children are at a higher risk); contact with a hot
object (8.8%); electrical (3.8%)
• Circumstances of injury: Home (66%); accident, non-work related (66%); accident, work
related (14.6%); accident, recreation (4.8%)
• Severe inflammation has been implicated with many post-burn complications: Triggers loss
of microvascular wall integrity, intravascular plasma and protein depletion, and interstitial
edema (peak edema occurs at 24 hours).
• Inhalation injury is direct damage to the upper and lower airways and lungs from heat,
smoke, or toxic fume inhalation. Inhalation of carbon monoxide produces
carboxyhemoglobin, and inhalation of cyanide fumes causes inhibition of the mitochondrial
electron transport chain.
• If inhalation injury or airway edema is suspected, secure the airway early before worsening
edema makes intubation difficult or impossible.
• Appropriate fluid management, maintenance of normothermia, glucose control, antibiotic
prophylaxis, and ventilatory management have been shown to improve outcome in the ICU
setting; these efforts should be extended perioperatively by the anesthesia provider.
SYMPTOMS
Symptoms of inhalation injury: Voice change, dysphagia, dyspnea
History
Etiology of burn injury, risk factors for inhalation injury (closed space, loss of consciousness),
associated injuries, pre-existing medical conditions
Signs/Physical Exam
• Signs of inhalation injury include singed eyebrows or nasal hair, facial burns, facial edema,
carbonaceous sputum, respiratory distress, and inspiratory stridor.
• Standard airway exam
• Size of burned area (%TBSA)
TREATMENT HISTORY
• Airway management, intravenous access, fluids
• Dialysis in patients with acute kidney injury; early continuous veno-venous hemofiltration
may reduce 28-day mortality, acute lung injury severity, and respiratory distress (1).
• Plasma exchange therapy may decrease the inflammatory response; this is still being
investigated (2).
• Blood transfusions; patients with comorbidities are more likely to receive blood, especially
with small burn injuries (<10% TBSA) (3). However, this may increase infectious
complications and mortality. Outcome studies have not provided information on the ideal
transfusion paradigm with significant comorbidities.
MEDICATIONS
• Naltrexone for pruritus may affect intraoperative opioid requirements.
• TPN should be continued perioperatively; patients are hypermetabolic and have increased
caloric requirements.
• Sedation for intubated patients
• Narcotics
Labs/Studies
• CBC
• Complete metabolic panel
• Coagulation panel
• ABG for baseline acid–base status, lactate, and base deficit trends
• Carbon monoxide and methemoglobin levels
• Type and cross
• Baseline chest radiography
• Cardiovascular: Intravascular volume depletion, decreased systemic vascular resistance,
myocardial depression, and deep vein thrombosis
• Pulmonary: Pulmonary edema, impaired gas exchange, reduced chest wall and airway
compliance, dysfunctional cilia, respiratory failure, PNA, and ARDS
• Renal: Acute kidney injury
• Hepatic: Congestion, fatty deposition, cholestasis, centrilobular necrosis, and activation of
acute phase reactants
• Gastrointestinal: Stress ulcers, decreased motility, ileus, decreased absorption, bacterial
translocation, edema, abdominal hypertension, and compartment syndrome
• Musculoskeletal: Acute and chronic wasting, contractures
• Neuroendocrine: Hypermetabolism increases catecholamines and catabolic hormones,
oxygen demand, production of carbon dioxide, muscle wastage, and glucose derangements.
The need to treat carbon monoxide poisoning with hyperbaric oxygen should be weighed
against the need for emergent surgery.
CLASSIFICATIONS
• Degrees of burn:
– First-degree, superficial burn extends into epidermis, blanches, does not blister, and is
intensely painful.
– Second-degree, superficial partial-thickness burn extends into superficial or papillary
dermis, blanches, blisters, and is severely painful.
– Second-degree, deep partial-thickness burn extends into deep or reticular dermis, does not
blanch or blister, and is less painful.
– Third-degree, full-thickness burn extends into subcutaneous tissue or deeper, is dry like
leather or white, and is minimally painful.
• Extent of burn:
– Wallace’s Rule of Nine can be used to estimate the %TBSA burned in adults.
– The Lund–Browder chart can be used to estimate %TBSA in children.
• ABA grading system:
– Minor burns: <10% TBSA in adults, <5% TBSA in children or elderly patients, <2% full-
thickness burn
– Moderate burn: 10–20% TBSA in adults, 5–10% TBSA in children or elderly patients, 2–
5% full-thickness burn; high-voltage burn, circumferential burn, suspected inhalation
injury, concomitant medical problems
– Major burn: >20% TBSA in adults, >10% TBSA in children or elderly, >5% full-
thickness burn, high-voltage burn, known inhalation injury; any significant burn to face,
eyes, genitalia, joints or significant associated injuries
TREATMENT
Premedications
• Benzodiazepines or ketamine may relieve anxiety and decrease opiate requirements.
• Dexmedetomidine has been shown to improve the level of sedation compared to
benzodiazepines in burn patients in the ICU (4).
• If unable to provide informed consent, a legal next of kin or 2 physicians’ consent may be
required for urgent treatment.
• Patients with severe burns to the head or neck may be impossible to intubate and can
require a surgical airway.
INTRAOPERATIVE CARE
General anesthesia is required for most burn injury patients; however, regional anesthesia is
an option in selected cases.
Monitors
• Intra-arterial blood pressure; femoral artery cannulation is often used in pediatric patients.
There is a 1.9% incidence of lost pulses, some requiring thrombectomies; monitoring of
distal pulses should be performed to avoid critical ischemia (5).
• Core temperature
• Foley catheter
• Vascular access: Place large-bore IV catheters in non-burned areas whenever possible; most
patients will require central venous access once stabilized; intraosseous access is acceptable
for primary resuscitation.
• Early rapid-sequence intubation or awake fiberoptic intubation may be the safest approach
in patients with inhalation injury or airway edema.
• Succinylcholine can be used during the first 48 hours following burn injury. It should not be
used after the initial 48 hours or within 1 year of burn injury (extrajunctional receptor
proliferation).
• Non-depolarizing muscle relaxants are safe in burn injury patients.
Maintenance
• Prophylactic antibiotics; the impairment of physical barriers and an immune-compromised
state increase the likelihood of infection (Pseudomonas aeruginosa is common).
• Inhalational anesthesia or TIVA is appropriate.
• Ventilation: High FIO2 in patients with carbon monoxide poisoning. High-frequency
oscillatory ventilation has been shown to improve oxygenation with concurrent ARDS;
consider utilizing an ICU ventilator intraoperatively.
• Fluid resuscitation to treat burn shock, maintain hemodynamic stability and urine output
– Parkland formula: Lactated Ringer’s 4 mL/kg/%TBSA over 24 hours with half in the first 8
hours and the remaining half over the next 16 hours
– Modified Brooke formula: Lactated Ringer’s 2 mL/kg/%TBSA over 24 hours
– Children <20 kg: Lactated Ringer’s 3 mL/kg/%TBSA over 24 hours plus hourly
maintenance thereafter (4 mL/kg for the first 10 kg + 2 mL/kg for next 10 kg + 1
mL/kg)
– Over-resuscitation or “fluid creep” can exacerbate pulmonary edema, chest wall edema, or
compartment syndrome of limbs or abdomen. Colloids have not been shown to improve
clinical outcomes (6)[A].
– Following inhalation injury, the 24-hour fluid requirement increases (6)[A], (7)[A].
Central venous pressures and urine output can aid with management.
• Avoid hypothermia; intraoperative hypothermia during burn excision has been linked to the
development of postoperative lung inflammation. Decreases of >1°C demonstrated
increased neutrophils 24 hours postsurgery compared to normothermics (8).
• Monitor hemoglobin, electrolytes, coagulation, as well as acid–base status.
• High-dose opiates for analgesia; the increased volume of distribution reduces drug
concentrations.
• Local anesthetic infiltration is often used with epinephrine to reduce blood loss.
• Tight glucose control (blood sugars <150 mg/dL) and decreased variability have a
decreased sepsis rate and mortality in ICU patients (9). Efforts should be continued
perioperatively by the anesthesia provider.
Patients with severe burns and/or inhalation injury are likely to remain intubated after
surgery and in the ICU during the acute post-burn injury period. Studies have shown that
they have a significantly higher rate of failed extubation; 30% compared to the general ICU
population (10)[B].
FOLLOW-UP
BED ACUITY
Transfer to a burn center is indicated for: Age <5 years or >60 years; burns to the face,
hands, perineum, joints, or other areas of function; >15% TBSA partial-thickness or >5%
full-thickness burn; inhalation injury; chemical, high voltage; concomitant trauma.
Severe burn injury is a permanent, life-altering experience for the patient and his or her
family and requires a multimodal approach and often long-term support: Pain specialists,
rehabilitation medicine specialists, plastic surgeons, psychiatrists, physical therapists, social
workers, and financial counselors.
COMPLICATIONS
Pneumonia (3%), urinary tract infection (2%), wound infection (2%), respiratory failure
(3%), septicemia (2%), cellulitis (1.5%), renal failure (1%)
REFERENCES
1. hung KK, Lundy JB, Matson JR, et al. Continuous veno-venous hemofiltration in severely
burned patients with acute kidney injury: A cohort study. Crit Care. 2009;13:R62.
2. Klein MB, Edwards JA, Kramer CB, et al. The beneficial effects of plasma exchange after
severe burn injury. J Burn Care Res. 2009;30:243–248.
3. Boral L, Kowal-Vern A, Yogore M, et al. Transfusions in burn patients with/without
comorbidities. J Burn Care Res. 2009;30:268–273.
4. Talon MD, Woodson LC, Sherwood ER, et al. Intranasal dexmedetomidine premedication is
comparable with midazolam in burn children undergoing reconstructive surgery. J Burn
Care Res. 2009;30:599–605.
5. Mourot JM, Oliveira HM, Woodson LC, et al. Complications of femoral artery
catheterization in pediatric burn patients. J Burn Care Res. 2009;30:432–436.
6. Saffle JR. The phenomenon of “fluid creep” in acute burn resuscitation. J Burn Care Res.
2007;28(3):382–395.
7. Latenser BA. Critical care of the burn patient: The first 48 hours. Crit Care Med.
2009;37(10):2819–2826.
8. Oda J, Kasai K, Noborio M, et al. Hypothermia during burn surgery and postoperative
acute lung injury in extensively burned patients. J Trauma. 2009;66:1525–1529.
9. Pidcoke HF, Salinas J, Wanek SM, et al. Glucose variability is associated with high
mortality after severe burn. J Trauma. 2009;67:990–995.
10. Smailes ST, Martin RV, McVicar AJ. The incidence and outcome of extubation failure in
burn intensive care patients. J Burn Care Res. 2009;30(3):393–394.
• Airway sires
CODES
ICD9
949.0 Burn of unspecified site, unspecified degree
ICD10
T30.0 Burn of unspecified body region, unspecified degree
CLINICAL PEARLS
• Consider anesthesia “stand by” for extubation and the possibility of extubating over a small
tube exchanger to facilitate re-intubation.
BURR HOLE
Dirk Younker, MD
BASICS
DESCRIPTION
General
• Burr hole craniotomy is a minimally invasive form of an ancient surgical procedure known
as “trephination.”
• It is performed to drain epidural (EDH) or subdural (SDH) hematomas, which may be either
acute or chronic in nature.
• The scalp is reflected over the area of the hematoma to expose the skull, followed by the use
of a drill to create the hole.
• In the case of an epidural clot, coagulum is simply removed and the wound is closed; clot
expansion tends to be restrained by the compartments formed by dura adherent to cranial
sutures.
• For SDHs, the dura is incised, as clot can be diffuse due to the lack of septations in the
subdural space. Irrigation may be used to remove the hematoma; a drain may be placed to
allow for postoperative drainage.
• In extreme, life-threatening conditions, burr holes may be performed with a simple, hand-
powered, manual twist drill.
Position
• Supine with the operating table turned 90 or 180°, depending on surgical preference and
physical layout of the OR
• The patient’s face points to the ceiling if a frontal incision is used. Alternatively, the
patient’s face is turned to the anesthesia team if a right or left temporal incision is
performed. Mayfield pins are often used, but the head may also be rested upon sterile
towels.
• Rarely, prone position may be required for infratentorial exposure (cerebellar clot).
Incision
• Scalp incision in the frontal, temporal, or base of skull
• Small, dime-sized hole made with twist drill or power drill
• 80% of acute EDHs are located below an existing fracture line.
• Incision may or may not be irrigated or drained (1)[A].
Approximate Time
60 minutes; longer if substantial bleeding is encountered
EBL Expected
Minimal, unless the patient is coagulopathic
Hospital Stay
• 23-hour admission for serial neurologic examinations, perhaps longer depending on
comorbidities
• Repeat, post-procedural CT scans are common in those patients with abnormal baseline
neurologic status (e.g., a demented patient from a nursing home).
• Manual, hand-twist drill
• Power drill
• Occasionally, endoscopic visualization is employed in nonemergent situations.
EPIDEMIOLOGY
Incidence
Acute post-traumatic SDH and EDH: 0.83/100,000 population
Prevalence
• Acute post-traumatic SDH and EDH: Median age 45 years, 80% male
• Chronic SDH: Median age 60 years; male:female ratio 5.63:1
Morbidity
• Acute post-traumatic SDH and EDH: 63% good outcome at 6 months
• Chronic SDH: 95.6% good outcome following surgery (most surgeries performed under local
anesthesia with sedation)
Mortality
Acute post-traumatic SDH and EDH: 23% mortality, greatest likelihood of death if age >60
AND surgery for acute SDH (2)[A], (3)[A]
• Acute post-traumatic SDH and EDH:
– Patients may have an increased risk of aspiration
– Cervical and thoracic spine precautions must be maintained for patients with multiple
trauma
– The traumatized brain needs oxygen and an adequate perfusion pressure (maintain
oxygenation, ventilation, and blood pressure)
– The need for optimum preoperative assessment and monitoring needs to be weighed
against the need for expeditious decompression when speed is of the essence
SYMPTOMS
• Headache
• Somnolence (sleepiness)
• Localizing neurologic signs
History
• Head trauma
• Anticoagulant therapy
• Acquired disorders of hemostasis NOT involving anticoagulant therapy (e.g., TTP)
• Concomitant drug or alcohol use
• Tobacco use (these patients may have significant carboxyhemoglobin levels and may also
cough upon emergence)
Signs/Physical Exam
• Trauma (especially orofacial trauma with cervical collar present)
• Focal neurologic signs
• Obtundation
• In elderly patients, look for signs of a pacemaker or an AICD.
MEDICATIONS
• Anticoagulants
• Drugs which inhibit the metabolism of warfarin compounds (INH, amiodarone,
metronidazole, omeprazole)
Labs/Studies
• Hematocrit, platelet count, INR
• Creatinine, blood glucose, LFTs
• A type and screen should be available if one anticipates the need for component therapy.
• EKG or CXR may be helpful in stable patients with multiple comorbidities.
• In deteriorating patients, the anaesthetist may need to progress without any laboratory
studies at all and obtain them intraoperatively later.
• Renal dysfunction may prolong the activity of anticoagulants, in particular clopidogrel.
• Liver dysfunction may alter warfarin metabolism.
• Hypothermia may complicate the emergence from a general anesthetic as well as impair
coagulation.
• Pre-existing hypertension may accentuate emergence hypertension.
TREATMENT
Premedications
• Doses of premedicants must NOT be so large as to obscure the neurologic exam or depress
spontaneous ventilation; a minimalist approach is best.
• Acid aspiration prophylaxis is warranted in those patients who have not fasted.
• Urgency of surgery may preclude truly informed consent.
• Patients with chronic SDHs may have a long-standing abnormal neurologic examination
which will preclude their giving informed consent themselves; a surrogate may be needed.
• Usually, coverage for common skin flora is sufficient.
• In trauma patients with dirty wounds, polymicrobial coverage is warranted.
INTRAOPERATIVE CARE
• General endotracheal anesthesia for the multiple trauma patient or the uncooperative
patient
• Cooperative patients with chronic SDH may be managed with a scalp block and judicious
intravenous sedation.
Monitors
• Invasive arterial and central venous monitoring may be warranted in some high-acuity
patients.
• Thiopental, propofol, or etomidate is chosen on the basis of the patient’s hemodynamic
status.
• Rapid-sequence induction with succinylcholine and cricoid pressure may be indicated.
• Esmolol may be used to attenuate the sympathetic response to laryngoscopy and intubation.
• Scalp block and intravenous sedation in selected patients who are cooperative and who have
fasted; a remifentanil or dexmedetomidine infusion may be considered (4)[A].
Maintenance
• Inhalational or intravenous anesthesia, or both may be utilized.
• Sedation may be maintained with an infusion of remifentanil or dexmedetomidine.
• Awake extubation should be performed if the patient is considered a “full stomach”;
intravenous lidocaine and esmolol may be useful in the suppression of coughing and
emergence hypertension, respectively.
• Insertion of an LMA or a deep extubation may be considered in selected patients who have
fasted, to avoid coughing and bucking.
POSTOPERATIVE CARE
BED ACUITY
• Elderly patients with multiple comorbidities or those patients with severe coexisting trauma
may require ICU admission and postoperative ventilation.
• Most patients can be discharged to a floor where the nursing personnel can perform repeat
neurologic examinations (“neuro-checks”).
ANALGESIA
• Postoperative pain tends to be managed well with small doses of IV or PO opiates.
• Reliance upon large doses of opiates for postoperative pain management may obscure the
neurologic examination or accentuate the nausea to which these patients are already prone.
COMPLICATIONS
• Re-accumulation of clot
• Lingering neurologic deficits
• Malignant cerebral edema
• Wound infections
• Injury to the brain
PROGNOSIS
Return to baseline neurologic function is expected if surgery has been expeditious and
without complications, in particular for chronic SDH.
REFERENCES
1. Donovan DJ, Moquin RR, Ecklund JM. Cranial burr holes and emergency craniotomy:
Review of indications and technique. Military Med. 2006;171(1):12–19.
2. Tallon JM, Ackroyd-Stolarz S, Karim SA, et al. The epidemiology of surgically treated acute
subdural and epidural hematomas in patients with head injuries: A population-based study.
Can J Surg. 2008;51(5):339–345.
3. Yuan L, Xia J, Wu A, et al. Burr-hole craniotomy treating chronic subdural hematoma: A
report of 398 cases. Chin J Traumatol. 2010;13(5):265–269.
4. Frost EAM, Booij LHDJ. Anesthesia in the patient for awake craniotomy. Curr Opin
Anaesthesiol. 2007;20:331–335.
5. Weigel R, Schmiedek P, Krauss JK. Outcome of contemporary surgery for chronic subdural
haematoma: Evidence-based review. J Neurol Neurosurg Psychiatry. 2003;74:937–943.
CLINICAL PEARLS
• In the patient who is rapidly deteriorating, insertion of intra-arterial catheters and
supplemental intravenous catheters can wait until AFTER the operating table is turned.
• Plasma levels of local anesthetics can reach high levels following scalp block; patients rarely
become symptomatic.
• Although very rare, chronic SDHs can occur in the healthy postpartum patient, almost
always following dural puncture.
• Burr holes are appropriate for both the pediatric and adult population. Studies have
demonstrated that results are better than a formal craniotomy for drainage of chronic SDH
(5)[A].
BURST SUPPRESSION
Victor Duval, MD
BASICS
DESCRIPTION
• The burst suppression (BS) pattern on electroencephalogram (EEG) was first demonstrated
in 1936 by Derbshire et al. in response to anesthetics. The term “burst suppression” was
introduced by Swank and Watson in 1948 in experiments studying the effects of
barbiturates on EEG patterns in various areas of the brain.
• BS is a periodic pattern of high-voltage, slow, sharp, spiking complexes that are interspersed
by low-voltage (<10 mV) complexes or isoelectric periods.
• At present, BS is usually induced with barbiturates or other anesthetics in order to decrease
cerebral metabolic activity in the setting of focal ischemia or status epilepticus.
• Neuronal electrical activity accounts for 50–60% of the brain’s oxygen consumption. Thus,
suppression of electrical activity with anesthetic and sedative medications can help restore a
favorable balance between oxygen delivery and consumption.
• Technique: EEG can be monitored with as little as 1 lead in the OR or a full EEG in the ICU.
In the ICU, it can be performed by an anesthesiologist or neuromonitoring team. An
amplitude-integrated EEG (aEEG) is used to simplify long-term monitoring of brain
function. It filters the EEG and displays it on a compressed time scale, providing a simplified
method to monitor brain activity.
• BS is defined as a burst of slow, sharp, and spiking activity followed by reduced or
suppressed electrical activity. There is no universal standard; however, most clinicians aim
for an interburst interval of about 10 s.
ANATOMY
• Barbiturates bind to the GABAA receptor (a chloride ion channel) and potentiate the effect of
GABAA neurotransmitter. This results in chloride ion entry into the cell and
hyperpolarization; the action potential of postsynaptic neurons is increased and neuronal
signaling activity is decreased.
• Inhaled anesthetic agents inhibit excitatory neurotransmission and potentiate inhibitory
receptors and ion channels. This leads to decreased oxygen requirements and ATP
production associated with signaling activity.
• It has been proposed that the thalamus generates a “fundamental brain-rhythm,” which is
relatively resistant to the effects of anesthetics. Modern agents act primarily on the cerebral
cortex; thus, the characteristic BS pattern emerges at this site before thalamic suppression.
• Hypothermia: Therapeutic hypothermia (TH) following adult cardiac arrest alters prognostic
accuracy. Monitoring the EEG for BS can aid with predicting outcome and titrating
temperature; the presence of BS is associated with unfavorable outcomes.
• Encephalopathy: Burst suppression is characteristic of early myoclonic encephalopathy
(EME) and Ohtahara syndrome—2 rare and devastating CNS disorders of infancy.
– EME is characterized by erratic myoclonic activity. Simple partial seizures, general
myoclonus, and tonic spasms can also occur. Severe developmental delay, marked
hypotonia, and altered level of consciousness are consistent findings. Some patients
deteriorate into a vegetative state.
– Ohtahara syndrome is a precursor to West Syndrome and Lennox–Gastaut syndrome.
Frequent tonic spasms appear in the 1st month of life and partial motor seizures may
occur. Marked developmental delay and intractable epilepsy are common in patients who
survive beyond infancy.
• Premature infants
– Intracranial hemorrhage: BS with low voltage has a 100% positive predictive value
although a lower negative predictive value.
– Hypoxia/asphyxia: The presence of BS suggests a poor prognosis.
• Induced BS: The BS pattern on EEG can be used clinically to titrate general anesthetics to
their maximally effective dose, as well as for any procedure where there is a chance of focal
brain ischemia (e.g., aneurysm clipping, carotid endarterectomy, large intracranial masses,
etc.). However, a growing body of evidence suggests that BS doses of anesthetics, especially
barbiturates, are not necessary for optimal brain protection.
– Barbiturates: Drug metabolism is slowed at levels required to achieve BS and it may take
several hours for the patient to emerge. This typically requires postoperative
intubation/continued ventilatory support and delays neurologic examination.
Consequently, this technique has fallen out of favor in modern neurosurgical anesthesia.
– Can be induced with any inhaled or intravenous induction agent; however, evidence of
brain protection is only available with isoflurane and barbiturates.
• Seizure treatment: Seizure activity is characterized by an abnormal increase in electrical
activity that increases the demand for oxygen. This can quickly lead to ischemia. Decreasing
oxygen consumption can effectively protect neurons from injury.
• Incomplete cerebral ischemia: In this setting, areas of the brain adjacent to the ischemic
region (penumbra) may be subject to low oxygen concentrations. Since neurons in the
penumbra remain intact immediately after an infarct, decreasing their oxygen demand can
limit the extent of neurologic injury
• Global ischemia: Anesthetic-induced BS following global ischemia, such as in cardiac arrest,
has not been shown to improve neurologic outcome since brain autoregulation remains
intact and the oxygen requirements to maintain electrical activity do not increase.
• BIS: Only the EEG pattern on the BIS may be correlated; BS does not correlate with any
particular BIS number.
GRAPHS/FIGURES
FIGURE 1. Burst suppression is characterized by a periodic pattern of high-voltage, slow, sharp, spiking complexes that are
interspersed by low-voltage complexes or isoelectric periods.
REFERENCES
1. Chalak LF, Sikes NC, Mason MJ, et al. Low-voltage aEEG as predictor of intracranial
hemorrhage in preterm infants. Pedtiatr Neurol. 2011;44(5):364–369.
2. Derbyshire AJ, Rempel B, Forbes A, et al. The effects of anesthetics on action potentials in
the cerebral cortex of the cat. Am J Physiol. 1936;116:577–596.
3. Drummond J. Brain protection during anesthesia: A reader’s guide. Anesthesiology.
1993;79:877–880.
4. Henry CE, Scoville WB. Suppression-burst activity from isolated cerebral cortex in man.
EEG Clin Neurophysiol. 1952;1:1–22.
5. Judy-Fray F, Kroeger D, Oana C, et al. Cortical inhibition during burst suppression induced
with isoflurane anesthesia. J Neurosci. 2009;29:9850–9860.
6. Niedermeyer E. The burst-suppression electroencephalogram. Am J Electroneuro-diagnostic
Technol. 2009;49:333–334.
7. Oddo M, Rossetti AO. Predicting neurological outcome after cardiac arrest. Curr Opin Crit
Care. 2011;17(3):254–259.
8. Swank RL, Watson CW. Effects of barbiturates and ether on spontaneous electrical activity
of dog brain. J Neurophysiol. 1949;12:137–160.
• Cerebral aneurysm clipping
• Electroencephalogram (EEG)
• Carotid endarterectomy
CODES
ICD9
794.02 Nonspecific abnormal electroencephalogram [EEG]
ICD10
R94.01 Abnormal electroencephalogram [EEG]
CLINICAL PEARLS
• The burst suppression pattern on EEG can be used to determine maximal effector site
concentration of various anesthetics used in general anesthesia.
• Pharmacologic suppression of cortical electrical activity may be beneficial in protecting the
brain after focal ischemia but has no neuroprotective effects following global ischemia.
• Intravenous anesthetic agents, such as barbiturates, propofol, and etomidate, may be used to
decrease ICP secondary to traumatic brain injury, but they have not been shown to decrease
the extent of neurologic injury.
CARBON DIOXIDE ABSORBERS
BASICS
DESCRIPTION
• Carbon dioxide (CO2) absorbers function to remove exhaled carbon dioxide from anesthesia
breathing systems at low fresh gas flow rates. They make rebreathing of exhaled volatile
agents and oxygen possible and thus conserve anesthetic agents and reduce pollution to the
environment.
• Absorbents
– Contain a chemical mixture of alkali metal hydroxides.
– Are used in closed and semi-closed circle breathing systems.
– Are contained in clear plastic containers to allow visualization of indicator color change.
– Are available as a single canister, two canisters (placed one over the other in series), or as
pre-filled plastic disposable cartridges.
• Current absorbents include
– Soda lime
– Calcium hydroxide lime (Amsorb); does not degrade inhalational agents to compound A (a
toxic breakdown product of sevoflurane) or carbon monoxide (CO).
– Barium hydroxide lime (Baralyme); was discontinued in late 2004 due to reports of
extreme heat and incidents of fire when desiccated absorbent was exposed to sevoflurane.
• Rebreathing of CO2 can result in hypercarbia and respiratory acidosis.
• Carbon dioxide is the gaseous waste product of body metabolism that is exhaled into
anesthesia breathing circuits. Absorbents eliminate CO2 from breathing circuits, thereby
preventing rebreathing and hypercarbia.
• An ideal CO2 absorbent is
– Non-toxic
– Does not interfere with anesthetic agents
– Has good CO2 absorption capacity
– Economical
– Easy to handle
• Soda lime
– Composition by weight: 80% calcium hydroxide, 15% water vapor, 4% sodium hydroxide,
1% potassium hydroxide.
– Setting (hardness) agent: Silicates; they also reduce dust formation.
– Capacity: 26 L of CO2 per 100 g of absorbent. Absorption capacity can decrease to 10–20 L
or less when gases are channeled through low resistance areas.
– Method: Absorbs and neutralizes CO2.
– Absorption involves the following:
CO2 + H2O H2CO3 + H2O H+ HC3-
HCO3− + Ca++ yields calcium carbonate and HCO3− + Na+ yields sodium carbonate
Sodium carbonate reacts with calcium hydroxide to form sodium hydroxide
Sodium hydroxide is more soluble and chemically more active than calcium hydroxide. It
is also responsible for soda lime’s “regeneration reaction.” Regeneration can occur when
soda lime is set aside for several hours, usually overnight and then used again; it has less
absorptive capacity and is more rapidly depleted.
– Neutralization is an exothermic reaction that occurs only in the presence of water vapor in
the granules. It has been calculated that the heat produced by the neutralization of each
gram molecule of CO2 (44 g) amounts to 13,700 calories. During this chemical reaction
water is liberated.
• Amsorb
– Composition by weight: Consists primarily of calcium hydroxide and calcium chloride;
does not contain strong alkalis.
– Setting agent: Small amounts of calcium sulfate and polyvinyl pyrrolidone.
• Baralyme
– Composition by weight: Approximately 20% barium hydroxide and 80% calcium
hydroxide.
– Setting agent: Most of the moisture is present in the form of water of crystallization and
not as a film on the surface of the granules.
• pH Indicator is added to signal when the absorptive capacity of the material has been
consumed. Ethyl violet (pKa 10.3) is present in all absorbents in the US; when the pH
changes secondary to CO2 absorption, it changes from colorless to violet. However,
prolonged exposure to fluorescent lights can produce photo deactivation of the dye; this
results in a white appearing absorbent, despite decreased pH and absorptive capacity.
• Shape and size of granules. The goal is to maximize surface area without increasing
resistance and work of breathing. To that extent, granules are:
– Porous
– Not too large (otherwise would reduce the surface for absorption)
– Not too small (otherwise would increase the resistance to breathing)
– Granule size is measured by a mesh number. Soda lime consists of granules in the range of
4–8 mesh. A 4 mesh granule is able to pass through sieves that have 4 openings per linear
inch, and an 8 mesh granule is able to pass through sieves that have 8 openings per linear
inch.
• Rebreathing of CO2 with resultant hypercarbia
– Occurs when absorbent is exhausted, channeling of gases increases circuit dead space, or a
leak in the canister assembly or incompetent one-way valves cause rebreathing of CO2.
– Can increase sympathetic drive with resultant increases in BP and heart rate (increased
surgical bleeding), skin flushing, sweating, and tachyarrhythmias.
• Carbon monoxide. Volatile agents that contain a difluoromethoxy moiety can react with
conventional CO2 absorbents and generate CO gas. Clinically significant CO generation only
occurs if the absorbent is absolutely dry. Desflurane > enflurane > isoflurane >
sevoflurane.
• Sevoflurane reacts chemically with desiccated Baralyme or soda lime to produce CO and
flammable organic compounds, including methanol and formaldehyde. The reaction
produces heat that increases the rate of sevoflurane breakdown. Sevoflurane may be so
extensively consumed that maintaining an adequate depth of anesthesia becomes difficult.
• An exhausted soda lime canister does not feel warm and changes from colorless to violet.
• Loose packing of soda lime granules in a canister can cause channeling of gases and
decrease CO2 absorption (increased dead space). If the granules are too tightly packed, it
may increase the resistance to breathing.
• Rebreathing and hypercarbia can be detected by steady increases in the end-tidal CO2
(EtCO2) concentration. Blood gas analysis may show respiratory acidosis.
• Excessive heating. Rapid changes in the color of some CO2 absorbents or an unusually
delayed rise in the delivered (inspired) gas concentration of sevoflurane (compared with the
vaporizer setting) may indicate excessive heating of the CO2 absorbent canister and
chemical breakdown of sevoflurane. Extremely rare cases of spontaneous fire in the
respiratory circuit have been reported with sevoflurane and desiccated CO2 absorbent.
• Carbon monoxide cannot be detected using routine anesthesia gas monitoring; it has the
same molecular weight as nitrogen (present in air). CO symptoms can be masked by general
anesthesia and pulse oximetry cannot distinguish between carboxyhemoglobin and
oxyhemoglobin. Blood co-oximetry can detect carboxyhemoglobin levels.
• Improperly fixed canister gaskets and defective prepacks larger than factory specifications
have been reported to cause leaks in the breathing circuits.
• Prepacked disposable canisters also cause total obstruction of the circle system if the clear
plastic shipping wrapper is not removed prior to use (6). This can result in high airway
pressures and difficulty with ventilation. The airway pressure may still appear high even on
disconnecting the breathing circuit from the patient but is easy to ventilate the patient with
an AMBU bag.
• Check that canisters are fitting well in canister housing and for leaks to prevent rebreathing.
• The new CO2 absorbent Amsorb does not contain strong bases like sodium and potassium
hydroxides. This eliminates the undesirable production of CO and the nephrotoxic substance
compound A. It may also reduce the possibility of fire in the breathing circuits. Amsorb has
less absorptive capacity than strong base containing absorbents and is more expensive.
REFERENCES
1. Yamakage M, Takahashi K, Satoh JI, et al. Performance of four carbon dioxide absorbents
in experimental and clinical settings. Anesthesia. 2009;64(3):287–292.
2. Wissing H, Kuhn I, Warnken U, et al. Carbon monoxide production from desflurane,
enflurane, halothane, isoflurane and sevoflurane with dry soda lime. Anesthesiology.
2001;95:1205–1212.
3. Laster MJ, Egler El 2nd. Temperatures in soda lime during degradation of desflurane,
isoflurane and sevoflurane by dessicated soda lime. Anesth Analg. 2005;101(3):753–757.
4. Baum JA, Woehlck HJ. Interaction of inhalation anesthetics with CO2 absorbents. Best
Pract Res Anesthesiol. 2003;17(1):63–76.
5. Kharasch ED, Powers KM, Artru AA. Comparison of Amsorb, sodalime, and Baralyme
degradation of volatile anesthetics and formation of carbon monoxide and compound A in
swine in vivo. Anesthesiology. 2002;96(1):173–182.
6. Norman PH, Daley MD, Walker JR, Fusetti S. Obstruction due to retained carbon dioxide
absorber canister wrapping. Anesth Analg. 1996;83(2):425–426.
7. Bagdasarian LA, Shah NK, Sharif MK. Carbon dioxide absorber as a cause of high airway
pressures. J Clin Anesth. 2008;20(1):48–49.
• Breathing circuit
• Carbon monoxide poisoning
• Respiratory acidosis
CLINICAL PEARLS
• Carbon dioxide absorbers prevent rebreathing of CO2 and development of hypercarbia and
respiratory acidosis.
• In patients under general anesthesia, detection of inspired CO2 (iCO2) and a steady increase
in EtCO2, despite increasing minute ventilation, is suggestive of rebreathing. This may be
due to exhaustion of the absorbent (detected by change in absorbent color to violet, canister
not warm to touch) or a defect in the expiratory valve. Other causes of increased
metabolism (e.g., malignant hyperthermia and thyroid storm) should also be considered and
ruled out.
• Desiccation of the absorbent can be avoided by
– Consistent use of low-flow techniques
– Routine change of the absorbent at least weekly
– Labeling the canisters with the filling date
– Carefully closing all gas flow controls after each anesthetic is complete
– Avoiding drying out the breathing system or the anesthetic ventilator overnight by leaving
a continuous flow of gases that may pass through the canister.
CARBON DIOXIDE TRANSPORT IN BLOOD
Melissa Flanigan, DO
BASICS
DESCRIPTION
• Carbon dioxide (CO2) is a by-product of cellular metabolic pathways. Rapid diffusion of CO2
from cells into capillaries occurs despite a partial pressure of only 1–6 mm Hg, compared
with ∼64 mm Hg for oxygen.
• CO2 is transported through the blood to alveoli for excretion in three different forms:
– Dissolved in blood
– Carbamino compounds
– Bicarbonate ion
• At a cardiac output of 5 L/min, each 100 mL of blood passing through the lungs unloads 4–5
mL of CO2. The amount circulating is a function of both CO2 elimination and production.
• Transport to the lungs occurs in three different forms; the sum comprises the total CO2
content of blood. The three forms are as follows:
– Physically dissolved in plasma solution (7%). CO2 is 20 times more soluble than oxygen
and results in the rapid transfer between tissues, blood, and the alveoli. Dissolved CO2
increases linearly with increases in PaCO2.
– Carbamino compounds (13%). CO2 can enter the erythrocyte and reversibly bind with
nonionized terminal amino groups of blood-borne proteins. The resulting compound is
called carbaminohemoglobin.
The Haldane effect facilitates the passage of CO2 in the blood and excretion by the
alveoli. In tissue, deoxyhemoglobin’s increased affinity to CO2 (3.5 times greater) results
in effective uptake. In the pulmonary capillaries, oxyhemoglobin’s reduced affinity to
CO2 results in “off-loading” and excretion. This liberates CO2 that then diffuses from
pulmonary capillary blood into alveoli.
– Bicarbonate (80%)
CO2 enters the erythrocyte where it reacts with water to form carbonic acid. This
reaction is almost immediate in the presence of the enzyme carbonic anhydrase: H2O +
CO2 ←→ H2CO3 ←→ H+ + HCO3− (Note: this enzyme is absent in plasma). Most of
the hydrogen ions combine with hemoglobin, a powerful buffer.
Buffering capacity. Bicarbonate is considered the most important buffer in extracellular
fluid. It provides immediate and effective chemical buffering against metabolic acid–
base disturbances. If a strong acid is added to the extracellular fluid, bicarbonate reacts
with the H+ to produce CO2.
Chloride effect: Occurs in the venous side of capillaries. Bicarbonate ions diffuse from
erythrocytes into plasma, accompanied by the opposite movement of chloride ions into
the cells to maintain electrochemical neutrality (chloride shift). The increase in
osmotically active ions (chloride and bicarbonate) in venous erythrocytes encourages the
entry of water, thus increasing their volume. This explains why the venous hematocrit is
∼3% higher than the arterial hematocrit.
• The kidneys indirectly affect CO2 homeostasis through its ability to control the amount of
HCO3− reabsorbed from filtrated tubular fluid, form new HCO3−, and eliminate H+ in the
form of titratable acids and ammonium ions.
– HCO3- is filtered at the glomerulus.
Approximately 85% is reabsorbed at the proximal tubules. After diffusing into the renal
tubular cell, CO2 combines with water to form carbonic acid (in the presence of carbonic
anhydrase). Carbonic acid rapidly dissociates into H+ and HCO3-; the bicarbonate ion
enters the bloodstream while H+ is secreted into the renal tubule.
HCO3- that is not reabsorbed may bind with H+ within the lumen to form carbonic acid.
Carbonic anhydrase on the luminal brush border catalyzes the dissociation of H2CO3 into
CO2 and H2O. This CO2 replaces the CO2 that was utilized in the renal tubular cell.
• Correction of the imbalance between production and elimination of CO2 takes about 30
minutes. Central chemoreceptors respond rapidly to a change in hydrogen ion concentration
(which is affected by the arterial CO2 content), while peripheral chemoreceptors respond to
the arterial content of oxygen.
• The fetus is dependent on the placenta for respiratory gas exchange. CO2 easily diffuses
across the placenta and is aided by maternal hyperventilation, which increases the gradient
for the transfer from the fetus into the maternal circulation.
• At birth, respiratory efforts occur within 30 seconds and are sustained to correct the hypoxia
and mild acidosis that occurs during the birthing process. Increases in oxygen tension cause
the release of chemical mediators that convert the fetal circulation to an adult circulation.
• Fetal hemoglobin (HbF) has a very high affinity for oxygen, which facilitates transfer of
oxygen from the placenta to the fetus. However, after birth the usefulness of HbF is limited
due to its impaired oxygen release to the tissues. It is replaced by adult hemoglobin by 4–6
months of age. HgF in the newborn has a reduced ability to carry and transport CO2.
• Pediatric renal function is diminished until about age 2. Premature neonates possess
multiple renal defects, including impaired bicarbonate reabsorption.
Maternal hyperventilation results in reductions in P2 to ∼30 Hg. However, the compensatory
decrease in plasma bicarbonate concentration results in only a mild respiratory alkalosis
ANATOMY
• PaCO2 in alveoli
• PaCO2 in tissue
• Imbalances in CO2 homeostasis can result in respiratory acidosis (pH <7.4) or alkalosis (pH
>7.4). Deviations can have adverse consequences and be deleterious.
• Respiratory acidosis occurs when there is alveolar hypoventilation or increased metabolism,
leading to the accumulation of CO2 and carbonic acid formation.
• Respiratory alkalosis occurs when the PaCO2 is decreased: The most likely perioperative
cause is iatrogenic hyperventilation, which can be corrected by ventilator setting
adjustments. Alkalosis is a normal occurrence with pregnancy; there is a 50% increase in
alveolar ventilation.
Geriatric Considerations
• Elderly patients can commonly present with chronic disease states and resultant
compensatory mechanisms
• Chronic pulmonary diseases can alter alveolar ventilation and the normal responses to
hypoxic and/or hypercarbic conditions.
• CO2 levels can be manipulated under anesthesia, especially with controlled ventilation.
• Central chemoreceptors, located in the medulla, are very sensitive to changes in CSF
hydrogen ion concentration. The blood–brain barrier is permeable to dissolved CO2 but not
to bicarbonate; therefore acute changes in arterial CO2 content are reflected in the CSF.
Increases in CO2 elevate the CSF hydrogen ion concentration and activate the
chemoreceptors.
– This change has an intense initial effect and occurs within seconds; in interstitial fluid, it
takes at least 1 minute. This stimulates the respiratory medullary centers to increase
alveolar ventilation. Of note, central chemoreceptor activity is depressed by hypoxia.
– After several hours, adaptation occurs and the CSF pH normalizes by active transport of
bicarbonate ions.
– The relationship between arterial CO2 and minute ventilation is nearly linear.
– Peripheral chemoreceptors are located outside the central nervous system; they include
the carotid and aortic bodies. The carotid body transmits signals via the glossopharyngeal
nerve to the respiratory center in the medulla. Carotid bodies affect ventilation primarily.
Removal or denervation, as with carotid endarterectomies, can result in loss of the
ventilatory response to arterial hypoxemia and about a 30% decrease in the ventilatory
response to CO2. The aortic body transmits signals via the vagus nerve and is primarily
responsible for cardiovascular responses.
• Apneic threshold is the highest PaCO2 at which ventilation is zero. Spontaneous respirations
are absent under anesthesia when PaCO2 falls below this value. This is not typically seen in
the awake state due to cortical influences that prevent apnea. Opioids and anesthetic
medications significantly depress ventilation by elevating the apneic threshold and hypoxic
drive
• Apneic oxygenation. When apnea occurs, the alveolar CO2 increases 5–10 mm Hg during the
first minute and 3 mm Hg/minute thereafter. The first minute increase is due to
equilibration of the alveolar gas with pulmonary capillary blood. After that first minute,
metabolic production is responsible for the steady rise. In practice, the end tidal CO2
monitor is utilized to assess and approximate alveolar CO2.
• Body temperature can directly affect the measurements of the partial pressures of a gas.
During hypothermia, both PaCO2 and PaO2 decrease because gas solubility is inversely
proportional to temperature (cold temperatures lead to a decrease in the partial pressure of
a gas in the solution). pH, on the other hand, increases because the bicarbonate ion remains
unchanged. However, transport of CO2 is not affected by body temperature.
• Hypermetabolism should be considered in a persistently hyperthermic patient in the
intraoperative and immediate postoperative period. Hypermetabolic states increase CO2
production and increase sympathetic activation. If not corrected, metabolic acidosis,
electrolyte imbalance, and muscle breakdown occur. The differential diagnosis should
include malignant hyperthermia, neuroleptic syndrome, thyroid storm, pheochromocytoma,
and serotonin syndrome. The end-tidal CO2 can double or triple in value. It is one of the
earliest and most sensitive indicators of malignant hyperthermia.
• Administration of acetazolamide, a carbonic anhydrase inhibitor, can impair CO2 transport
between tissues and alveoli.
EQUATIONS
H2O + CO2 H2CO3 H+ + HCO3−
REFERENCES
1. Carlson BE, Anderson JC, Raymond GM, et al. Modeling oxygen and carbon dioxide
transport and exchange using a closed loop circulatory system. Adv Exp Med Biol.
2006;614:353–360.
2. Andreassen S, Rees SE. Mathematical models of oxygen and carbon dioxide storage and
transport: Interstitial fluid and tissue stores and whole-body transport. Crit Rev Biomed
Eng. 2005;33(3):265–298.
3. Duffin J. Role of acid-base balance in the chemoreflex control of breathing. J Appl Physiol.
2005;99(6):2255–2265.
4. Smith CA, Rodman JR, Chenuel BJ, et al. Response time and sensitivity of the ventilator
response to CO2 in unanesthetized intact dogs: Central v. peripheral chemoreceptors. J
Appl Physiol. 2006;100(1):13–19.
ADDITIONAL READING
• Boron WF. Acid-base transport by the renal proximal tubule. Jam Soc Nephrol.
2006;17:2368–2382.
• Jensen FB. Red blood cell pH, the Bohr effect and other oxygenation-linked phenomena in
blood and CO2 transport. Acta Physiol Scand. 2004;182:216–227.

• Carotid body
• Malignant hyperthermia
• Buffering systems
CLINICAL PEARLS
CO2 is transported in three forms:
• Dissolved in plasma solution
• Bound to carbamino compounds
• As bicarbonate ion
CARCINOID
Lori Gilbert, MD
BASICS
DESCRIPTION
• Carcinoid tumors are rare neoplasms of neuroendocrine tissue and are derived from
enterochromaffin cells.
• Carcinoid syndrome results from the direct release of vasoactive amines and peptides into
the systemic circulation, usually from liver metastases associated with midgut carcinoids, or
from bronchial or ovarian primary tumors. Patients commonly experience flushing,
diarrhea, bronchospasm, and tachycardia.
• Carcinoid crisis is a potentially life-threatening complication of metastatic carcinoid.
EPIDEMIOLOGY
Prevalence
• Varies with gender, age, and race.
• In the US: 2 per 100,000 per year; higher in males with African descent.
• Location: GI tract 65%, bronchopulmonary tract 25%, unknown primary 10%; GI tract
tumors have increased significantly over the past 25 years.
Prevalence
• Most commonly diagnosed in the 5th or 6th decade; average age is 60.9 years. Additional
peaks between 15 and 25 years as well as 65 and 75 years.
• Female:male is approximately 2:1 under the age of 50; at older ages, there is a male
predominance.
Morbidity
• Relatively slow growing and patients may go many years without diagnosis; at presentation,
40–60% are asymptomatic.
• Disability arises from flushing, diarrhea, and wheezing.
• Cardiac involvement in up to 66% of patients; characterized by fibrous plaques that cover
the valves of the right heart (tricuspid valve) with eventual right heart failure.
Mortality
• Five-year survival rate: 70–80%; improved survival with appendiceal and lung carcinoid
tumors due to low metastatic spread.
• Carcinoid crisis accounts for 50% of deaths.
• Mostly sporadic
• MEN-1 gene (multiple endocrine neoplasia type 1). In a minority of patients,
neuroendocrine tumors of the lungs, thymus, and stomach can be associated with neoplasia
of the parathyroid glands, pancreas, anterior pituitary. About 5–10% of gastric carcinoids
are associated with Zollinger–Ellison syndrome and the MEN-1 gene.
• First-degree relative: Relative risk of 3.6
• Carcinoid tumors secrete vasoactive peptides. When the tumor is outside of the portal
system, the peptides cannot be metabolized and symptoms manifest. This occurs in
approximately 10% of patients.
– Serotonin (5-hydroxytryptamine) is the most prominent.
– However, other peptides, however, can be produced such as 5-hydroxytryptophan,
bradykinins, tachykinins, histamine, substance P, and adrenocorticotropic hormone.
– The two most common symptoms are flushing and diarrhea. Other clinical manifestations
include wheezing and skin lesions as well as increased fibrous tissue that can cause
retroperitoneal fibrosis resulting in urethral obstruction.
– GI tract tumors do not commonly present with symptoms because the released peptides
must pass through the liver (and are metabolized) prior to entering the systemic
circulation.
• Serotonin is a monoamine neurotransmitter that is derived from tryptophan. Normally, the
majority of serotonin is secreted by enterochromaffin cells in the gut and stored by platelets.
Platelets release serotonin when they bind to a clot; it causes vasoconstriction and aids with
hemostasis. Serotonin is metabolized to 5-hydroxyindoleacetic acid (5-HIAA) that can be
measured. In high doses, serotonin has abnormal growth promoting effects on the
myocardium, and causes myocyte proliferation.
• Kallikrein is a serine protease enzyme that converts kininogen to lysyl-bradykinin, which is
ultimately converted to bradykinin. It also converts plasminogen to plasmin. Kallikrein is
believed to be responsible for flushing.
• Bradykinin is an endogenous peptide with potent vasodilator activity and can increase
vascular permeability; it stimulates endothelial release of prostacyclin and nitric oxide. It
also results in contraction of nonvascular smooth muscle (lungs).
• The severity of symptoms is an indicator of perioperative morbidity. Assess for overt
symptoms of carcinoid syndrome (diarrhea, flushing, wheezing) as well as heart function
and hypertension/hypotension related to carcinoid crisis.
• Medications should be optimized, circulating volume restored, and electrolytes replaced
prior to surgery. Octreotide has a half-life of 60–90 minutes and will typically require
perioperative administration.
• The release of peptides can be augmented by stress, surgical manipulation, and beta-
adrenergic agents. The anesthetic plan should focus on the prevention of mediator release
and avoidance of triggering factors; as well as preparation for the management of
perioperative carcinoid crisis.
SYMPTOMS
• Diarrhea, flushing, shortness of breath, wheezing, palpitations
• Reduced exercise tolerance, orthopnea, paroxysmal dyspnea, peripheral edema may suggest
signs of heart failure.
History
• Age of onset
• Triggers such as stress, alcohol, exercise, certain foods such as cheese, or agents such as
catecholamines and serotonin reuptake inhibitors
Signs/Physical Exam
• Tachycardia, flushing, lacrimation, wheezing, facial edema, regurgitant murmur
• Dehydration
• Hypotension
• Arrhythmias
TREATMENT HISTORY
• Chemotherapy
• Embolization
• Hospitalizations or intensive care unit (ICU) admissions
• Surgeries; gastric carcinoids can cause intestinal obstruction
MEDICATIONS
• Octreotide mimics natural somatostatin and decreases the secretion of serotonin (as well as
gastrin, vasoactive intestinal peptide). It is a potent inhibitor of GH, insulin, and glucagon
secretion and is useful in treating flushing and diarrhea. Available in SQ and IV
formulations.
• Interferon alpha is believed to exert pleiotropic effects (antiproliferation, impair hormone
synthesis, alter the major histocompatibility complex, and increase expression of class I
antigens on the tumor cells)
• Methyldopa inhibits aromatic amino acid decarboxylation (serotonin synthesis)
• Ondansetron is an antiserotonergic agent
• Nicotinamide treats low levels of tryptophan and pellagra
• Diuretics and heart failure medications
• Aprotinin is a kallikrein inhibitor
Labs/Studies
• Chemistry panel (may show effects of chronic diarrhea on electrolytes)
• Liver function tests (LFTs)
• CBC
• Urinary 5-HIAA can indicate progression of carcinoid heart disease
• EKG (may show right ventricular hypertrophy)
• Chest x-ray
• Echocardiogram to assess for right heart and tricuspid valve disease
• Cardiac stress test
• Carcinoid heart disease is a late complication, and can occur in 20–70% of patients. The
characteristic lesion consists of fibrous plaques covering normal endothelium of the
chambers and valves of the right heart (tricuspid valve)
• Bronchial involvement
• Dermatologic manifestations (pellagra-like lesions)
• Skeletal metastases in 10% of patients
• Carcinoid crisis. Diarrhea can lead to dehydration, hypotension, and arrhythmias along with
unconsciousness; it is potentially life-threatening
• Electrolyte abnormalities
• Active bronchospasm
CLASSIFICATIONS
• Nonsecretory carcinoid is asymptomatic
• Secretory carcinoid (vasopeptides) is symptomatic
TREATMENT
Premedications
• Avoid histamine-releasing premedications
• Ondansetron has antiserotonin properties
• Octreotide 150–250 mcg q6–8 hours for 24–48 hours prior to the surgery. Alternatively, an
infusion at 50 mcg/hour for at least 12 hours immediately before surgery
• Hydration should be started prior to surgery
INTRAOPERATIVE CARE
• General endotracheal anesthesia. Intubation allows control of the airway and the ability to
provide positive pressure ventilation
• Epidural catheter placement may be considered depending on the type of surgery and
volume status of the patient. It should be cautiously bolused and dosed, as patients can have
extreme variability in BP
Monitors
• Large bore IV access
• Fluid warmers
• Invasive monitoring (arterial line, central line, pulmonary artery catheter) can aid with
monitoring and diagnosis of a carcinoid crisis
• Laryngoscopy and intubation can trigger the release of carcinoid mediators. Airway
instrumentation should not begin until the patient is “deep.”
• Opioids such as fentanyl or remifentanil can blunt noxious and pressor responses associated
with intubation.
• Lidocaine to the vocal cords can help blunt reflexes.
• Avoid succinylcholine, mivacurium, atracurium, or thiopental; they can provoke histamine
or other mediator release.
Maintenance
• Octreotide should be continued throughout the procedure; it has a half-life of 90–120
minutes
• Patients should be kept at a “deep” level of anesthesia to prevent surgical stimulation from
releasing peptides
• Hemodynamics
– Hypotension: Avoid vasoconstrictors such as norepinephrine and epinephrine as they can
release substances such as bradykinin and worsen hypotension. IV fluid administration
and phenylephrine in small doses are the preferred choices
– Hypertension: Labetalol and esmolol deepen the anesthetic
• Fluids should be carefully monitored; tumors involving the liver portal system may
contribute to large, rapid blood loss
• Opioids: Avoid morphine (histamine release); remifentanil and fentanyl are good choices
• Carcinoid syndrome intraoperatively is best treated with IV boluses of octreotide 20–50 mcg
(titrated to hemodynamics)
• Consider a deep extubation or extubation while running a low dose of remifentanil to avoid
coughing and straining
• Observe for signs of bronchospasm and flushing
• Have drugs available for BP control
FOLLOW-UP
BED ACUITY
ICU setting for IV octreotide, invasive monitoring, fluid management, and analgesia,
particularly in patients with a history of carcinoid syndrome or crisis
• Octreotide IV, followed by subcutaneous
• Fluid management
• Cardiac studies dictated by hemodynamics
• Electrolytes/LFTs
COMPLICATIONS
• Complications of octreotide: GI tract pain, nausea, diarrhea, gallstone formation, steatorrhea
• Inadequate resection may manifest as carcinoid crisis
REFERENCES
1. Zuetenhorst JM, Taal BG. Metastatic carcinoid tumors: A clinical review. The Oncologist.
2005; 10:123–131.
2. Powell B, Mukhtar AA, Mills G. Carcinoid: The disease and its implications for anaesthesia.
Contin Educ Anaesth Crit Care Pain. 2011;11(1):9–13.
3. Maggard M, O’connell JB, Ko C. Updated population-base review of carcinoid tumors. Ann
Surg. 2004;240(1):117–122.
4. Schnirer I, Yao J, Ajani J. Carcinoid—A comprehensive review. Acta Oncologica. 2003;
42(7):672–692.
5. Farling PA, Durairaju AK. Remifentanil and anaesthesia for carcinoid syndrome. Br J
Anaesth. 2004;92:893–895.
ADDITIONAL READING
• www.carcinoid.org (The Carcinoid Cancer Foundation)
• Epidural
• Pheochromocytoma
CODES
ICD9
• 209.20 Malignant carcinoid tumor of unknown primary site
• 209.60 Benign carcinoid tumor of unknown primary site
• 259.2 Carcinoid syndrome
ICD10
• C7A.00 Malignant carcinoid tumor of unspecified site
• D3A.00 Benign carcinoid tumor of unspecified site
• E34.0 Carcinoid syndrome
CLINICAL PEARLS
• Carcinoid crisis may be provoked by stress, chemotherapy, certain foods such as cheese and
alcohol, and anesthetic administration. Prophylactic measures should always be taken
before anesthesia and surgery such as octreotide and hydration.
• Carcinoid syndrome is very rare in patients with pulmonary carcinoids but very common in
patients with GI tumor or with liver metastases
CARDIAC ACTION POTENTIAL
Jacques Prince Neelankavil, MD
BASICS
DESCRIPTION
• The heart consists of pacemaker and myocyte cells that undergo depolarization in order to
produce their function. However, their action potentials (APs) are markedly different in
regard to how they are initiated, the types of ion channels that are involved, and their
repolarization.
• Myocytes are responsible for the contractile/mechanical function of the heart. Their APs are
not spontaneous; instead they result when adjacent cells (pacemaker and myocytes) are
depolarized, similar to dominos. Their AP duration varies depending on the type of
myocyte: atrial potentials are ∼150 ms in duration; ventricular potentials are ∼400 ms;
and Purkinje potentials are ∼450 ms. Each AP consists of 5 phases (in order of occurrence):
– Phase 4: resting membrane potential
– Phase 0: rapid depolarization
– Phase 1: early repolarization
– Phase 2: plateau
– Phase 3: repolarization
• Pacemaker cells are responsible for initiating the myocyte contraction and depolarize
spontaneously; they are found in the sinoatrial (SA) node, interatrial tracts, atrioventricular
(AV) node, Bundle of His, Purkinje fibers, and other abnormal sites. Their AP consists of 3
phases:
– Phase 4: slow spontaneous depolarization (pacemaker potential)
– Phase 0: faster depolarization phase
– Phase 3: repolarization
– There is no well-defined Phase 1 or 2.
• The membrane potential is regulated by voltage-gated ion channels and pumps within the
cell membrane that maintain transmembrane concentration gradients.
• Myocytes
– Phase 4. The intracellular resting potential of the ventricular cardiomyocyte is between
−80 mV and −90 mV. It is created and maintained due to the cell membrane’s high
permeability to potassium, while sodium and calcium channels are mostly closed.
The high intracellular potassium concentration allows diffusion out of the cell along the
concentration gradient. Loss of net positive charge during this phase creates a more
negative membrane potential.
Extracellular sodium ion concentration is high. The sodium–potassium adenosine
triphosphate (ATP) pump prevents complete equilibration of potassium and sodium
across the cell membrane. This ATP-dependent process drives extracellular transport of
three sodium ions and intracellular transport of two potassium ions (2 K+ out, 3 Na+
in).
Intracellular calcium concentrations are regulated by a sodium–calcium exchanger that
maintains a low intracellular calcium concentration. It expels one calcium ion for every
three sodium ions that diffuse down its concentration gradient.
– Phase 0 marks cell membrane depolarization. At a threshold of −60 mV, fast sodium
channels open and sodium ions rapidly move down their electrochemical gradient into the
myocyte. The cell depolarizes to +20 mV to +30 mV.
Fast sodium channels have activation and inactivation gates. At resting potential, the
activation gate is closed and the inactivation gate is open. Upon depolarization, the
activation gates open rapidly and the inactivation gates close more slowly. Sodium ions
may only enter the cell while both gates are open.
A positive feedback loop is created that opens more fast sodium channels and leads to
the membrane being depolarized to a positive value. Phase 0 ends as the inactivation
gates close.
Fast sodium channels activate quickly (<1 ms) in the vast majority of depolarizations.
– Phase 1 is the inactivation of fast sodium channels. During this phase, there is a small
decrease in membrane potential (early repolarization). Chloride permeability increases
and chloride ions move into the cell. Simultaneously, there is a transient efflux of
potassium ions. These two ion currents lead to early repolarization.
– Phase 2 is the plateau period and its duration is the primary determinant for the length of
AP. The plateau portion of the AP is unique to cardiac myocytes.
An inward current of calcium ions prevents the cell from repolarizing. The long shoulder
of the AP is where calcium enters the cell and facilitates mechanical contraction.
There are 2 types of voltage-gated calcium channels in the heart: iCa(T), or transient
calcium channels, and iCaL, or long-lasting channels. iCaT have rapid kinetics, whereas
iCaL have slower kinetics because they open more slowly at higher membrane potentials
and remain open longer. iCaL are found in all cardiac cells, while iCaT are found mainly
in pacemaker and Purkinje cells.
During the plateau, slow delayed-rectifier potassium channels allow outward movement
of potassium ions, which balance the inward calcium current.
– Phase 3 marks repolarization, leading to the closure of the remaining calcium channels. As
the calcium channels inactivate, the slow delayed-rectifier potassium ions remain open,
making the membrane potential more negative. Potassium permeability increases
secondary to rapid delayed-rectifier (voltage-dependent) potassium channels (iK). The
membrane then repolarizes to resting potential at 1/1000th the rate of depolarization.
During repolarization, the fast sodium channels convert from inactive to closed. This
prepares the channel for the next AP.
The absolute refractory period is when the muscle fiber cannot produce another AP due
to the inactivation of the fast sodium channels. This period starts during rapid
depolarization and lasts until approximately midway through repolarization.
The period from the midpoint of repolarization to full repolarization is the relative
refractory period. A larger than normal electrical signal may result in an AP. Inactivation
is the basis for refractoriness in cardiac muscle, and is important for prevention of re-
excitation.
The duration of the ventricular AP is reflected in the QT interval. The QT interval in men
and women are equal in childhood; at puberty the QT interval shortens in men.
• Pacemaker cells
– Phase 4 spontaneous depolarization (pacemaker potential) triggers the AP once the
membrane potential reaches threshold between −40 and −30 mV. Unlike the fast sodium
channels in myocytes, Phase 4 depends on slow If sodium channels (called funny currents)
and calcium channels for depolarization. There is no stable resting membrane potential
due to the repeated spontaneous depolarizations.
– Phase 0 is the depolarization phase of the AP.
– Phase 3 marks repolarization. Once the cell is completely repolarized (about −60 mV),
the cycle is spontaneously repeated.
ANATOMY
• The sarcolemma is a specialized lipid bilayer within the myocyte that contains a plasma and
basement membrane; it forms the intercalated disks and the transverse tubules (T tubules)
as well as contains the pumps and channels responsible for calcium storage and the AP. The
intercalated disks allow for rapid conduction of the AP; the T tubules bring the iCaL close to
the sarcoplasmic reticulum; and the internal stores of calcium are responsible for converting
the AP into a myocardial contraction.
• Mitochondria make up ∼40% of the cell’s volume; this is a function of the large amount of
ATP required by the myocyte.
• Ischemia. There are ATP-sensitive potassium channels that change shape depending on the
metabolic state of the cell. During ischemia, the change in the ADP:ATP ratio activates these
channels, and shortens the AP, leading to less force generation, which may be
cardioprotective. With worsening ischemia and depletion of ATP, the energy-consuming ion
channels can no longer maintain the necessary resting potentials and repolarize the cell.
This can precipitate fatal arrhythmias.
• Prolonged QT interval can result from defects in ion channels that place the myocardium at
risk for fatal arrhythmias.
– Abnormality of the delayed-rectifier potassium channels (responsible for repolarization)
can cause a long QT interval.
– Sodium channels may have defects in inactivation that lead to persistent sodium current.
This can lead to long QT syndrome.
• Brugada syndrome may result from sodium channel mutations in 20% of patients.
• Dilated cardiomyopathy may result from defects in sodium channels via an unknown
mechanism.
• Mutations in the genes for potassium channels are the primary cause of arrhythmias that
result from abnormal repolarization. Gain of function of inward-rectifier potassium channels
causes marked acceleration of repolarization and short QT syndrome.
• Adrenergic receptor agonists such as epinephrine can lead to increased calcium current. The
increase in intracellular calcium results in stronger contractions by increasing cross-bridge
formation.
• The sodium–potassium ATPase pump that helps maintain the resting membrane potential is
the site of digitalis binding.
• Antiarrhythmic medications primarily exert their effects on ion channels and receptors
located on the myocyte membrane. The Vaughan Williams system is the most common
classification system for these medications.
– Class I medications primarily block fast sodium channels.
– Class IA medications (quinidine, procainamide, disopyramide) prolong the repolarization
and refractory period as well as blocking fast sodium channels. This may lengthen the
QRS and QT interval.
– Class IB medications (lidocaine, tocainide, mexiletine) have minimal effect on the QRS
and QT interval, and they are the weakest of class I medications for blocking sodium
channels.
– Class IC medications (flecainide, propafenone) increase the QRS interval more than other
class I medications, and they are the most potent sodium channel blockers.
– Class II medications (propranolol) are beta-adrenergic antagonists. They slow the SA and
AV node without an appreciable change in the QT or QRS interval.
– Class III medications (sotalol, amiodarone) affect the potassium current and lengthen
repolarization and the refractory period.
– Class IV medications (verapamil, diltiazem) are calcium channel blockers, which prolong
the PR interval. There is no appreciable change in the QRS or QT interval.
• The Vaughan Williams classification is useful, but many antiarrhythmic drugs have complex
mechanisms of action.
– Quinidine has class I and class III effects.
– Sotalol has class II and III effects.
– Amiodarone has a mechanism of action that involves all 4 classes.
– Approximately 50% of patients with ICDs receive antiarrhythmic medications.
– Class IC medications affect pacemaker thresholds.
– Many antiarrhythmic medications increase defibrillation thresholds.
– The biotransformation of most antiarrhythmic drugs occurs in the liver. Amiodarone,
propafenone and verapamil are almost exclusively hepatically metabolized. Procainamide,
bretylium, and sotalol have minimal hepatic metabolism.
GRAPHS/FIGURES
FIGURE 1. Action Potential of a Ventricular Myocyte. ERP—Effective Refractory Period.
FIGURE 2. Action Potential of a Spontaneously Depolarizing Nodal Myocyte. iCa —Transient Calcium Channels. iCa —
(T) (L)
Long-Lasting Calcium Channels, If Channels (funny current). iK —Rapid Delayed-Rectifier (Voltage-Dependent) Potassium
Channels.
REFERENCES
1. Grant A. Cardiac ion channels. Circ Arrhythm Electrophysiol. 2009;2:185–194.
2. Kowey PR. Pharmacological effects of antiarrhythmic drugs. Review and update. Arch
Intern Med. 1998;158(4):325–332.
3. Walker CA, Sinale F. The structure and function of the cardiac myocyte: A review of
fundamental concepts. J Thorac Cardiovasc Surg. 1999;118:375–382.
4. Zaza A. Control of the cardiac action potential: The role of repolarization dynamics. J Mol
Cell Cardiol. 2010;48:106–111.
5. Whalley DW, Wendt DJ, Grant AO. Basic concepts in cellular cardiac electrophysiology.
Pacing Clin Electrophysiol. 1995;18(8):1556–1574.
ADDITIONAL READING
• Zipes DP, Jalife J. Cardiac Electrophysiology: From Cell to Bedside. Philadelphia, PA:
Saunders/Elsevier; 2009.
• Ventricular tachycardia
• QT prolongation
• Premature ventricular contractions
CLINICAL PEARLS
• Abnormalities of cardiac AP may lead to different cardiac arrhythmias.
• Different classes of antiarrhythmic medications exert their effect by modifying the different
phases of cardiac AP. However, most of the drugs do not have totally isolated effects on
different phases of the AP.
• There are classes of potassium channels that are activated by acetylcholine, which decreases
the slope of depolarization in pacemaker cells and are part of the mechanism of the vagal
control of the heart.
CARDIAC CATHETERIZATION
Wanda M. Popescu, MD
BASICS
DESCRIPTION
General
• Left heart catheterization is performed to diagnose and treat coronary artery conditions. It
allows real-time visualization of the coronary arterial circulation via injection of contrast
under fluoroscopic guidance. Indications include the following (1):
– Diagnostic procedures: Confirm and assess the severity of suspected heart disease
(chambers and circulation) after a failed stress test.
– Therapeutic procedures: Percutaneous coronary interventions (PCI); valvuloplasties and
percutaneous valve insertions; septostomy and septal reduction; myocardial biopsy.
• Diagnostic uses: Vascular sheaths are introduced, typically into the femoral arteries, and
function as a conduit by which other instruments are then inserted.
– Coronary angiography is performed by advancing a balloon-tipped catheter into the aorta
and through the coronary ostia to access the coronary circulation; dye is injected to
delineate the anatomy, collaterals, and blockages.
– Ventriculogram is performed by subsequently pulling the catheter back into the ascending
aorta and advancing it through the aortic valve (AV); dye is injected into the left ventricle
(LV) to assess its function.
– Pressures in chambers and gradients across valves are also measured.
• Therapeutic uses
– Percutaneous transluminal coronary angioplasty (PTCA) consists of inflating a balloon at
the level of the narrowed coronary artery to improve blood flow.
– Stenting consists of deployment of mesh-like structures that are loaded onto angioplasty
balloons. They fixate to the coronary wall via hooks and prevent acute recoil. Bare metal
stents (BMS), introduced in the 1990s, are metallic mesh-like structures. Drug-eluting
stents (DES), FDA approved in 2003, are similar to BMS but release a medication designed
to inhibit restenosis.
– The presence of a raw surface on the coronary artery (stent) mandates preprocedure
loading with dual antiplatelet therapy (DAPT) and treatment continuation until stent
endothelialization is complete; BMS require ~2 months, whereas DES require 1 year or
more.
– Valvuloplasties are performed to dilate stenotic valves (aortic, mitral) by inflating a
balloon at the level of the valve. More recently, aortic valves have been successfully
inserted percutaneously.
– Septal reductions are performed in patients with hypertrophic obstructive
cardiomyopathies. During cardiac catheterization, alcohol is injected in the septal
perforator artery that supplies the area of hypertrophied interventricular septum (induces
necrosis of the area and thus reduces outflow tract obstruction).
– Septostomies are performed in patients with congenital heart disease requiring a right-to-
left shunt. A balloon-tipped catheter is inserted percutaneously into the venous system and
advanced via the right atrium into the fossa ovalis, which is dilated by balloon inflation.
• Right heart cardiac catheterization allows for measurement of right heart and pulmonary
circulation pressures as well as oxygen saturation via blood sampling (not addressed here).
• Advantages of PCI over coronary artery bypass surgery (CABG) include the following:
– Less invasive treatment of coronary artery disease (CAD)
– Decreased impact on major organ function
– Decreased intensive care unit (ICU) or hospital stay
– Faster recovery to full activity, reduced postoperative pain
– Outcome studies in patients with 3-vessel or left main disease show similar rates of major
adverse cardiac events or cerebrovascular events at 1 or 2 years when comparing PCI with
DES versus CABG (2,3,4)
• Disadvantages of PCI over CABG
– Prolonged treatment with DAPT and increased risk of spontaneous or surgical bleeding
– May require repeat target lesion revascularization
– No long-term survival benefit
Position
Supine
Incision
• Femoral artery puncture
• Other possible puncture sites: Axillary, brachial, or radial artery
Approximate Time
1–2 hours
Expected Blood Loss
• Usually minimal
• Potential for significant blood loss with major vessel or cardiac injury
Hospital Stay
• In elective cases, may be discharged home the same day
• In acute coronary syndrome (ACS) situations, 2–3 days, possibly longer
• In cardiogenic shock, prolonged ICU stays may be necessary
• Cardiac catheterization laboratory
• Fluoroscopy machine, IV contrast dye injector, intravascular ultrasound
• Ideally: Cardiac operating room available within the same building
EPIDEMIOLOGY
Prevalence
• 1 million PCI/year in the US
• During PCI, 90% of patients receive at least 1 stent
Morbidity
• Coronary artery restenosis manifests as reoccurrence of anginal symptoms
– PTCA: 30–40%
– BMS: 20–30%
– DES: <10%
• Late stent thrombosis manifests as death or myocardial infarction
– BMS rare
– DES 0.5–3.1%, possibly higher
Mortality
• At the time of PCI: 1%
• Acute vessel recoil post-PTCA: 20%
• Late stent thrombosis: 45–75%
• Anesthetic care is usually requested for patients with significant comorbidities or
hemodynamic instability.
• Anticoagulation requirements: High-dose loading with antiplatelet drugs pre-PCI, IV
antiplatelet therapy, as well as systemic anticoagulation during and post-PCI (5).
• Preoperative PCI may increase the risk of major adverse cardiac events at the time of
surgery. Perioperatively, the risk of surgical bleeding incurred by maintaining DAPT should
be balanced against the risk of stent thrombosis and possible death encountered when
aspirin and clopidogrel are discontinued prematurely.
• Out-of-OR case. Anesthesia machine and cart, as well as availability of suction are
mandatory. Establish communication with the OR floor manager and anesthesia technician
such that, in case of an emergency, help is easily available.
SYMPTOMS
• Elective: Asymptomatic, exercise-induced or atypical angina
• Emergency: Unstable angina or ACS ± cardiogenic shock
History
• Often identified as a failed stress test
• Associated comorbidities: Hypertension, heart failure, arrhythmias, diabetes, peripheral
vascular disease, smoking history, chronic obstructive pulmonary disease (COPD), chronic
kidney injury
Signs/Physical Exam
S3, S4 heart sounds and bibasilar crackles in patients with heart failure
MEDICATIONS
• Beta-blockers are beneficial by decreasing heart rate, vascular shear stress, and by
attenuating the sympathetic output and thereby decreases platelet reactivity.
• ACE-inhibitors and angiotensin receptor blockers (ARBs) decrease afterload and revert LV
remodeling
• Diuretics decrease preload
• DAPT prevents acute stent thrombosis.
• Statins have pleiotropic effects (lipid lowering, coronary plaque stabilization).
Labs/Studies
• Hematocrit/hemoglobin, potassium, creatinine, coagulation profile; platelet function assay
(if available)
• Echocardiography results (if available)
• Stress test results (if available)
TREATMENT
Premedications
• Loading with high-dose clopidogrel (300–600 mg) and aspirin (PO or orogastric
tube/nasogastric tube)
• Anxiolysis as appropriate
• Low ejection fraction (EF) or high-grade left main disease patients may require pre-PCI
placement of intra-aortic balloon pump (IABP)
• Cardiogenic shock patients may require pre-PCI placement of a percutaneous LV assist
device (pVAD) like the Impella® or TandemHeart®
• Potential for conversion to open heart surgery
• Consent for possible blood transfusions
INTRAOPERATIVE CARE
• Most cases are performed without anesthesia care under mild/moderate sedation
administered by a cath lab nurse (6).
• Situations where anesthesia services are required include patients that are critically ill,
hemodynamically unstable, morbidly obese with significant sleep apnea, cannot lie flat,
claustrophobic, or mentally impaired. General anesthesia (usually with endotracheal tube
[ETT]) is often performed.
Monitors
• Arterial waveform can be derived from the groin access lines placed by the cardiologist.
• Good IV access for rapid resuscitation in case of vascular damage or emergency cardiac
surgery
• Foley catheter
• Transesophageal echocardiography/transthoracic echocardiography (TEE/TTE) is useful to
assess cardiac function, detect complications, and guide management.
• Controlled induction to avoid hemodynamic instability
• Emergency airway tools readily available (LMA, indirect video laryngoscopy)
Maintenance
• Volatile or IV agents can be used for maintenance of anesthesia. Volatile agents offer the
theoretical advantage of ischemic preconditioning of the myocardium. There is no data to
suggest that decreases in myocardial contractility seen with volatile or IV anesthetics impact
overall patient outcome.
• Anticoagulation
– Systemic heparinization is administered to a desired activated clotting time (ACT) of 300–
350 seconds. For patients with heparin-induced thrombocytopenia, direct thrombin
inhibitors, factor Xa inhibitors, or defibrinogenating agents are used. No test is available
to monitor the effect of these agents. Patients may be overdosed (manifests as generalized
bleeding).
– IV antiplatelet drugs (glycoprotein IIb/IIIa inhibitors) may be required.
• Significant hypotension suggests cardiogenic shock or hypovolemic shock due to massive
hemorrhage (cardiac or vascular injury).
• Standard extubation criteria; consider postoperative intubation if the patient is
hemodynamically unstable.
• Control BP and heart rate during emergence with IV agents such as beta-blockers,
nitroglycerin, diltiazem, and clevidipine.
• Neurologic exam (potential for cerebral embolic event)
FOLLOW-UP
BED ACUITY
• Elective, noncomplicated case: Discharged home or admitted to regular floor overnight
• Technically difficult case or hemodynamically unstable: Telemetry or cardiac care unit
(CCU)
• Antiplatelet medications will need to be continued post-PCI
• Avoid groin flexion
ANALGESIA
Usually minimal pain, controlled with acetaminophen or PO opioids
COMPLICATIONS
• Acute vessel recoil post-PTCA
• Stent thrombosis
– Early (within 1 month of PCI): Usually represents a technical error
– Late (after 1 month): Usually when DAPT is prematurely stopped.
• Major vessel or coronary artery injury (dissection, laceration)
• Cardiac perforation with pericardial tamponade and shock
• Embolization of atheromatous debris (stroke, abdominal organ ischemia)
• Major bleeding (from aggressive anticoagulation and antiplatelet therapy)
• Access site hematoma, pseudoaneurysm formation, or infection
• Contrast-induced acute kidney injury
REFERENCES
1. hook DC, Gross W. Offsite anesthesiology in the cardiac catheterization lab. Curr Opin
Anesthesiol. 2007;20:352–358.
2. Bravata DM, Gienger AL, McDonald KM, et al. Systematic review: The comparative
effectiveness of percutaneous coronary interventions and coronary artery bypass graft
surgery. Ann Intern Med. 2007;147:703–716.
3. Serryus PW, Morice M-C, Kappetein AP, et al. Percutaneous coronary interventions versus
coronary artery bypass grafting for severe coronary artery disease. N Engl J Med.
2009;360:961–972.
4. Park S-J, Kim Y-H, Park D-W, et al. Randomized trial of stents versus bypass surgery for
left main coronary artery disease. N Engl J Med. 2011;364(18):1718–1727.
5. evine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI Guidelines for
Percutaneous Coronary Interventions.
http://content.onlinejacc.org/cgi/content/full/j.jacc.2011.08.007v1
6. Braithwaite S, Kluin J, Buhre WF, et al. Anesthesia in the cardiac catheterization
laboratory. Curr Opin Anethsiol. 2010;23:507–512.
• Coronary artery bypass grafting
• Cardiac tamponade
CLINICAL PEARLS
• PCI is a less invasive modality compared to coronary artery bypass for the treatment of CAD
when medical therapy is insufficient.
• Patient population with multiple comorbidities
• Requires systemic anticoagulation and high-dose antiplatelet medications. Thus, patients
have an increased risk of spontaneous bleeding.
• In cardiogenic shock, IABP or pVAD can be place pre-procedure.
• May require repeat interventions for restenosis or stent thrombosis
• 1- and 2-year outcomes of PCI are similar to CABG. There are no long-term survival benefits
demonstrated.
CARDIAC OUTPUT
Rebecca L. Reeves, DO
Nanhi Mitter, MD
BASICS
DESCRIPTION
• Circulating blood is necessary for meeting the nutritional demands of tissues, removing
wastes, delivering hormones, and keeping an environment in all tissue that is optimal for
cell function and survival.
• The rate of blood flow to tissue is dependent on its nutritional needs. Cardiac output (CO) is
maintained by alterations in the heart and blood vessels.
• CO is the amount of blood pumped out of the heart into the aorta each minute; it is blood
flow.
– Average CO for adults: 5.6 L/minute for males, 4.9 L/minute for females.
– Varies with age, physical activity, body surface area (BSA), and metabolism.
– Cardiac index (CI). Because CO increases proportionally with BSA, CI can be used as a
measurement. Average CI is approximately 3 L/min/m2.
• Extrinsic factors that control CO:
– The Frank–Starling law is the heart’s built-in mechanism to control CO. It states that
increased venous return (end diastolic volume; EDV) increases wall stretch of the heart
chambers and myocardial cells; this allows cardiac muscle to have greater contractile
force resulting in an increase in SV and therefore CO (Figure 1). An analogy is a bow and
arrow; the greater the stretch, the greater the force exerted on the arrow. However, past a
certain EDV, further filling can become ineffective (will exceed troponin and myosin
overlap and result in a decrease in contractile force and decrease in CO).
FIGURE 1. Effects of changes in afterload on Frank-Starling curves. A shift from A to B occurs with increased afterload,
and from A to C with decreased afterload. From Richard Klabunde. www.cyphysiology.com, 2011, with permission.
– Stretch of the sinus node in the wall of the right atrium (RA) has a direct effect on heart
rate (HR), increasing HR by as much as 10–15%.
– The Bainbridge reflex is a nervous system reflex, also initiated by a stretched RA, that
increases HR.
– In translation, the heart, itself, is not principally responsible for CO. Under normal,
unstressful situations, CO is controlled by extrinsic factors, mainly venous return.
• Intrinsic factors that control CO:
– HR depends on the diastolic interval. The diastolic interval is controlled by the sinoatrial
(SA) node pacemaker (dependent on calcium and potassium channels).
– EDV depends on filling pressure, filling time, and ventricular compliance.
Longer filling times → increases EDV.
Increased ventricular compliance → increased EDV.
• End systolic volume (ESV) depends on
– HR: Increased HR is secondary to increased calcium in pacemaker/myocardial cells; this
also results in increased contractility, and decreased ESV.
– Contractility: Increased inotropy will result from increases in calcium within myocardial
cells, with resultant increases in contractility and HR and decreases in ESV.
– Preload: Increased EDV increases stretch and consequently contractile forces, with a
resultant decrease in ESV.
– Afterload: Increases prevent the heart from emptying with resultant increases in ESV.
• Ejection fraction (EF) is a term that is utilized to describe the systolic function of the heart
in terms of SV and EDV. It is the percentage of blood that is ejected by the ventricles with
heart beat; normal is ∼55–65%.
ANATOMY
• Arteries: High pressure, high flow, strong vascular walls. Function: Transport of blood to
tissues.
• Arterioles: Small branches of arteries, variable flow and pressure. Function: Control
conduits; muscular walls are able to contract and dilate to vary local blood flow in tissue
beds.
• Capillaries: Small thin-walled vessels. Function: Nutrient/waste exchange site.
• Venules: Collect blood from capillaries and form progressively larger veins.
• Veins: Low volume, thin walls, low pressure. Function: Return blood back to the heart,
serves as a reservoir of blood, can also contract/dilate depending on circulatory needs.
• SA node: Located at the junction of the SVC and RA. Serves as the cardiac pacemaker,
largely dependent on calcium channels.
• Cardiac myocytes: Striated muscle with gap junctions that allow muscle fibers to function as
a unit.
• Distribution of CO to organs: Brain 15%, heart 5%, kidneys 20%, liver 25%, muscle 15%
(can increase to up to 65% with exercise), skin 10%, bones/fat/ other 15%.
• High CO states (usually as a result of decreased SVR or shunts): Activates the renin-
angiotensin system and increases sympathetic output with resultant increases in heart rate,
vasoconstriction, and salt and water retention. Leads to ventricular remodeling and failure.
– Beri beri: Thiamine deficiency that leads to peripheral vasodilation, increased CO, salt
retention, and edema. Because of a high CO, the myocardium sustains overuse injuries
that can lead to tachycardia, edema, high pressures, and chest pain.
– AV shunt (fistula): Reduces SVR and arterial BP; this is compensated by increasing the CO.
– Hyperthyroid: Increased metabolism results in decreased SVR that is compensated by
increasing the CO.
– Anemia: Decreases blood viscosity and SVR along with vasodilation from increased nitric
oxide synthase.
– Obesity: Increases blood volume and CO to sustain excess body mass.
– Cirrhosis: Results in splanchnic vasodilation, and also development of shunts.
– Pregnancy: Increased metabolic demand is compensated for with an increase in the
circulating blood volume and HR.
– Shock: The release of cytokines results in extreme vasodilation and decreased SVR; this is
compensated for by an increase in CO.
• Low CO states:
– Hypovolemia: Decreased venous return and EDV result in decreased CO
– Acute venous dilatation: similar to hypovolemia, with decreased EDV.
– Obstruction of large veins: Again, decreased venous return leading to a decrease in the
EDV
– Arrhythmias: Decreased ventricular filling time and decreased SV lead to decreased CO.
– Decreased metabolic rate
– Late sepsis: Inadequate tissue oxygenation leads to multiorgan failure, including heart
failure.
– Regional wall motion abnormalities due to ischemia: Decreased contractility resulting in
decreased EF.
– Valvular disease: Leads to structural changes in the heart muscle and eventual decreases in
systolic function (EF).
– Cardiomyopathy: Impaired ventricular compliance resulting in decreased contractility via
Frank–Starling law.
• Mean arterial pressure (MAP) is the perfusion pressure to organs. MAP = CO × SVR.
• As preoperative clinicians, we need to understand the interrelationship of these physiologic
parameters in order to intervene appropriately, as too high or too low CO can be
detrimental to the patient.
• Measuring CO. In the perioperative setting, this is typically done via invasive monitoring.
Furthermore, CO measurements do not provide information about end-organ blood flow and
oxygen utilization by tissue. Currently, the only monitor that addresses this is mixed venous
oxygen saturation (SvO2).
– Thermodilution technique via the Swan–Ganz catheter is frequently used.
– Echocardiography measures changes in the ventricular volumes to calculate stroke
volume, which is then multiplied by the HR.
– Velocity encoded MRI. Very accurate method to measure velocity based on detection of
changes in the phase of proton precession.
– Arterial line waveform analysis. Area under the curve equals work or stroke volume.
– Invasive pulse pressure, involves inserting a manometer in the artery, the waveform is
analyzed and CO calculated.
– SvO2: Blood samples are collected viaa pulmonary artery catheter. Reflects balance of
oxygen delivery, determined by CO, and oxygen consumption.
– Receptors
β1: Directly increases HR (chronotropy) by stimulating the SA node, and increases
contractility (inotropy) and automaticity of cardiac muscle all increase CO.
β2: Dilates arteries to skeletal muscle which ↓ afterload and ↑ stroke volume and
therefore CO, but to a lesser degree than β1 receptors.
α1: Principle effect is vasoconstriction which increases the SVR.
Dopamine: Increases HR and BP. Low doses: Vasodilates and increases renal blood flow.
Intermediate doses: Increases CO by positive chronotropy and inotropy. High doses: Acts
as a pressor causing vasoconstriction.
• Drugs and receptors
– Epinephrine: Has both β and α activity
– Norepinephrine: Predominantly α activity
– Dobutamine: β1 selective
– Isoproterenol: β1 and β2
– Phosphodiesterase inhibitors: Increases contractility, pulmonary, and systemic
vasodilation
– Calcium: Directly increases myocardial contractility
– Glucagon: Acts as a positive inotrope and increases CO. Also, decreases SVR by arterial
and venous vasodilation
• Hypotension. Workup should include an assessment of preload, afterload, contractility, HR,
and rhythm in light of the clinical picture. The ASA/SCA recommends obtaining
transesophageal echocardiography when the diagnostic information will alter the
management – this includes unexplained persistent hypotension.
• Decreased CO likely results in a longer IV drug circulation time and slower onset of action.
Conversely, volatile agents have a quickened onset due to a more quickly increased alveolar
concentration (less volatile agent is carried away). Increased CO results in a faster IV drug
onset time, while volatile agents have a slower onset (slower increase in alveolar
concentrations).
EQUATIONS
• OHM’s law: V = I / R or Flow = Pressure/Resistance
• CO = MAP/SVR (PVR for right heart, SVR for left heart)
• CO = SV × HR
• SV = EDV – ESV
• Fick principle: CO = VO2/(CaO2 −CvO2); where VO2 is oxygen consumption, CaO2 is
arterial oxygen concentration, and CvO2 is venous oxygen concentration
• CI = CO/BSA
– BSA = 0.20247 × height (m)0.725 × weight (kg)0.425
REFERENCES
1. Guyton AC. The relationship of cardiac output and arterial pressure control. Circulation.
1981;64:1079–1088.
2. de Waal EE, Wappler F, Buhre WF. Cardiac output monitoring. Curr Opin Anaesthesiol.
2009;22:71–77.
3. Rothe CF. Physiology of venous return. An unappreciated boost to the heart. Arch Intern
Med. 1986;146:977–982.
4. Thys DM, Abel MD, Brooker RF, et al. Practice guidelines for perioperative TEE: An
updated report by the American Society of Anesthesiologists (ASA) and the Society of
Cardiovascular Anesthesiologists (SCA) Task Force on TEE. Anesthesiology. 2010;112:1084–
1096.
ADDITIONAL READING
• Ejection fraction
• Cardiac output methods to measure
• High output cardiac failure
CLINICAL PEARLS
• Circulatory shock is inadequate tissue perfusion caused by inadequate CO.
• Hypovolemic shock → the pump is empty. Administer either crystalloid, colloid, or blood
products.
• Distributive/vasogenic shock → SVR is low. Give pressors with strong α1 activity:
Phenylephrine, norepinephrine, ephedrine
• Cardiogenic shock → pump failure. Administer pressors with strong β1 properties,
epinephrine, dopamine, etc. until the underlying cause can be fixed.
• Obstruction to flow → valvular lesions, pulmonary HTN. Surgical correction, inhaled nitric
oxide, and phosphodiesterase inhibitors.
• Bradycardia, heart block → ACLS protocols or treat with atropine, glycopyrrolate, cardiac
pacing.
CARDIAC OUTPUT METHODS TO MEASURE
Amrik Singh, MD
BASICS
DESCRIPTION
• Cardiac output (CO) is the volume of blood pumped by the heart per unit time and is
measured in liters/minute. In the absence of any intracardiac shunt, both right and left
ventricular output are roughly equal.
• Continuous CO monitoring provides dynamic information that can facilitate rapid
adjustments in therapy.
• Fick’s method. Originally described by Adolph Fick in 1870.
– Technique: CO is measured by dividing the body’s oxygen consumption (VO2) by the
difference in arterial and mixed venous blood oxygen content (CaO2–CvO2). CO =
VO2/(CaO2–CvO2). O2 content of arterial or venous blood is determined by adding the O2
bound to hemoglobin (Hb) with that dissolved in blood: [Hb × 1.36 × O2 saturation] +
[PaO2 × 0.003].
– Equipment: VO2 can be measured via spirometry or a closed rebreathing circuit. The PaO2
is attained from an arterial blood gas (ideally pulmonary vein) and the PvO2 from the
pulmonary artery.
– Pros
The original reference standard by which all others are evaluated
Good accuracy in low CO states because the arterial to venous O2 content difference is
reliably augmented
– Cons
Technically difficult to attain VO2 values. To that extent, it can be estimated from an
individual’s height and weight (Fick’s determination) using a value of 125 mL
O2/min/m2.
Fick’s method is not reliable in patients with varying O2 demands, impaired lung gas
exchange, and unstable hemodynamics because the O2 content and consumption are
rapidly changing.
• Pulmonary artery catheter thermodilution method (PAC TD)
– Technique: Based on the modified Steward–Hamilton indicator diffusion equation. A
known amount of cold solution at a known temperature is injected at one port and
measured at a downstream port; the change in temperature is calculated and extrapolated
into a CO measurement. In low CO states, lower blood flow results in greater temperature
change (more time to equilibrate with the body’s warmer temperature), whereas in high
CO states, the blood moves more quickly and there is less time for a change in
temperature.
– Equipment: Heat is used as an indicator instead of lithium or other dyes (e.g., indocyanine
green). A known amount of cold solution is injected in the proximal port that lies in the
right atrium, and the change in blood temperature is detected by a thermistor at the
catheter tip located in the pulmonary artery.
– Pros
Considered the clinical gold standard due to extensive experience with this technique
Allows quick successive measurements
No blood sampling is required
– Cons
Several measurements are needed to calculate an average since the pulmonary blood
flow changes during the respiratory cycle
Many factors including temperature and volume of the injectate, concomitant rapid
intravenous fluid administration, and presence of pulmonic or tricuspid regurgitation
can affect the accuracy
A right-to-left intracardiac shunt will enable some of the indicator to bypass the
thermistor and overestimate the cardiac output
A left-to-right intracardiac shunt will result in recirculation of dye resulting in
underestimation of the cardiac output
There is an inherent 10–20% error in measurement
• Pulmonary artery catheter continuous cardiac output (PAC CCO)
– Technique: Continuous detection of temperature changes from the proximal to distal port.
Utilizes dissipation of heat instead of cold injectate used in the bolus thermodilution
method. The CO value is averaged over 4–6 minutes, although a STAT mode is available
to display it every sixty seconds.
– Equipment: An embedded heat filament that rests between the right atrium and ventricle
emits small thermal pulses every 30–60 seconds.
– Pros
Good correlation with bolus thermodilution method
Provides hands-free continuous data
– Cons: Prone to error with sudden changes in blood flow or concomitant rapid infusions of
cold or warm fluids.
• Partial CO2 rebreathing (NiCO2)
– Technique: Utilizes the differential Fick’s principle; carbon dioxide elimination is
measured in lieu of measuring VO2. CO is based on breath-by-breath measurements of
CO2 elimination.
– Equipment: The NiCO2 system is noninvasive and has a built in rebreathing valve and
loop. Infrared sensors and flow meters measure and calculate CO2 elimination after a brief
period of partial rebreathing.
– Pros: CO2 elimination is easier to measure accurately than O2 due to its high diffusion
rate.
– Cons
Requires mechanical ventilation
Not accurate in the presence of intrapulmonary shunts (however this is present in most
critically ill patients)
• Transpulmonary thermodilution (TPCO)
– Technique: Measures the temperature change in a central artery after injection of cold
saline into a central vein.
– Equipment: A known amount of cold saline is injected in a central line. After passing
through the right heart, pulmonary circulation and left heart, the final temperature
change is measured by a thermistor-tipped catheter placed in a central artery (axillary or
femoral).
– Pros
Less invasive than PAC
Validity is comparable to more invasive techniques
Simultaneous injection of indocyanine green (which stays in the intravascular space) and
cold saline (which equilibrates with the extravascular space) can provide measurements
of the total thoracic intravascular volume and extravascular fluid volume
– Cons
Requires invasive intravascular lines
Concomitant rapid intravenous fluid administration can affect accuracy
• Pulse dye densitometry
– Technique: Dye is injected intravenously, and the arterial concentration is measured.
Calculation of CO is based on a concentration versus time curve.
– Equipment: Indocyanine green dye distributes exclusively in the intravascular space.
Noninvasive arterial concentration is measured with a fingertip sensor. The same principle
of pulse oximetry is utilized (the ratio of the pulse absorbance signals is obtained at two
wavelengths).
– Pros: Noninvasive (indirect sampling)
– Cons: The accuracy of this technique has not yet been validated.
• Doppler ultrasound (esophageal Doppler probe)
– Technique: Aortic blood flow is calculated by multiplying blood flow velocity over time
with the cross-sectional area of the aorta.
– Equipment: An esophageal probe is placed at the level of the descending aorta,
approximately 35 cm from the incisors. The probe position is optimized by slow
penetration and rotation to obtain a clear Doppler signal and blood flow velocity in the
aorta. Aortic diameter is obtained either from a built in nomogram linked to patient
demographics or using an M-Mode echo transducer built into the probe.
– Pros: The shape of the velocity versus time wave can also be used to estimate preload,
afterload, and contractility.
– Cons
Poorly tolerated in awake, unintubated patients
Accuracy is dependent on nonturbulent blood flow, angle of the Doppler beam and aorta,
and the relative distribution of blood flow to the upper part of the body
• Transesophageal echocardiography (TEE)
– Technique: Based on measuring the area and blood flow velocity at a particular location in
the heart. The left ventricular outflow tract (LVOT) is the most commonly used site due to
its nearly circular shape. LVOT area is calculated using the mid-esophageal long axis or
transgastric long axis view. Velocity time integral (VTI) is obtained by placing pulse wave
Doppler sample volume at the same location in the LVOT: Stroke volume = LVOT area ×
VTI.
– Equipment: Echocardiography
– Pros
Avoids blood distribution assumptions made in the esophageal Doppler method
3D echocardiograms can calculate the CO by direct stroke volume (SV) measurements
– Cons
Transesophageal echocardiography is invasive; alternatively, the transthoracic approach
can be utilized, but the image quality may be suboptimal
Technically more demanding and requires special expertise
• Pulse contour analysis-based methods
– LiDCO system
Technique: Based on pulse power analysis, not pulse morphology. The arterial pressure
wave is transferred to a volume wave and the net power is calculated (proportional to
the net flow/SV).
Equipment: External calibration is performed using the lithium dilution method. Isotonic
lithium chloride is injected into a peripheral vein and its concentration is measured with
an electrode attached to a peripheral arterial line.
Pros: Less invasive. Measures CO independent of sampling site.
Cons: The external calibration needs to be repeated after significant changes in
hemodynamics or arterial compliance. However, the newer LiDCO plus system is capable
of self-calibration.
– PiCCO system
Technique: Based on BP waveform morphology and calculates CO by using an algorithm
described by Wesseling and colleagues.
Equipment: Peripheral arterial catheterization provides the pressure waveform. It
requires external calibration by the transpulmonary thermodilution method as described
above.
Pros: Less invasive. Accuracy validated in a number of studies.
Cons: Frequent recalibration is required in the presence of intravascular volume changes
or hemodynamic instability.
– FloTrac/Vigileo system
Technique: Works on the principle that the pulse pressure is directly proportional to the
SV and inversely proportional to aortic compliance. Uses arterial pulse analysis in
conjunction with patient’s height, weight, age, and gender. The system recalibrates itself
frequently.
Equipment: Standard peripheral arterial catheter attached to a special high-fidelity
pressure transducer and monitor. Arterial site not important but the quality of pulse
tracing is relevant.
Pros: No external calibration is required. Derives percent stroke volume variation (SVV)
that has been shown to be a reliable indicator of intravascular volume status. Good
correlation with PAC-based thermodilution method.
Cons: Unlike PAC, right heart filling pressure and mixed venous O2 saturation level not
provided.
• Bioimpedance cardiography
– Technique: Based on changes to electrical resistance in the thoracic cavity associated with
varying amounts of aortic blood volume during systole and diastole. Higher thoracic blood
volume reduces impedance. SV is calculated using a built-in algorithm.
– Equipment: Four pairs of electrodes apply high-frequency, low-amplitude alternating
current and sense impedance changes related to pulsatile blood flow.
– Pros
Completely noninvasive
Can also measure intrathoracic fluid volume and LV ejetion time
– Cons
Accuracy is questionable in the setting of significant ambient electrical noise and body
motion
A new device (NICOM, Cheetah Medical) that uses phase shifts of the received signal
relative to the applied signal resulting from blood volume induced bioreactance changes
in the thorax, may be less susceptible to external noise
– CO is determined by preload, afterload, and contractility; therefore, the etiology of low CO
state could be traced to three fundamental causes:
– Pump failure from ischemic or nonischemic causes
– Hypovolemia
– Low systemic vascular resistance (SVR)
• Intraoperative hypotension is a common occurrence. Since MAP = CO X SVR, measuring CO
will help in the treatment of persistent hypotension unresponsive to simple empirical
treatment.
• Knowing CO is also helpful in monitoring the response of inotropic/vasoactive drugs.
EQUATIONS
• Fick’s equation: CO = VO2/(CaO2–CvO2) where VO2 = O2 consumption and (CaO2–CvO2)
= arterial and mixed venous oxygen content difference.
• CO = VCO2/(CvCO2–CaCO2) where VCO2 = CO2 production and (CvCO2–CaCO2) =
venous and arterial CO2 concentration difference.
• VTI = Velocity time integral measured by Doppler ultrasound = stroke distance.
• Stroke volume = stroke distance X cross-sectional area at the sampling site.
REFERENCES
1. eyton PJ, Chong SW. Minimally invasive measurement of cardiac output during surgery
and critical care: A meta-analysis of accuracy and precision. Anesthesiology.
2010;113(5):1220–1235.
2. Mathews L, Singh RK. Cardiac output monitoring. Ann Card Anaesth. 2008;11:56–68.
3. Pugsley J, Lerner AB. Cardiac output monitoring: Is there a gold standard and how do the
newer technologies compare? Semin Cardiothorac Vasc Anesth. 2010;14:274–282.
4. Skowno JJ, Broadhead M. Cardiac output measurement in pediatric anesthesia. Paediatr
Anaesth. 2008;18:1019–1028.
5. de Waal EE, Wappler F, Buhre WF. Cardiac output monitoring. Curr Opin Anaesthesiol.
2009;22:71–77.
• Cardiac output, high
• Cardiac output
CLINICAL PEARLS
• Fick’s method, traditionally considered the gold standard by many, is technically
challenging. PAC TD has been the practical gold standard in recent decades but the use of
PACs is declining.
• Arterial pulse contour analysis-based monitors, especially the Flo Trac system, are gaining
popularity (reliable and use-friendly). SVV calculation adds additional value to these
methods.
• Not all methods can be used in the pediatric population. For example, the PAC, TP TD, and
esophageal Doppler method have patient size limitations.
• Given the variability of measurements with any modality, trends in CO may be more useful
than absolute values.
CARDIAC OUTPUT, HIGH
Rashmi R. Rathor, MD
BASICS
DESCRIPTION
• High cardiac output (HCO) is a hyperdynamic circulatory state marked by low mean arterial
blood pressure (MAP) and tachycardia:
– Cardiac output (CO) > 8 L/min or cardiac index (CI) > 4 L/min/m2
– Systemic vascular resistance (SVR) <900 dynes × seconds/cm5 or SVR index (SVRI)
<1680 dynes × seconds/cm5/m2
EPIDEMIOLOGY
Prevalence
HCO in the general population: Unknown
Prevalence
• End-stage liver disease (ESLD): Over 400,000 (0.15%) in the US
• SIRS/sepsis over 130 per 100,000 persons
• Hyperthyroidism: 1.5% in general population, more common in women than men (5:1).
Mortality
• ESLD: About 35,000 deaths per year and the 9th leading cause of death in the US.
• Sepsis: In hospital mortality is 30–50%; it is the 10th leading cause of death in the US.
• Thyroid storm mortality is 10–20%.
• Physiologic causes: Anxiety, exercise, pregnancy, fever
• Common pathologic causes: ESLD, SIRS/sepsis, hyperthyroidism, obesity
• Less common pathologic causes: Arteriovenous (AV) fistula, anemia (Hg <7 g/dL),
carcinoid, beriberi, hereditary hemorrhagic telangiectasia, dermatologic diseases, Kaposi
sarcoma, multiple myeloma, Paget’s disease.
• Decreased SVR leading to a low MAP is often the primary circulatory derangement leading
to HCO. Two principal causes of low SVR are as follows:
– Vasodilated small and precapillary arterioles
– AV shunting, including iatrogenic AV fistulas
• Compensatory mechanisms are triggered by a low SVR and MAP:
– Chronic activation of the sympathetic nervous system (SNS) causes tachycardia and
increases plasma catecholamines, vasomotor tone, myocardial contractility, and CO.
– Activated renin-angiotensin-aldosterone system (RAAS) maintains systemic BP by
vasoconstriction and sodium retention.
– Nonosmotic hypersecretion of arginine vasopressin results in retention of free water in
order to preserve the circulatory volume.
• Heart failure may occur regardless of the etiology of HCO; it is defined by clinical evidence
of heart failure and a CI > 4 L/min/m2 (3)[A]. Chronic SNS activation and an excess of
catecholamines cause tachycardia, arrhythmogenesis, β1 receptor down-regulation,
increased myocardial oxygen consumption VO2, and tachycardia-mediated dilated
cardiomyopathy.
• ESLD: Mesenteric vasodilators (nitric oxide [NO], carbon monoxide, cytokines, etc.) cause
splanchnic arterial and venous vasodilatation (1)[A].
– Splanchnic arterial dilatation is so profound that it lowers the overall systemic SVR.
– Splanchnic venous dilatation causes pooling of venous blood and functional hypovolemia.
– A dual circulation exists with a (1)[A]:
Primary derangement causing a low resistance-high capacitance splanchnic circulation
Compensatory response causing a high resistance-low capacitance extrasplanchnic
circulation
• Cirrhotic cardiomyopathy: Describes systolic dysfunction in the setting of HCO and low SVR,
diastolic dysfunction, and supportive criteria (e.g., long QTc and abnormal chronotropy due
to β1 receptor down-regulation). Pharmacologic and physiologic stress can unmask an
impaired LVEF and elevated LVEDV (1)[A].
• SIRS/sepsis: Adequately fluid-resuscitated patients have a hyperdynamic circulation and low
SVR. The extent of SVR reduction appears to be related to mortality (2)[B].
– Mechanisms of low SVR: A blunted rise of intracellular Ca2+ in vascular smooth muscle by
activated KATP channels, increased expression of NO synthase, and depletion of
vasopressin stores due to sustained baroreflex stimulation (2)[A].
– Septic cardiomyopathy presents as an isolated or combined diastolic and systolic
dysfunction. The etiology is unknown but appears to include NO, TNF-α, and cytokines.
Impaired LVEF is associated with poor prognosis in septic patients (2)[A].
– Increased troponins (nonischemic “leak”) predict LV dysfunction and mortality (2)[A].
• Hyperthyroidism: Decreased SVR combined with increased chronotropy and inotropy can
result in a greater than 250%.
• Ensure adequate perioperative organ/tissue perfusion and oxygenation.
• The degree of circulatory derangement and type of surgery determine the invasiveness of
monitoring and the acuity of postop care.
SYMPTOMS
• Anxiety
• Palpitations, angina-like chest pain
• Dyspnea, orthopnea
• Fatigue, poor exercise tolerance
• Lower extremity swelling
• Symptoms related to primary disease
History
Etiology of HCO, functional status, end-organ dysfunction, degree of circulatory compromise
Signs/Physical Exam
• Tachycardia, tachypnea
• Hypotension, wide pulse pressure
• Jugular venous distention and hum
• Hyperdynamic precordium
• Midsystolic murmur (2nd and 3rd LICS), S3
• Bounding femoral artery pulses (pistol shots)
• Warm extremities
TREATMENT HISTORY
• Treatment of primary etiology
• Treatment of heart failure
MEDICATIONS
• α-1 Adrenergic agonist (phenylephrine, norepinephrine, midodrine) (3)[A]
• Dopamine (dosed as α-1 agonist; lower doses act to lower the SVR) (3)[A]
• Vasopressin, terlipressin (4)[A]
• Catecholamine inotropes have decreased efficacy due to β1 receptor downregulation.
Alternative inotropic agents include milrinone (phosphodiesterase inhibitor) and
levosimendan (troponin C sensitizer to Ca2+) (4)[C].
• Diuretics, digoxin if in heart failure (1)[A]
• Drugs specific to underlying cause
Labs/Studies
• BMP to assess for acidosis, renal insufficiency
• CBC: Pancytopenia, leukocytosis
• LFTs, PT/INR, PTT: Hepatocellular integrity, ESLD, sepsis, liver function, coagulopathy
• Fibrinogen, FDP: Fibrinolysis in sepsis, ESLD
• ABG and lactate: Acid–base, hypoperfusion
• Troponins: Myocardial ischemia or leak
• BNP > 400 pg/ml implies CHF
• CXR: Cardiomegaly, effusions, edema.
• EKG: Tachycardia, ischemia, long QTc
• Poorly managed primary pathology (e.g., poorly controlled hyperthyroidism)
• Symptoms and signs of heart failure
CLASSIFICATIONS
No classification specific to HCO
TREATMENT
INTRAOPERATIVE CARE
• Neuraxial anesthesia is not recommended as it further reduces preload and afterload (4)[B].
• Peripheral nerve blocks should be considered, as appropriate.
• No evidence favors either inhalational versus TIVA; both techniques reduce SVR (4)[A].
• Regardless of the anesthetic technique, vasopressors should be in line and ready for
immediate administration.
Monitors
• Standard ASA monitors may be adequate in minor surgery and in the absence of heart
failure.
• Invasive monitors: Indicated when compromised hemodynamics suggest heart failure.
• Arterial line for continuous BP and metabolic assessment (serial ABGs, lactate levels, etc.).
• Central venous pressure does not accurately reflect intravascular volume but is still used to
guide volume therapy. Central venous access is optimal for vasoactive drug administration.
• CO monitors: Most have limited absolute precision and accuracy in the setting of HCO but
provide trends, which is clinically useful information for goal-directed volume therapy and
hemodynamic management.
– Pulmonary artery catheter thermodilution (PAC-TD): Despite its lack of precision and
accuracy, it is still considered the clinical gold standard to validate novel CO monitoring
modalities (5)[A]. Compared to Fick CO determination, PAC-TD systematically
underestimates CO in the HCO range (>7 L/min).
– Continuous venous oximetry: Central venous (SCVO2) and pulmonary artery mixed venous
(SVO2) oximetry estimate adequacy of CO based on the difference between the oxygen
delivery (DO2) and VO2. It is of limited value in the setting of diffuse systemic AV
shunting as high oxygen saturation does not rule out organ hypoperfusion.
– Arterial pressure-based CO monitors (APCOs) exhibit poor agreement in unstable
hemodynamics compared to PAC-TD, may underestimate CO in HCO states, and is
conceptually deficient when the artery used is in the setting of vasoconstriction (ESLD).
– Esophageal Doppler (ED) estimates CO by measuring descending aortic flow velocity and
has been used to successfully guide volume therapy; it has increased bias with increasing
COs (5)[A].
– Transesophageal echocardiography (TEE): Visual assessment of ventricular filling,
contractility, and regional wall motion. It is a useful hemodynamic monitor in HCO.
• Near-infrared spectroscopy (NIRS) continuously displays regional oxygen saturation (rSO2)
of blood in target tissues. Conceptually, NIRS may be the best method of assessing adequacy
of CO in low BP and shunt physiology but data is limited at this time.
• Most agents lower SVR, contractility, and MAP. Tachycardia increases VO2; bradycardia
decreases CO.
• Etomidate has minimal decrease in SVR; however, adrenal suppression is possible even after
a single dose.
• Ketamine can drop SVR if catecholamines are depleted.
Maintenance
• Inhalational anesthesia or TIVA; no evidence exists to suggest superiority of one technique
over another.
• Volume and hemodynamic management can be guided by dynamic monitors (stroke volume
variation, SVV), TEE, or tissue DO2 (tissue oximetry, lactate); not by a preset value of CO or
MAP (4)[B].
• Point of care testing for frequent ABGs and lactate
• Protective ventilator lung strategies:
– Low tidal volumes minimize the impact of positive pressure on the lungs but may be
inadequate for SVV or CO estimates by APCOs.
– Permissive hypercapnia should be carefully considered as it may aggravate an already low
pH due to hypoperfusion (4)[A].
• Patients often cannot tolerate a full MAC of volatile anesthetic; however, this constitutes a
high risk for recall; EEG or BIS monitoring may be appropriate.
Standard extubation criteria
FOLLOW-UP
BED ACUITY
Telemetry, intensive care unit (ICU) based on underlying condition, hemodynamic status, and
extent of surgery
• Dependent on extent of surgery
• ECG, cardiac enzymes, BNP if in HCO failure
COMPLICATIONS
• Heart failure, ischemia/MI, arrhythmias
• Instability, dynamic LVOT obstruction
• Decreased organ perfusion, circulatory shock
REFERENCES
1. Moller S, Henricksen J. Cirrhotic cardiomyopathy. J Hepatol. 2010;53:179–190.
2. Hunter J, Doddi M. Sepsis and the heart. Br J Anaesth. 2010;104(1):3–11.
3. Mehta PA, Dubrey SW. High output heart failure. QJM. 2009;102(4):235–241.
4. Eissa D, Carton EG, Buggy DJ. Anaesthetic management of patients with severe sepsis. Br J
Anaesth. 2010;105(6):734–743.
5. Mayer J, Suttner S. Cardiac output derived from arterial pressure waveform. Curr Op
Anaesth. 2009;22(6):804–808.
ADDITIONAL READING
• LeDoux D, Astiz M, Carpati C, Rackow EC. Effects of perfusion pressure on tissue perfusion
in septic shock. Crit Care Med. 2000;28(8):2729–2732.
• Cardiac output
• Hyperthyroidism
CLINICAL PEARLS
• Decreased SVR is a part of a HCO state.
• Cardiomyopathy may be masked by a low SVR.
• Currently available monitors are often not accurate in HCO states; however, CO/SVR
trending information can be clinically useful.
• Organ perfusion is key to intraoperative management.
CARDIAC PACEMAKER CELLS
BASICS
DESCRIPTION
• In the mammalian heart, three major structures create rhythmical impulses and are able to
drive the heartbeat: The sinoatrial (SA) node, the atrioventricular (AV) node, and the
Purkinje fiber network.
• The SA node region serves as the primary (physiological) pacemaker, while the AV node and
Purkinje fibers serve as secondary (or accessory) pacemakers.
• Spontaneous (Phase 4) diastolic depolarization underlies the electrophysiological property of
automaticity of cells in the SA and AV nodes, His–Purkinje system, coronary sinus, and
possibly the pulmonary vein.
• SA node. Initiates the heart beat and sets the rate and rhythm of cardiac contraction. SA
nodal cells are characterized as having no true resting potential, but instead generate
regular, spontaneous action potentials.
– The ionic mechanism underlying the pacemaker depolarization is the activation of the
hyperpolarization-activated current (If); this current is crucial in the generation of diastolic
depolarization and hence of spontaneous activity. Depolarizing current is carried into the
cell primarily by relatively slow Ca2+ currents.
– The action potential, initiated in the center of node, propagates to the periphery of the
node, and then into the musculature of the terminal crest.
– In the center of the node, the action potential is slow and small compared with the action
potential in the surrounding atrial muscle.
– Autonomic regulation. The nodal region has an abundance of parasympathetic and
sympathetic nerve endings.
Acetylcholine increases (makes more negative) the transmembrane resting potential and
reduces the spontaneous Phase 4 (diastolic) slope, thereby tending to reduce the rate at
which depolarization occurs. Acetylcholine also tends to prolong refractoriness of SA
node cells. Excessive parasympathetic influence may induce marked sinus bradycardia,
sinus arrest, and exit block.
Catecholamines (norepinephrine and epinephrine) increase the rate of Phase 4
depolarization, thereby increasing the sinus rate. The sympathetic autonomic nervous
system (ANS) increases the heart rate and may reverse sinus arrest and SA exit block.
During aging, the SA node structure undergoes remodeling associated with an
augmentation of collagen content. Parasympathetic influence on SA node chronotropism
progressively diminishes with increasing age. Maintenance of an appropriate heart rate
and chronotropic responsiveness in older individuals is increasingly dependent on the
integrity of the sympathetic tone.
• AV node. From the SA node, the wave of depolarization spreads across the atria to the AV
node. The AV node sets the appropriate frequency-dependent conduction delay between the
atria and ventricles. It also limits ventricular activation during atrial tachyarrhythmias,
thereby protecting the ventricular rhythm.
– Action potentials have relatively low resting potentials, slow upstrokes (Ca2+ dependent),
and properties of refractoriness that persist well after repolarization has been completed
(i.e., time-dependent refractoriness).
– Dromotropic responsiveness in the resting patient is under relatively balanced sympathetic
and parasympathetic neural influence. The relationship between ANS control of the SA
rate and AV conduction properties appears to foster both maintenance of 1:1 AV
conduction and a relatively optimal AV conduction interval.
Parasympathetic predominance (i.e., sleep, very fit resting subjects) markedly enhances
AV nodal dromotropic properties; in the extreme this can be associated with transient
complete AV nodal block.
AV node can become dominant in case of sympathetic block or failure.
• Purkinje fibers. His bundle and bundle branches are composed of cells with larger surface
area, more negative resting membrane potentials, and faster (Na+ dependent) action
potentials than those of the AV node.
– Automaticity in Purkinje fibers is slower than in the SA node and AV node. Depending on
the species considered, the pacemaking rate in Purkinje fibers varies between 25 and 40
beats/minute, which is usually sufficient to set a viable cardiac output.
– The Purkinje fibers network can pace the heart in cases of complete AV block.
– Action potentials propagate within thin Purkinje fiber bundles from base to apex before
activation of the surrounding myocytes occurs.
• Purkinje fibers appear to be more resistant to ischemia than ordinary myocardial fibers.
ANATOMY
• SA node. Situated laterally in the epicardial groove (less than 1 mm from the epicardial
surface) of the sulcus terminalis near the right atrium–superior vena cava junction. In
addition to the SA node, spontaneously active pacemaker cells can also be found in the area
of the crista terminalis, the left and right branch of the SA ring bundle, and the interatrial
septum.
– The SA node is a spindle-shaped structure with a fibrous tissue matrix that is comprised of
closely packed cells with a wide variety of morphologies. Only the spindle- and spider-
shaped cells exhibit the typical electrophysiological characteristics of pacemaker cells.
– 10–20 mm long, 2–3 mm wide, and thick, tending to narrow caudally toward the inferior
vena cava.
– Besides pacemaker cells, the SA node also contains atrial cells, fibroblasts, and adipocytes.
– Arterial supply to the SA node arises from the right coronary artery 55–60% of the time
and the left circumflex artery 40–45% of the time; this is often referred to as right or left
dominance
• AV node. A superficial structure lying just beneath the right atrial endocardium, anterior to
the ostium of the coronary sinus, and directly above the insertion of the septal leaflet of the
tricuspid valve.
– It is located at the apex of a triangle (triangle of Koch) formed by the tricuspid annulus
and the tendon of Todaro, which originates in the central fibrous body and passes
posterior through the atrial septum.
– The cells are small and dispersed in a complex fibrous tissue matrix with relatively large
extracellular space.
– Arterial supply to the AV node typically arises from a branch of the right coronary artery
80–85% of the time.
• Purkinje fibers. Cells are found in the His bundle and bundle branches; they cover much of
the endocardium of both ventricles. In humans, they penetrate only the inner 1/3rd of the
endocardium. Purkinje fibers tend to be less concentrated at the base of the ventricle and at
the papillary muscle tips.
• Sinus node dysfunction (sick sinus syndrome) includes the following:
– Abnormalities of sinus node impulse generation
– Disturbances of impulse emergence into the atrium
– Abnormal impulse transmission within the atria (and in some cases from the atria to the
ventricles)
– Increased susceptibility to atrial tachycardias (particularly atrial fibrillation) and
chronotropic incompetence
– Inappropriate sinus tachycardia
– Persistent or inappropriate sinus tachycardia includes abnormal enhanced automaticity
within the SA node or nearby atrial regions
– Bradycardia–tachycardia syndrome includes periods of bradyarrhythmia interspersed with
bouts of atrial fibrillation, or less commonly other paroxysmal primary atrial tachycardias
• AV conduction disturbances include AV blocks (first degree, second degree, third degree)
– First- and second-degree type 1 AV blocks are most often the result of conduction
disturbances at the level of the AV node and are frequently attributable to ANS influences.
– In the presence of a narrow QRS complex, first-degree AV block is due to AV nodal delay
in more than 85% of patients and due to delay within the His bundle in less than 15%.
– Complete heart block is almost always associated with structural heart disease and, more
often is associated with a wide QRS morphology.
• Drug effects
– Cardiac glycosides: First- or second-degree type 1 AV block occurs as a result of glycoside-
induced enhanced vagal tone at the AV node.
– Beta-adrenergic blockers result in AV nodal conduction slowing, block, or both by
diminishing sympathetic effects on the AV junction.
– Calcium channel blockers (particularly verapamil and diltiazem) and most antiarrhythmic
drugs (especially from class 1C) act directly to slow conduction in the AV node.
– Quinidine and disopyramide manifest prominent vagolytic actions, which tends to
counterbalance their negative dromotropic direct effects
• Loss of pacemaker activity from the SA node may result in circulatory collapse, necessitating
the implantation of an electronic pacemaker.
• “Intrinsic” sinus node dysfunction is related to idiopathic degenerative and fibrotic changes
associated with the aging process.
• “Extrinsic” sinus node dysfunction can be caused by beta-adrenergic blockers, calcium
channel blockers, membrane-active antiarrhythmics, and digitalis.
• Drugs can alter SA node function as a result of direct pharmacologic effects (e.g., flecainide,
sotalol, and verapamil) or indirectly via the autonomic nervous system (e.g., beta-
adrenergic blockers), or both (e.g., quinidine, disopyramide, propafenone, amiodarone, and
digitalis).
• Parasympathetic predominance can result in sinus bradycardia, sinus pauses, SA exit block,
and slow ventricular responses in atrial fibrillation.
• Assessment of SA node function:
– Responses to pharmacologic interventions (e.g., autonomic blockade)
– Neural reflexes (e.g., carotid sinus massage, Valsalva maneuver, heart rate response to
upright tilt)
• Responses to induced hypotension (e.g., by administration of amyl nitrite)
GRAPHS/FIGURES
FIGURE 1. Schematic organization of the pacemaker cells in the conduction system of the heart.
FIGURE 2. Anatomical localization of the pacemaker cells and conduction system in the human heart. The AV node tapers
down into the bundle of His, which passes into the ventricular septum and divides into two bundle branches, the left and
right bundles.
FIGURE 3. SA nodal action potentials are divided into three phases. Phase 4 is the spontaneous depolarization (pacemaker
potential) that triggers the action potential once the membrane potential reaches threshold between –40 and –30 mV.
Phase 0 is the depolarization phase of the action potential. This is followed by Phase 3 repolarization. Once the cell is
completely repolarized at about –60 mV, the cycle is spontaneously repeated.
FIGURE 4. Effects of Parasympathetic (Vagal) and Sympathetic Nerve Activation on SA Nodal Action Potentials. Dashed
line represents a normal action potential.
REFERENCES
1. Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: Promoting
understanding of sick sinus syndrome. Circulation. 2007;115:1921–1932.
2. Mangoni ME, Nargeot J. Genesis and regulation of the heart automaticity. Physiol Rev.
2008;88:919–982.
3. Anderson RH, Yanni J, Boyett MR, et al. The anatomy of the cardiac conduction system.
Clin Anat. 2009;22:99–113.
• Bradycardia
• Tachycardia
• Authonomic nervous system
• Sick syndrome
CLINICAL PEARLS
• Heart failure and atrial fibrillation may be associated with significant SA node dysfunction.
• SA node dysfunction can be caused by beta-adrenergic blockers, calcium channel blockers,
membrane-active antiarrhythmics, and digitalis.
• Complete heart block is almost always associated with structural heart disease.
• First- and second-degree AV blocks can be caused by beta-adrenergic blockers, calcium
channel blockers, membrane-active antiarrhythmics, and digitalis.
CARDIOGENIC PULMONARY EDEMA
Eric W. Nelson, MD
BASICS
DESCRIPTION
• Cardiogenic pulmonary edema (CPE) is the accumulation of fluid with a low protein content
in the lung interstitium and alveoli. It results from the left ventricular (LV) output being
lower than pulmonary and left atrial venous return.
• CPE is the end-result of several different pathological processes that cause increased
hydrostatic pressure. Alternatively, increased permeability is seen more commonly with
primary pulmonary processes such as acute respiratory distress syndrome or acute lung
injury (noncardiogenic pulmonary edema).
• Analogy: The heart functions like a dam, and the lungs are the banks along the river. When
the dam does not let the water through, the river rises, backs up, and overflows onto the
banks. In CPE, the heart pump malfunctions and thus causes backup and overflow leading
to edema in the lungs.
EPIDEMIOLOGY
Prevalence
Difficult to assess exact incidence; however, pulmonary edema occurs in 1–2% of the general
population.
Prevalence
CHF, a major cause of CPE, affects nearly 5 million Americans.
Mortality
• In-hospital mortality: 15–20%
• CPE resulting from an acute myocardial infarction (MI) has a 40% mortality; this can reach
80% when the patient is hypotensive.
• Acute MI (1)
• Severe myocardial ischemia
• Cardiomyopathies (low ejection fraction)
• LV volume overload
• LV outflow obstruction (aortic stenosis)
• Diastolic dysfunction
• Acute mitral regurgitation
• Left atrial myxoma
• Atrial fibrillation, due to low LV filling
• LV pump dysfunction increases left atrial volume and pressure that transmits to the
pulmonary vasculature. The increased hydrostatic pressures initially cause dilation and
recruitment of pulmonary vessels, followed by extravasation into the interstitial space, and
entry into alveoli. This manifests as follows:
– Atelectasis and decreased functional residual capacity; results in V/Q mismatching and
increased Alveolar-artery (A-a) gradient
– Increased work of breathing
• Ischemia and infarction
– Increase myocardial oxygen supply
Increase the FIO2
Increase hemoglobin levels (if appropriate)
Increase diastolic perfusion pressure
Decrease heart rate (increases diastolic perfusion time)
Avoid hyperventilation (which can cause vasospasm of the coronary arteries)
– Decrease myocardial oxygen demand
Decrease heart rate (as appropriate)
Decrease contractility (as appropriate)
Decrease preload (as appropriate)
Decrease afterload (as appropriate
Maintain sinus rhythm (if possible)
– Cardiac catheterization and percutaneous intervention
– Emergency coronary artery bypass surgery
• Hypertensive emergency. Aggressively treat BP to decrease myocardial wall tension (and
decrease oxygen consumption). Insert invasive monitors as needed
• Diastolic dysfunction. Avoid volume overload, increase lusitropy (myocardial relaxation),
maintain sinus rhythm (atrial kick is important for adequate end diastolic volumes)
• Systolic dysfunction. Avoid volume overload, promote afterload reduction
• Aortic stenosis. Maintain normal sinus rhythm, slow heart rate, adequate diastolic perfusion
pressures, and volume status (preload dependent)
• Mitral stenosis. Maintain normal sinus rhythm, slow heart rate, avoid volume overload.
• Atrial fibrillation. Convert to a sinus rhythm if possible; if not, maintain rate control.
• Under general anesthesia, the intraoperative diagnosis may be difficult; many signs and
symptoms will be masked or are nonspecific.
– There is usually a history of an acute cardiac or coronary event prior to its onset, or
conversely volume overload in the setting of baseline cardiac dysfunction.
– Hypoxia and desaturation can result from atelectasis. Auscultation can reveal crackles,
rales, wheezing, and murmurs.
– Arterial blood gas measurements can reveal an increased A-a gradient.
– Increased sympathetic tone can result in tachycardia and hypertension. However, in the
setting of severe LV dysfunction, hypotension may be present.
– S3 gallop or jugular venous distention may be observed.
– Pink, frothy sputum in the endotracheal tube or laryngeal mask airway may be seen.
• Invasive monitoring
– PCWP is useful in differentiating causes of pulmonary edema, as CPE will usually have a
PCWP >18 mm Hg, pulmonary edema from other causes typically has a PCWP <18 mm
Hg.
– Transesophageal echocardiogram (TEE) is useful when a patient is under anesthesia to
help determine if the cause of pulmonary edema is from a cardiac cause. Ventricular
dysfunctions (wall motion, ejection fraction), ventricular pathology (stenosis,
regurgitation), and volume status can be determined.
• Aspiration
• Sepsis
• Anaphylaxis
• Acute asthma exacerbation
• Pneumonia
• Pneumothorax
TREATMENT
• Should be aimed at the underlying cause while supporting cardiac pump function (2).
• Preload reduction decreases the volume that the heart needs to pump forward; akin to
decreasing the river flow to the dam.
– Venodilators. Nitroglycerin is fast acting and easily titratable (increases capacitance, does
not decrease intravascular volume).
– Diuretics. Loop diuretics such as furosemide reduce intravascular volume, but require
∼20 minutes for onset. In the setting of poor renal perfusion, it may be even longer.
– Hemodialysis may be necessary in the setting of renal failure and volume overload.
• Afterload reduction improves forward flow (stroke volume and hence cardiac output) for a
given contractility; it decreases wall tension and myocardial oxygen demand. This is
accomplished via vasodilators (3).
– Nitroprusside is a potent arterial dilator and easily titratable (4).
– Intravenous calcium channel blockers may also be utilized.
– Volatile anesthetics
• Inotropic support should be considered when CPE is refractory to preload and afterload
reduction, or when hypotension prevents the use of these strategies. Improved pump
function allows improved management of venous return and forward flow with resultant:
– Decreases in LV end-diastolic pressure (LVEDP) and volume; results in decreased wall
tension (decreased radius, as per LaPlace’s Law).
– Improvement in coronary perfusion during diastole (CPP = MAP–LVEDP)
– Improvement in cerebral and systemic perfusion
– However, this comes at the cost of increased myocardial oxygen consumption secondary
to enhancing the contractile state.
• Inotropic agents include the following:
– Dobutamine is a β-1 agonist; it causes a mild reduction in afterload that helps to increase
cardiac output.
– Milrinone is a phosphodiesterase inhibitor, which increases inotropy and decreases both
SVR and PVR (5).
– Dopamine has β and alpha effects depending on the dosage. At high doses, it can cause
tachycardia and has arrhythmogenic potential.
– Norepinephrine is a potent alpha-1 agonist with some β activity. It is typically reserved for
patients with refractory hypotension as it tends to cause a much greater increase in
afterload than the other inotropes.
• Oxygenation
– Increase the FiO2
– Increase hemoglobin levels with packed red blood cell transfusion, if appropriate
– PEEP should be optimized in an attempt to keep the SpO2 >90%
FOLLOW-UP
• Treatment of the underlying cause should be the initial step in managing these patients once
they are stabilized.
• Any arrhythmias must be corrected.
• If CPE is caused by an acute valvular dysfunction, emergent valve surgery is required.
• CPE from an acute MI typically requires either aggressive medical management,
percutaneous intervention, or bypass surgery
• Left ventricular assist device (LVAD) or heart transplants may be warranted.
REFERENCES
1. eConte P, Coutant V, Nguyen JM, et al. Prognostic factors in acute cardiogenic pulmonary
edema. Am J Emerg Med. 1999;17(4):329–332.
2. Mattu A, Martinez JP, Kelly BS. Modern management of cardiogenic pulmonary edema.
Emerg Med Clin North Am. 2005;23(4):1105–1025.
3. Annane D, Bellissant E, Pussard E. Placebo-controlled, randomized, double-blind study of
intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema.
Circulation. 1996;94(6):1316–1324.
4. Dupuis J. Nitrates in congestive heart failure. Cardiovasc Drugs Ther. 1994;8(3):501–507.
5. Karlsberg RP, DeWood MA, DeMaria AN. Comparative efficacy of short-term intravenous
infusions of milrinone and dobutamine in acute congestive heart failure following acute
myocardial infarction. Milrinone-Dobutamine Study Group. Clin Cardiol. 1996;19(1):21–
30.
6. Gropper MA, Wiener-Kronish JP, Hashimoto S. Acute cardiogenic pulmonary edema. Clin
Chest Med. 1994;15(3):501–515.
7. Teerlink JR. Overview of randomized clinical trials in acute heart failure syndromes. Am J
Cardiol. 2005;96(6A):59G–67G.
ADDITIONAL READING
• www.uptodate.com
• Myocardial oxygen demand
CODES
ICD9
428.1 Left heart failure
ICD10
I50.1 Left ventricular failure
CLINICAL PEARLS
• CPE carries a high mortality. Treatment should focus on the underlying cause, while
supporting pump function, and providing supportive measures as appropriate.
– Oxygenation should be optimized by titrating the FiO2 and PEEP to keep the SpO2 >90%
– Rate control, maintenance of sinus rhythm, preload reduction, and inotropic support
CARDIOPLEGIA
Ali Salehi, MD
BASICS
DESCRIPTION
• Cardioplegia is a specialized solution that is delivered to the myocardium during
cardiopulmonary bypass (CPB) to cease electrical activity and hence mechanical function. It
– Brings the heart to a standstill and provides a quiet operating environment for the surgeon
– Decreases oxygen (O2) demand by decreasing electrical activity and mechanical
contraction
– Supplies the myocardium with O2 and nutrients in order to protect it from ischemic injury
• Cardiac myocardium has a high O2 demand and requires a high, sustained supply of O2 and
nutrients.
– Normal myocardium: 8 mLO2/100 g/min
– Empty beating heart: 5.6 mLO2/100 g/min
– K+ arrested heart: 1.1 mLO2/100 g/min
– Myocardial arrest and cooling decreases consumption to 0.3 mLO2/100 g/min (1,2).
• Ischemia results when there is an imbalance in O2 supply and demand. O2 delivery depends
on the following:
– Hemoglobin concentration
– Arterial O2 saturation
– Blood flow to the heart. This is dependent on the coronary perfusion pressure and is equal
to diastolic blood pressure minus the left ventricular end diastolic pressure.
• Cardiac contractility is dependent on adenosine triphosphate (ATP). Aerobic metabolism
produces 36 ATP for each glucose molecule; anaerobic metabolism produces only 2 ATP and
also results in lactic acid and H+ accumulating in the myocardium (suppresses glycolysis).
• Cardioplegia during CPB functions to:
– Provide a quiet surgical field to facilitate the surgical procedure (arrest electrical activity
and hence myocardial contractility).
– Decrease myocardial energy requirements and O2 demand in order to protect and preserve
myocardial function during the period in which aortic cross-clamp is placed and
myocardial perfusion is disrupted.
– Provide O2 and nutrients to the myocardium while it is ischemic (no coronary artery
perfusion).
– Of note: Myocardial arrest time can be prolonged or shortened by the administration of
additional cardioplegia or washing out of cardioplegia.
• Composition of cardioplegia: Crystalloid or crystalloid and blood:
– Crystalloid cardioplegia only contains dissolved O2 due to the lack of hemoglobin. Its O2
carrying capacity is sufficient to provide enough O2 to cold myocardium, hence, it
requires a hypothermic strategy for myocardial protection. Its composition can be altered
by the addition of additives that replace substances present in blood cardioplegia.
Intracellular solutions have a [Na+] similar to the intracellular [Na+]; this abolishes the
Na+ gradient and thereby prevents action potentials and myocardial contraction. The
lack of Ca++ further hinders myocardial contractility. Procaine chloride and magnesium
chloride are added to provide membrane stability, and mannitol maintains the
osmolarity of the solution. Today, it is mostly used for organ preservation in cardiac
transplantation.
Extracellular solutions have a [Na+] similar to the extracellular [Na+] but with a high
[K+], 8–30 mmol/L, that is responsible for causing diastolic arrest of cardiac action
potentials. Today, it is more commonly used during CPB.
– Blood cardioplegia is made by mixing blood and crystalloid cardioplegia. The ratio of
blood:crystalloid is typically 4:1, but may vary based on the practitioner or institution. It
has a higher O2 carrying capacity because it contains hemoglobin and can be used for
both cold and warm cardioplegia. Cold cardioplegia, however, causes a left-shift on the
oxyhemoglobin saturation curve; thus, hemoglobin has an increased affinity and will not
offload O2 to tissues as readily. Benefits of blood cardioplegia include having natural
buffers, free radical scavengers, and colloids, thus decreasing the need for additives. Blood
cardioplegia solution is used more commonly than crystalloid cardioplegia. The most
recent meta-analysis of the current literature indicates that blood cardioplegia is
associated with a decreased incidence of low cardiac output state and creatine
phosphokinase isoenzyme MB (CK-MB) release, but there is no difference in the incidence
of myocardial infarction or mortality (3).
• Cardioplegia temperature, desired myocardial temperature, and protective strategies: The
optimal myocardial temperature is dependent on the particular patient and surgery; it
affects the choice between cold and warm cardioplegia as well as other protective strategies.
– Cold (hypothermic) cardioplegia at a temperature of 4–10°C is typically administered to
produce myocardial cooling. Myocardial metabolic rate and O2 consumption decrease by
50% for every 10°C drop in temperature; the greatest benefit is achieved at a myocardial
temperature of 25°C. Further cooling of the heart will result in smaller reductions in O2
demand. Drawbacks of hypothermia include myocardial edema and injury that can result
in post-CPB myocardial dysfunction (4).
– Warm cardioplegia is used to achieve a “warm induction,” or arrest prior to the initiation
of ischemia. Electrical and mechanical arrest results from a high [K+] of 20–25 mEq/L
(decreases O2 consumption to ∼1.1 mLO2/100 g/min), while providing O2 and nutrients
to the myocardium (maintains O2 supply). It can be used throughout the entire procedure
if prolonged ischemia is not anticipated. However, because it is not hypothermic, it does
not aid with decreasing cellular metabolism. It also requires blood cardioplegia (contains
hemoglobin and hence a higher O2 carrying capacity) and continuous administration.
Studies have shown that warm cardioplegia results in a decreased incidence of myocardial
dysfunction and impaired cardiac output in the post-bypass period, particularly in the
setting of significant prebypass myocardial dysfunction and low ejection fraction (i.e.,
cardiogenic shock, progressing myocardial infarction, and advanced valvular disease)
(4,5,6).
• Route of delivery:
– Anterograde delivery is through a cannula placed in the ascending aorta proximal to the
aortic cross-clamp. Flow is usually adjusted to achieve and maintain a pressure of 70–100
mm Hg in the aortic root. A rapid rate or low perfusion pressure will result in uneven
distribution of cardioplegia.
– Retrograde delivery is through a cannula placed in the coronary sinus (CS). Right
ventricular (RV) venous return enters the CS near the CS ostium or directly into the right
atrium (RA) which may result in inadequate RV myocardial protection through retrograde
cardiolegia.
– Additionally, cardioplegia can be delivered directly in the coronary ostia (Ostial), or
through the bypass grafts to the distal coronary arteries (7).
• Frequency of delivery. Single dosing is appropriate when bypass time is short and there is no
coronary disease. Multiple dose delivery is used in most cases, however, and is given to
replace the solution washed away through noncoronary collateral flow. It is given for 1–2
minutes every 10–20 minutes. Advantages of multiple dose delivery include the following:
– Maintain myocardial arrest
– Maintain myocardial hypothermia (cold cardioplegia)
– Supply substrates
– Clear metabolites
– Counteract myocardial edema
• Additives. Counteract the potential myocardial injury and dysfunction during myocardial
arrest and reperfusion. Blood cardioplegia needs fewer additives in comparison to
crystalloid cardioplegia, as previously discussed.
– Calcium reduces the risk of reperfusion injury.
– Magnesium not only stabilizes the myocardial cell membrane but also antagonizes the
effect of calcium (preventing the need to eliminate Ca++ from the solution). It has been
shown that there is no benefit to adding magnesium to calcium-free cardioplegia.
– Buffers. Natural (histidine, imidazole groups on proteins, bicarbonate) and synthetic
buffers (THAM) are added to offset the accumulation of lactic acid in the myocardium
during CPB. Blood cardioplegia contains only natural buffers.
– Increasing osmolality to that of extracellular fluid helps prevent myocardial edema and
preserve ventricular function. Mannitol, albumin, and glucose are used to increase the
osmolarity of solutions.
– Energy substrates. Addition of glutamate and aspartate can help replete the high-energy
phosphates in the myocardium and preserve myocardial function.
ANATOMY
• Anterograde cannula is placed just proximal to the site selected for aortic cross-clamp in the
ascending aorta. The cannula has 3 ports, one for delivering cardioplegia, one for pressure
monitoring, and one for venting. If the patient is undergoing aortic aneurysm repair or
aortic valve surgery, anterograde cardioplegia can be delivered directly into the relative
coronary ostia.
• Retrograde cannula is placed through a small incision through the RA after the placement of
the venous cannula. The surgeon feels the inferior vena cava–right atrial junction and
guides the tip of the cannula into the CS ostium. This can also be guided by transesophageal
echocardiography. Presence of a large Thebesian valve in the entrance of the CS can prevent
the placement of the cannula. The cannula is advanced until resistance is felt or a pressure
of >20 mm Hg is measured. This means that the cannula is wedged and is at the junction of
the CS and great coronary vein; it should be pulled back 1 cm and secured.
• The left ventricular free wall is perfused and cooled equally well by anterograde and
retrograde techniques in the presence of a patent coronary vasculature. Subendocardial
muscle is perfused as well as the epicardial muscle or even hyperperfused (Endo:Epi 1.4:1).
If the left anterior descending artery is obstructed and anterograde cardioplegia is used,
subendocardial muscle will be underperfused (Endo:Epi <0.2). Selective subendocardial
hyperperfusion can be restored with retrograde cardioplegia (6).
• Left ventricular septal cooling is more profound with retrograde cardioplegia because it
reduces the septal blood flow. It has been suggested that this effect is due to a rich network
of venovenous collateral vessels. Retrograde flow passes this network and cools the septum
without nourishing the capillary bed.
• Blood flow in the RV capillary bed is maintained with anterograde cardioplegia. Retrograde
cardioplegia decreases RV perfusion by 20% in comparison to anterograde cardioplegia but
moderate cooling (20°C) can be achieved.
In coronary artery bypass grafting, doses are alternatively given anterograde and retrograde.
In mitral valve procedures, they are given mostly retrograde.
• Anterograde cardioplegia is used first to induce rapid arrest and limit the total amount of
perfusate used. It is started after initiation of bypass and before cross-clamping the aorta to
ensure aortic valve competency. Transesophageal echocardiography can be used to
determine left ventricular distension at this time.
• A pressure of 70–100 mm Hg should be achieved during administration of anterograde
cardioplegia. Pressure is transduced through the side port of the anterograde cardioplegia
cannula. If the CS pressure rises during administration of anterograde cardioplegia, it
indicates that the venous return from the coronary flow is entering the cannula tip. Pressure
never exceeds 50 mm Hg because a portion of the venous return is drained directly into the
RA and ventricle through the Thebesian veins. If arrest is not achieved within 1 minute,
several reasons need to be considered:
– Incomplete aortic cross-clamping. The cross-clamp may need to be adjusted or a new
clamp used.
– Aortic valve insufficiency (AI). If AI is mild, then increasing the cardioplegia flow to 500
cc/min will be sufficient. If significant, anterograde cardioplegia should be abandoned and
switched to retrograde.
– Distortion of the noncoronary cusp by the venous cannula. In this situation, the venous
cannula should be repositioned.
– Inadequate venous drainage. Cardioplegia should be started after the collapse of the
pulmonary artery to confirm adequate drainage.
– Insufficient potassium in the cardioplegia solution
• Retrograde cardioplegia is delivered at a rate of 200–250 cc/hr to achieve a pressure of 30–
50 mm Hg. It is important that the pressure in the system and in the cannula be monitored
closely. A CS pressure >20 mm Hg after insertion, or >50 mm Hg while on pump, means
that the cannula is too far or wedged and needs to be pulled back and resecured. The
cannula has a self-inflating balloon 1.8 cm in length with low intramural pressure and flows
of 200–250 cc/hr to prevent barotrauma during infusions.
• Return of electromechanical activity after 2–5 minutes of administration of cardioplegia
indicates that the cardioplegia solution was washed away by noncardioplegic blood. This
could be due to inadequate venous drainage, low perfusate potassium concentration, or
incomplete aortic clamping.
• Preparation for separation from CPB. The temperature is raised to 37°C and reperfusion is
done with substrate enriched blood cardioplegia to buffer acidosis and limit the calcium
load. Rewarming is started about 5 minutes before warm reperfusion. Warm reperfusate has
a low potassium concentration (8–10 mmol/L) and is rich in substrates (aspartate,
glutamate), CPD (to reduce calcium), and buffers (THAM). The first dose is given via
anterograde cardioplegia and then alternated between anterograde and retrograde
cardioplegia; the flow rate is 150 cc/hr for 3–5 minutes. The aortic cross-clamp is then
removed and electromechanical activity usually resumes within 1–2 minutes. If this does
not occur, it is indicative of a high serum and myocardial K+. Usually furosemide (0.5
mg/kg) and 1 g CaCl2 are given to ease the return of rhythm and contractility.
REFERENCES
1. uckberg GD, Braizer JR, Nelson RI, et al. Studies of the effects of hypothermia on regional
myocardial blood flow and metabolism during cardiopulmonary bypass. I. The adequately
perfused beating, fibrillating, and arrested heart. J Thorac Cardiovasc Surg. 1977;73:87–
94.
2. Sink JD, Hill RC, Attarian DE, et al. Myocardial blood flow and oxygen consumption in the
empty-beating, fibrillating, and potassium arrested hypertrophied canine heart. Ann
Thorac Surg. 1983;35:372–379.
3. Hayashida N, Economides JS, Weasel RD, et al. The optimal cardioplegic temperature. Ann
Thoracic Surg. 1994;58:961–971.
4. Rosenkranz ER, Buckberg GD, Mulder DG, et al. Warm induction of cardioplegia with
glutamate enriched blood in coronary patients with cardiogenic shock who are dependent
on inotropic drugs and intra-aortic balloon pump support: Initial experience and operative
strategy. J Thorac Cardiovasc Surg. 1983;86:507.
5. aylaor CD, Lichtenstein SV, Fremes SE, et al. Randomised trial of Normothermic vs
Hypothermic coronary bypass surgery. Lancet. 1994;343:559–563.
6. Buckberg GD. Antegrade/retrograde blood cardioplegia to ensure cardioplegic distribution:
Operative techniques and objectives. J Card Surg. 1989;4(3):216–238.
7. Jacob S, Kallikourdis A, Sellke F, et al. Is blood cardioplegia superior to crystalloid
cardioplegia? Interact Cardiovasc Thorac Surg. 2008;7:491–498.
ADDITIONAL READING
• Hensley FA, Martin DE, Gravlee GP, ed. A Practical Approach to Cardiac Anesthesia, 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2008:604–624.
• Shiroishi MS. Myocardial perfusion: The rebirth of potassium based cardioplegia. Tex Heart
Inst J. 1999;26(1):71–86.
Cardiopulmonary bypass
CLINICAL PEARLS
Blood cardioplegia is most commonly used for CPB procedures; the choice between warm and
cold solution depends on the procedure and patient factors; additives are surgeon and center
dependent.
CARDIOPULMONARY BYPASS
Daniel Castillo, MD
BASICS
DESCRIPTION
• Cardiopulmonary bypass (CPB) machines temporarily take over the function of the heart
and lungs. It is often referred to as a “heart-lung-machine.”
– It redirects venous blood return away from the heart to the bypass machine where it adds
oxygen and removes carbon dioxide. It returns the blood to the systemic circulation via a
large artery.
– Nearly all blood flow through the heart and the lungs stops.
– Machines are operated by allied health professionals known as perfusionists.
• Surgical procedures in which CPB are used:
– Coronary artery bypass surgery
– Cardiac valve repair and/or replacement
– Repair of large septal defects
– Repair and/or palliation of congenital heart defects
– Repair of some large aneurysm (cerebral aneurysm, aortic aneurysm)
– Pulmonary thrombectomy
– Heroic measures when oxygenation or perfusion of organs cannot be maintained by other
means (e.g., local anesthetic systemic toxicity, anterior mediastinal mass).
• Basic circuit of the CPB machine:
– Venous cannulae are placed in the right atrium and/or in the inferior or superior vena
cava to receive and redirect the patient’s blood away from the heart and lungs into a
venous reservoir.
– Oxygenator: From the venous reservoir, the blood passes through an oxygenator where
oxygen is added (membrane oxygenators are less traumatic than bubble oxygenators).
– Heat exchanger: The blood then passes through a heat exchanger that functions to cool or
warm the patient to the desired temperature.
– Main pump: either a roller head pump or a centrifugal pump.
Roller pump: The pump console is made of several rotating motor-driven pumps that
peristaltically “massage” the tubing. This action gently propels the blood through the
tubing.
Centrifugal pump: By altering the speed of revolution of the pump head, blood flow is
produced by centrifugal force. This type of pumping action is considered by many to be
superior to the action of the roller pump because it is thought to produce less blood
damage.
– Arterial cannula: Placed in the ascending aorta; the main pump returns the blood through
an arterial cannula to the patient’s systemic circulation.
– Arterial line filter: Is incorporated in the CPB circuit to minimize the embolic load
delivered to the patient.
• Other components of CPB Machine:
– “LV vent” is a cannula that suctions blood out of the left ventricle to prevent its dilatation
(per LaPlace’s law, Tension = {Pressure * Radius}/Wall thickness; increases in radius
increase tension and myocardial oxygen consumption). The blood originates from
Thebesian and bronchial veins that empty directly into the left ventricle.
– “Cardiotomy suction” is a suction cannula that removes and salvages undiluted or “clean”
blood from the open cardiac chambers or the surgical field.
– “Cellsaver” system collects and washes red blood cells from diluted field blood and blood
that has been exposed to potentially harmful elements (e.g., inflammatory cytokines).
– “Cardioplegia pump” administers a cardioplegic solution.
• Monitoring and access:
– Arterial line is placed prior to initiation of CPB: The flow on bypass is usually nonpulsatile
and thus a noninvasive BP cuff will not work.
– Large-bore intravenous access is also established in case of significant fluid shifts and/or
blood loss prior to or after CPB.
– Central venous access is routinely placed after induction; a pulmonary artery catheter
(PAC) may be considered.
– Transesophageal echocardiography probe is placed as indicated by the procedure in the
absence of contraindications.
• Anesthetic management:
– Balanced anesthesia with shorter-acting narcotics (fentanyl), short-acting intravenous
agents, such as propofol, and modern volatile agents are utilized. Volatile agents appear to
improve cardiac cell conditioning when administered prior to the onset of ischemia.
– High-dose narcotic techniques are not commonly used today.
– Supplemental techniques have increased in popularity (e.g., paraspinal blocks) to reduce
the use of systemic agents, improve analgesic control, and improve postoperative
pulmonary function.
• Systemic inflammatory response syndrome (SIRS): can result from cardiac surgery with CPB.
– Possible causes include contact of the blood components with the artificial surface of the
bypass circuit, ischemia-reperfusion injury, endotoxemia, and operative trauma.
– Data indicate that a complex sequence of events leads to the activation of leukocytes and
endothelial cells, which is responsible for cell dysfunction in different organs.
– There may be some benefit of steroid use in patients undergoing CPB (see additional
reading).
• Complications of CPB (3)[B]:
– Capillary leak syndrome secondary to inflammatory response (see above)
– Hemolysis
– Clotting of blood can block the circuit (particularly the oxygenator) or send a clot into the
patient.
– Air embolism
– Exsanguination (loss of blood perfusion of tissues) if a line becomes disconnected.
– Type I CNS events in 3–6% of patients.
– Long-term cognitive dysfunction in up to 15% of patients.
– Acute respiratory distress syndrome in up to 1.5% of patients.
– Renal dysfunction, with 1–2% of patients requiring hemodialysis.
• As a consequence, CPB is only used during the several hours a cardiac surgery may take.
Most oxygenators come with a manufacturer’s recommendation that they are only used for a
maximum of 6 hours, although they are sometimes used for up to 10 hours. When longer
periods of cardiopulmonary support are required, extracorporeal membrane oxygenation
(ECMO) or a ventricular assist device (VAD) should be utilized.
• Initiation of bypass is defined as the moment that the patient’s venous blood is allowed to
flow through the venous cannula, away from the heart into the bypass machine. A clamp is
typically placed on the venous cannula while preparing for CPB; thus removal of the clamp
usually marks initiation.
– Use of CPB requires suppression of the clotting cascade with heparin because the
components of the bypass pump and the surgical wound are powerful stimuli for
thrombus formation.
– Heparin is given intravenously before placement of the aortic cannula and the activated
clotting time (ACT) is checked; the targeted ACT varies with the type of CPB used
(heparin-coated versus nonheparin coated) and the type of surgical procedure.
– After acceptable pump flows have been achieved and the mean BP is stabilized, the aorta
is cross-clamped, cold cardioplegia (see below) is infused, and the heart is also topically
cooled with a saline slush solution to stop it from beating.
• Cardioplegia is a solution that contains a high concentration of potassium and other
electrolytes. It is designed to arrest and protect the heart muscle. The solution is typically
administered every 20–30 minutes throughout the on-bypass time when there is no blood
flow through the heart.
– Anterograde cardioplegia is administered through the coronary artery os and the flow is
anterograde.
– Retrograde cardioplegia is administered through a catheter in the right atrium directly
into the coronary sinus. The flow is retrograde through the coronary veins.
• Optimal conduct of CPB:
– Currently, the management of patients during CPB varies substantially by institution and
practitioner (surgeon, anesthesiologist, perfusionist involved).
– Evidence-based guidelines for best perfusion practices have been developed (1)[A,B], (2)
[A]. The guidelines describe physiologic parameters (mean arterial BP, pump flow rate,
hematocrit, temperature) and technologies (heparinized versus nonheparinized circuits,
arterial line filters, pulsatile versus nonpulsatlie pumps, centrifuge versus roller pumps)
that may optimize perfusion.
• Alpha stat versus pH stat:
– Alpha stat arterial blood gases are not temperature corrected. During hypothermia on
bypass, an alkaline shift occurs as carbon dioxide leaves the gas form and dissolves in the
blood (less kinetic energy to keep in gas form; resulting in decreased PaCO2). This leads to
a leftward shift of the oxyhemoglobin dissociation curve that remains uncorrected; carbon
dioxide is not added to the system and total body carbon dioxide remains the same. Alpha
stat is most commonly used in adults.
– pH stat arterial blood gases are temperature corrected. Carbon dioxide is added to the
oxygenator to correct for the alkaline drift at lower temperatures and increases the PaCO2
to normal levels. This counteracts the leftward shift of the oxyhemoglobin dissociation
curve. It is most commonly used in neonatal and infant cardiac surgery as it may offer
neurologic protection for this patient population.
• Comparison of adult and pediatric CPB: There are significant differences in the conduct of
CPB between adult and pediatric patients (see Table 1).
Table 1. Comparison of adult versus pediatric cardiopulmonary bypass
• Deep hypothermic circulatory arrest (DHCA) describes maintaining the body without any
perfusion (blood flow).
– It is most frequently used in pediatric cardiac surgery and aortic arch aneurysm repairs in
adults.
– The patient is put on the CPB and cooled to induce total body hypothermia, which is the
prerequisite for initiation of DHCA.
– Additional measures are instituted in an attempt to further reduce the metabolic
requirement of the brain and provide brain protection during DHCA: Ice packing of the
head, administration of barbiturates and mannitol.
– Finally, blood flow to all organs, including the brain, is stopped.
– In adults, DHCA may offer brain protection for up to 30–45 minutes.
• Termination of CPB:
– Weaning from CPB is only begun once the patient’s core temperature is adequate (about
36.5°C) and ventilation is re-established.
– The aortic cross-clamp is removed and the heart beat most often resumes spontaneously;
temporary pacing wires can be used if heart rate is inadequate.
– Weaning from CPB is usually done gradually: The pump flow rates are slowly reduced,
while the amount of blood flow back into the heart is slowly increased at the same time
(“partial bypass”).
– Once the patient is completely off CPB and vital signs are stable, venous and arterial
cannulae are removed.
– Protamine is then administered to reverse the heparin-induced anticoagulation. Always
start with a test dose of protamine (typically 10 mg IV) before giving the full dose in case
of an allergic reaction (severe pulmonary hypertension requiring reinstitution of the CPB).
REFERENCES
1. Murphy GS, Hessel EA II, Groom RC. Optiomal perfusion during cardiopulmonary bypass:
An evidence-based approach. Anesth Analg. 2009;108(5):1394–1417.
2. Oakes DA, Managno CTM. Cardiopulmonary bypass in 2009: Achieving and circulating
best practices. Anesth Analg. 2009;108(5):1368–1370.
3. Shann KG, Likosky DS, Murkin JM, et al. An evidence-based review of the practice of
cardiopulmonary bypass in adults: A focus on neurologic injury, glycemic control,
hemodilution, and the inflammatory response. J Thorac Cardiovasc Surg. 2006;132:283–
290.
ADDITIONAL READING
• Conolly S, Arrowsmith JE, Klein AA. Deep hypothermic circulatory arrest. Contin Edu
Anaesth Crit Care Pain. 2010;10:138–142.
• Whitlock RP, Chan S, Devereaux PJ, et al. Clinical benefit of steroid use in patients
undergoing cardiopulmonary bypass: A meta-analysis of randomized trials. Eur Heart J.
2008;29:2592–2600.
• Circulatory arrest
• Cardioplegia
• Left ventricular assist device
• pH measurements
CLINICAL PEARLS
• CPB is a technique that temporarily takes over the function of the heart and lungs.
• Certain surgical procedures are only possible to perform with the help of CPB.
• CPB carries its own pathophysiology and complications.
• There are significant differences in the indications and the conduct of CPB in adult and
pediatric patients.
• Evidence-based practice guidelines have been developed to optimize perfusion and outcome.
CAROTID BODY
Robert S. Fitzgerald, LittB, STB, MA, STM, PhD
BASICS
DESCRIPTION
• The carotid body (CB) comprises chemoreceptors and their supporting cells at the
bifurcation of the carotid artery. It functions to detect oxygen and carbon dioxide partial
pressures as well as changes in pH, glucose, and temperature.
• From the available literature, the CB was first reported in 1743 in a dissertation from the lab
of the famous German physiologist, Albrecht von Haller. In 1938, Corneille Heymans
received the Nobel Prize in Physiology or Medicine for his discovery of the role carotid and
aortic mechanisms played in cardiopulmonary control. Heymans’ work owed a great debt to
the pioneering histological work of Fernando De Castro who knew the difference between
the CB and carotid sinus before the Heymans’ group (1).
• The CB is sometimes confused with the carotid sinus, located at the base of the internal
carotid artery; this latter structure is the principal detector and regulator of BP in mammals.
• The CB, however, is arguably the most important interoreceptor in humans.
• In human subjects, the CB is football-shaped with a volume of ∼12 mm3. The human CB
weighs ∼14 mg but has an enormous blood flow, the highest of any organ measured.
• The CB “tastes” the blood; that is, it is sensitive to qualitative changes in arterial blood
composition.
– When PaO2 or glucose drops, carbon dioxide tension (PaCO2) or hydrogen ion rises. The
neurotransmitter-containing chemosensitive glomus cells in the CB become depolarized
and extracellular calcium rises in these cells. This provokes the release of excitatory
(acetylcholine, adenosine triphosphate [ATP]) and inhibitory (dopamine) transmitters.
– Serotonin and GABA, slower acting agents, are subsequently released (2). These
neurotransmitters cross a synaptic-like cleft between the glomus cell and the abutting
sensory afferent neuron, a branch of the glossopharyngeal nerve to bind to appropriate
receptors.
– The afferent neurons have their cell bodies in the petrosal ganglion and insert into nucleus
tractus solitarii in the medulla.
– The neurotransmitters also bind to autoreceptors on the glomus cells to promote or
attenuate further release of the agents.
• Stimulation of the CB initiates an impressive array of systemic reflex responses.
– Pulmonary
Increase in tidal volume
Increase in respiratory frequency
Increase in FRC (a static lung volume)
Increase in airway resistance
Increase in secretions
Decrease in pulmonary vascular resistance.
– Cardiovascular
Increase in sympathetic nerve output leading to tachycardia after an initial brief
bradycardia
Peripheral vasoconstriction
Some of the cardiovascular responses are modified by the stimulated lung receptors due
to the hyperpnea (increase in depth and rate of respiration).
– Endocrine
Release of some adrenal medullary contents as well as 17-OH corticosteroids
Increase in plasma renin
– Renal. CB stimulation increases renal sodium and water excretion in normoxic mammals.
Bilateral CB denervation abolishes the natriuresis (3).
ANATOMY
Located bilaterally at the bifurcations of the common carotid arteries into their external and
internal branches.
• Respiratory concerns
– Obstructive sleep apnea (OSA). This condition, which affects over 11 million Americans
including children, results from the relaxing and collapse of the upper airway muscles
during sleep.
Since metabolism continues, oxygen is consumed and PaO2 falls. Likewise CO2 is
produced and PaCO2 rises.
This modest form of asphyxia strongly stimulates the CBs first; this provokes a minimal
arousal and taking in of a breath. The stimulus to the CB also provokes a significant
increase in sympathetic nervous system (SNS) output. This is not attenuated by input
from the stretch receptors in the lung since the subject is apneic.
As a consequence of the increased SNS output, heart rate and contractility increase as
well as vascular resistance in some beds. This results in an increase in BP, a very
undesirable consequence for subjects who have suffered a previous stroke. BP never
returns to normal. The nocturnal hypertension frequently carries over into the daylight
hours.
Episodes of OSA can occur as frequently as 30–40 times per hour.
Hypoxia also increases pulmonary arterial pressure by local mechanisms; this is
somewhat attenuated by CB stimulation.
– Sudden infant death syndrome. Though this condition has been greatly reduced by proper
positioning of the infant during sleep, the CBs are still thought to function as above in the
periodic apneas observed in children throughout their first year of postnatal life as their
respiratory control system undergoes development.
• Cardiovascular concerns
– Chronic heart failure. As the population ages, the occurrence of heart failure (HF) is on
the rise. In the US, almost 5 million people experience this condition with about 20%
mortality within 1 year and about 50% mortality within 5 years (4,5).
Recent research using the rabbit as an animal model has illustrated that the CB plays a
key role in CHF (6). Heart failure results in decreased blood flow in the common carotid
artery with a resultant decrease in blood flow to the CB. The rabbits demonstrated an
increase in CB neural output and renal sympathetic nerve activity.
Decreased blood flow reduces sheer stress on the endothelial cells in the CB vasculature.
This factor initiates a cascade of events that reduces nitric oxide synthase (nNOS)
activity and NO in the CB. NO is a well-known attenuator of CB neural output (7,8).
When an adenovirus was loaded with the gene for nNOS and injected into the CBs of the
HF rabbits, CB neural output as well as SNS output were reduced (9).
Modest exercise, which increases blood flow, also reduced CB neural output.
• Effect of sedation on the CB
– Many drugs used in anesthesia depress regulation of breathing during acute hypoxia,
among which are propofol, halogenated inhaled general anesthetics, and neuromuscular
blocking agents.
– In a recent study of human CBs, mechanisms behind this action were studied (5). And
though many of the elements operating to depress ventilation and hypoxia-induced
increases in CB neural output in animal models were the same in humans, not all of the
implicated nonhuman elements could be found in human CBs. The authors speculate that
in humans, propofol acts on the GABAA receptor in the CB, while inhaled halogenated
anesthetics were found to target both K+ channels and neuronal acetylcholine receptors
(nAChRs). Human CB nAChRs having the α3, α7, and β2 subunits would also be blocked
by atracurium and vecuronium.
REFERENCES
1. DeCastro F. The discovery of sensory nature of the carotid bodies – Invited article. Adv
Exptl Med Biol. 2009;648:1–18.
2. Nurse C. Neurotransmission and neuromodulation in the chemosensory carotid body.
Auton Neurosc Bas Clin. 2005;120:1–9.
3. itzgerald RS, Shirahata M. Systemic responses elicited by stimulating the carotid body:
Primary and secondary mechanisms. In: The Carotid Body Chemoreceptors, Ed. Gonzalez
C. Heidelberg, Germany, Springer, 1997, pp. 171–191.
4. Paterson DJ. Targeting arterial chemoreceptor over-activity in heart failure with a gas. Circ
Res. 2005;97:1–6.
5. Fagerlund M, Kahlin J, Ebberyd A, et al. The human carotid body – Expression of oxygen
sensing and signaling genes of relevance for anesthesia. Anesthesiol. 2010;113:1270–1279.
6. Ding Y, Li YL, Schultz H. Role of blood flow in carotid body chemoreflex function in heart
failure. J Physiol. 2011;589:245–257.
7. Wang ZZ, Stensaas L, Bredt D, et al. Mechanisms of carotid body inhibition. Adv Exptl Med
Biol. 1994;360:229–235.
8. Fitzgerald RS, Shirahata M, Chang I, et al. L-arginine’s effect on the hypoxia-induced
release of acetylcholine from the in vitro cat carotid body. Respir Physiol Neurobiol.
2005;147:11–17.
9. Schultz H, Li YL. Carotid body function in heart failure. Respir Physiol Neurobiol.
2007;157:171–185.
10. eath D, Smith P. Diseases of the human carotid body. London, Springer-Verlag, 1992, pp.
88–89.
• Carotid sinus
CLINICAL PEARLS
• Aging has an effect on the human CB: In three groups of adults with mean ages of 26, 52,
and 79, the mean cross-sectional area of the CB (mm2) was 2.71, 3.12, and 4.42
respectively. But the mean percent of type I cell tissue was 45, 39, and 29. This suggests
that the reflex responses to CB stimulation by hypoxia, hypercapnia, and hypoglycemia
would become less as one ages.
• A further consequence of aging is the diffuse infiltration of lymphocytes. In a group of 38
male and 37 female subjects, only 2 of 18 subjects under 50 years of age exhibited this
phenomenon, while 32 of the 57 subjects greater than 50 years showed it.
• The CB is affected by COPD. There is usually an accompanying right ventricular
hypertrophy that is associated with alveolar hypoxia, hypercarbia, and muscularization of
pulmonary arterioles. In emphysematous patients presenting without right ventricular
hypertrophy, the mean weight of the combined CBs was 32.4 mg. In the presence of
hypertrophy, the mean weight of the combined CBs was 56.2 mg.
• In asthma, one might expect enlarged CBs due to the mild hypoxemia resulting from
bronchospasm and mucus secretion. Stimulated CBs normally provoke contraction of
airways smooth muscle. However, in asthmatic subjects who had undergone CB removal,
the structures were not enlarged. But the proportion of sustentacular cells had doubled in
the asthmatics compared to controls. And of the two types of type I (chief) cells, the dark
type had increased from ∼28% of all type I cells in the normal CBs to 43% in the
asthmatics. This suggests the possibility of an abnormal CB sensitivity (10).
• A commonly used neuromuscular blocker during anesthesia, vecuronium has been shown in
rats to decrease the neural output from the CB. It is believed that halothane, enflurane, and
isoflurane prolong the effects of vecuronium, and this would suggest that the CB would
remain hyporesponsive.
CAROTID ENDARTERECTOMY
Jared Feinman, MD
BASICS
DESCRIPTION
General
• Carotid endarterectomy (CEA) is an open surgical procedure to remove stenotic material
from inside the carotid artery and improve perfusion to the brain.
• An oblique incision is made along the anterior border of the sternocleidomastoid muscle and
the platysma is divided on top of the carotid bifurcation; the omohyoid muscle will often
also be divided. The carotid fascia is then incised and the common carotid artery (CCA) is
exposed.
• A soft, noncrushing clamp is applied to the internal carotid artery (ICA), and the external
and CCA are subsequently clamped to provide a “bloodless" operating field. A shunt may be
inserted above and below the clamps to maintain perfusion to the brain.
• An arteriotomy is made in the CCA, extended past the occlusion in the ICA, and the plaque
is removed.
• Arterial closure is via a primary closure or patch, and the patient’s neurological status
should be assessed before leaving the OR.
• Embolic phenomena from the atheroma can be dislodged during clamping or plaque
removal and travel up to the brain, causing infarction or TIAs.
• The decision to proceed with a CEA versus medical management is based on the degree of
stenosis, presence or absence of symptoms, and concomitant risk factors (1).
– 70–99% stenosis/symptomatic: Proceed with CEA, shown to reduce 2-year stroke risk
from 26% to 9%
– 50–69% stenosis/symptomatic: Consider CEA, especially if male, >5-year life expectancy
and surgical risk of stroke/death is <6%
– <50% stenosis/symptomatic: Medical management
– 60–99% stenosis/asymptomatic: Consider CEA, especially if age <75, life expectancy >5
years, and surgical stroke/death risk <3%
– <50% stenosis/asymptomatic: Medical management
• Endovascular carotid angioplasty and stenting are also available. It involves threading a
catheter via a femoral arteriotomy, expanding a balloon (angioplasty), and inserting a stent
to keep the artery patent. It carries an increased morbidity and mortality compared to CEA
and higher rates of restenosis.
Position
• Supine
• Head extended and turned to the contralateral side
• Shoulder roll facilitates exposure
Incision
Two inch incision over the left or right carotid
Approximate Time
2–4 hours
EBL Expected
50–250 mL
Hospital Stay
2–3 days
• Fluoroscopy, IV contrast dye
• Vascular shunt
EPIDEMIOLOGY
Incidence
• Stroke is the 3rd leading cause of death in the US. 700,000 strokes occur each year (of which
200,000 are recurrent).
• 180,000 CEAs are performed in the US annually and an additional 30,000 carotid stents.
Prevalence
Increases with age, male gender, hypertension, tobacco use, diabetes mellitus,
hyperlipidemia, and homocysteinemia
Morbidity
• Stroke (embolic or ischemic) in 5–7% of CEAs
• Intracerebral hemorrhage in 0.6% of cases (60% are fatal)
• Increased risk of perioperative myocardial infarction
Mortality
30-day postoperative mortality: 0.4%
• Patient population with significant comorbidities.
• Heparinization, and sometimes protamine reversal, is required.
• Stroke is the most devastating complication; thus, preoperative, intraoperative (when
possible), and postoperative neurological assessments are crucial.
SYMPTOMS
• Often asymptomatic, found in workup for other illness or carotid bruit heard on exam
• May present as TIA or stroke
History
• Baseline neurological assessment; symptomatic patients will often have a history of stroke or
TIAs.
• Assessment for cerebral, coronary, renal, and/or peripheral vascular disease.
• Assess stenosis in contralateral carotid artery, as this may impact collateral flow during
surgery.
Signs/Physical Exam
Carotid bruit
MEDICATIONS
• Statins
• Antiplatelet medications (aspirin, IIB/IIIA)
• Antihypertensives (beta-blockers, calcium channel blockers, ACE inhibitors or ARBs,
diuretics)
Labs/Studies
• Creatinine
• PT/PTT, INR
• Hemoglobin
• Electrolytes if on diuretics, ACE inhibitors, renal insufficiency
• Carotid Doppler ultrasound
• Carotid angiography
• Magnetic resonance angiography (MRA)
• Computed tomography angiography (CTA)
• Peripheral vascular disease
TREATMENT
Premedications
• Perioperative beta-blockers may be considered; they have been shown to reduce cardiac
morbidity and mortality in open repair; however, may increase the risk of stroke. Titrate to
heart rate.
• Perioperative statins may reduce hospital length of stay, postoperative complications,
overall cost, and renal complications.
• Blood consent
• If using regional anesthesia and sedation, discuss realistic sedation goals.
INTRAOPERATIVE CARE
• Regional: Superficial and/or deep cervical block
– Pros: Allows for awake neurological exam and avoids hemodynamic shifts. Shunts are less
commonly utilized.
– Cons: Patient interference, neuroprotective qualities of anesthetic agents are lacking, and
if the airway needs to be secured in the event of stroke, hemorrhage, seizure, agitation, or
hypoxia, it must be done under less than optimal conditions.
• General anesthesia (GA) with ETT
– Pros: Secure airway, controlled surgical field, anesthetic meds may be neuroprotective.
Reduced total procedural cost.
– Cons: Hemodynamic changes, inability to perform an intraoperative neurological exam.
• The General Anaesthesia Versus Local Anaesthesia for carotid surgery (GALA) trial showed
no significant difference in stroke or death between GA and regional (2).
Monitors
• Arterial line; consider awake placement if hemodynamic instability can be detrimental.
• Awake neurological exam (if possible)
• Indirect neurological monitoring
– Flow/pressure
Stump pressure: Needle tip transducer inserted cephalad to the clamp, measuring back
pressure in the ICA from collateral flow. Pressure goals vary by surgeon. Not very
sensitive or specific for clinically significant ischemia.
Transcranial Doppler (TCD) at the zygomatic arch to assess MCA blood flow via the
Circle of Willis. Also has the ability to detect microemboli, but these are often not
clinically significant. TCD is very operator dependent and its position may interfere with
the surgical field.
– Functional
EEG: Raw and processed EEG has been used. Well-established EEG changes occur due to
cerebral ischemia, but there are many limitations, including changes due to anesthesia,
the inability to detect ischemia in deeper structures, and the need for specially trained
personnel to interpret EEG.
SSEP (somatosensory-evoked potential): Monitors transmission of signals from peripheral
nerves to the sensory cortex (can identify ischemia in deeper structures). Amplitude is
decreased by many anesthetic medications and requires trained personnel to operate.
MEP (motor-evoked potential): Monitors transmission of signals from the motor cortex to
peripheral nerves. More sensitive than SSEP to effects of anesthesia, muscle relaxation
cannot be used, and specially trained personnel are required.
– Consumption
JVO2: Catheter placed in the jugular bulb to measure SpO2. Dependent on arterial
oxygen saturation, cerebral blood flow (CBF) and CRMO2. Unclear yet if this is sensitive
or specific for ischemia, and no clear threshold level has been established.
• If EEG neuromonitoring is chosen, a baseline reading is performed prior to induction.
• Slow, controlled induction is performed to avoid and treat significant hypotension that may
exacerbate ischemia while achieving an adequate depth of anesthesia.
Maintenance
• Surgical traction on the carotid sinus can result in vagal stimulation, leading to hypotension
and bradycardia. Releasing traction, or administration of glycopyrrolate/atropine may be
required. Local anesthetic infiltration may abolish the response; however may last into the
• Heparinization should be performed prior to cross-clamping of the carotid artery.
• Placement of the cross-clamp often leads to hypertension via baroreceptor activity and
increased sympathetic tone that may require treatment. It is important not to overtreat and
cause hypotension, increasing the risk of ischemia.
• Shunt placement to allow distal blood flow is based on surgeon preference. Some place a
shunt routinely while others do so only if there is an indication (change in neuromonitoring
indicating ischemia).
• Elevation of the BP during cross-clamp time is often performed to maintain brain perfusion
through collaterals and the contralateral carotid artery via the Circle of Willis.
• Unclamping may be accompanied by reflex vasodilation and bradycardia.
• Avoid coughing and bucking and hypertension that could disrupt repair.
• Neurologic exam should be performed post-op (an awake and oriented patient is beneficial).
POSTOPERATIVE CARE
BED ACUITY
• Telemetry or intensive care unit (ICU) for frequent neurological exams and tight BP control.
• Antiplatelet therapy (clopidogrel, aspirin), statins, and beta-blockers may need to be started
or continued postoperatively.
• Expanding neck hematoma may compromise airway.
ANALGESIA
• Pain is typically minimal, especially if regional anesthesia is used.
• IV PCA if NPO, then NSAIDs and opioids.
COMPLICATIONS
• Stroke (embolic or ischemic) in 5–7% of CEAs
• Hematoma in 5.5% of cases
• Cerebral hyperperfusion syndrome (CHS) may lead to brain edema. Hypoperfusion is
defined as a >100% increase in blood flow compared to preoperative values; it is due to
impaired CBP autoregulation, hypertension, and ischemia-reperfusion injury. CHS can
present as a triad of ipsilateral headache, seizure, and focal neurological symptoms.
• Seizures in 3% of cases
• Cranial nerve injury (reported incidence ranges from 1% to 30%), often hypoglossal nerve
• Intracerebral hemorrhage in 0.6% of cases (60% of these are fatal)
• Recurrent stenosis
• Increased risk of perioperative myocardial infarction
REFERENCES
1. Charturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy: An evidence-based
review. Neurology. 2005;65:794–801.
2. GALA trial collaborative group. General anaesthesia versus local anaesthesia for carotid
surgery (GALA): A multicentre, randomized control trial. Lancet. 2008;372:2132–2142.
3. Goldstein LB, McCrory DC, Landsman PB, et al. Multicenter review of preoperative risk
factors for carotid endarterectomy in patients with ipsilateral symptoms. Stroke.
1994;25:1116–1121.
ADDITIONAL READING
• NASCET trial group. Beneficial effect of carotid endarterectomy in symptomatic patients
with high-grade carotid stenosis. N Engl J Med. 1991;325:445–453.
• ESCT trial group. Randomized trial of endarterectomy for recently symptomatic carotid
stenosis. Lancet. 1998;351:1379–1387.
• Somatosensory- and motor-evoked potentials
CODES
ICD9
433.10 Occlusion and stenosis of carotid artery without mention of cerebral infarction
ICD10
• I65.21 Occlusion and stenosis of right carotid artery
• I65.22 Occlusion and stenosis of left carotid artery
• I65.29 Occlusion and stenosis of unspecified carotid artery
CLINICAL PEARLS
• Beta-blockers and statins should be continued perioperatively; some evidence to suggest that
initiation of therapy confers a survival benefit and discontinuation may increase morbidity
or mortality.
• GA or regional anesthesia has equivalent outcome data.
• Risk of embolic or ischemic stroke due to CEA is significant, and serial neurological exams
must be documented.
CAROTID SINUS
BASICS
DESCRIPTION
The carotid sinus is a baroreceptor that is located at the bifurcation of the internal and
external carotid artery. It is involved in blood pressure and heart rate homeostasis.
• The carotid sinus reflex describes baroreceptor-mediated hemodynamic suppression to high
arterial wall tensions resulting in hypotension and bradycardia.
• When a rise in arterial pressure stretches the baroreceptors, sodium channels are activated
and afferent signals (via the glossopharyngeal nerve) travel to central nuclei, including the
nucleus tractus solitarius. From there, long preganglionic efferent fibers via the vagus nerve
propagate to the heart and synapse on postganglionic neurons in myocardial tissue. These
postganglionic neurons directly stimulate pacemaker cells and conducting pathways to slow
down the heart. The reflex can be elicited manually by external carotid massage.
• Bronchoconstriction is another possible side effect of direct stimulation of the carotid sinus.
ANATOMY
The carotid sinus is located within the bifurcation of the internal and external carotid
arteries.
FIGURE 1. Carotid Sinus. The baroreceptor is located at the bifurcation of the internal and external carotid arteries. It
sends afferent input to the central nuclei via the glossopharyngeal nerve and efferent input travels to the heart via the
vagus nerve. Illustration by Brooke Albright, MD
• Atheromatous plaques located within the region of the carotid sinus impair the sensitivity of
the baroreceptor stretch receptors. Once these plaques are removed, such as in carotid
endarterectomy surgery, an exaggerated response to changes in BP and cardiac rhythms
may be encountered (1).
• Increased age, hypertension, and diabetes can all lead to impaired cardio-vagal reflex
responses and increased cardiovascular morbidity (1).
• In the transplanted heart, vagus nerve innervation is severed. Parasympathetic stimulation
via carotid massage, arterial wall stretch of the carotid sinus, and the Valsalva maneuver are
not effective in slowing the heart rate. Indirect acting medications are also ineffective in the
denervated heart.
• Carotid sinus syndrome (CSS) is a disease characterized by nausea, vomiting, dizziness,
syncope, severe hypotension, and asystole due to hypersensitivity of the carotid sinus. It is a
recognized complication following carotid endarterectomy surgery in some patients.
Treatment may require a pacemaker, glossopharyngeal nerve block/ablation, or surgical
denervation of the glossopharyngeal nerve at the level of the carotid bifurcation (2). If a
regional nerve block is selected for therapy, an electrical stimulating needle is passed
anterior to the styloid process until the patient complains of vague sensations in the regions
supplied by the nerve, such as the external ear or pharynx. If performance of block
successfully reduces symptoms after testing with carotid massage, then the nerve is ablated
with ethanol.
• New technology development and testing related to stimulation of the carotid sinus is
underway for the treatment of drug-resistant hypertension. The Rheos Multicenter
Feasibility Trial is currently investigating an implantable pulse generator and bilateral
perivascular carotid sinus leads that electrically activate the afferent limbs of the carotid
sinus baroreflex and reduce overall sympathetic vascular tone over time. FDA-approved
phase II clinical trials have been promising (3).
• Carotid artery stenting can lead to severe bradycardia and cardiac rhythm disturbances
during balloon angioplasty. Different techniques have been utilized with varying degrees of
success to prevent episodes of bradycardia, including intravenous injection of atropine, and
injection of local anesthetic into the carotid sinus prior to dilation. Infiltration of the carotid
sinus with 5 mL of 1% lidocaine 3 minutes before dilation allowed stable hemodynamics
and did not lead to bradycardia in one study (4).
• Carotid endarterectomy surgery may lead to deterioration of baroreceptor function at the
point when the atheromatous plaque is removed, although the exact mechanism by which
this happens is unclear.
– Some theories suggest that removal of the plaque results in denervation of the
baroreceptor nerve fibers within the arterial wall, which could result in sympathomimetic
electrocardiographic changes and hypertension.
– If carotid afferent fibers are maintained intact, then postoperative hypotension is possible
due to hyperactivity of the newly exposed carotid sinus to the increased perceived BP.
• Prophylactic administration of intravenous atropine is advocated by some anaesthetists
whenever manipulation of the carotid sinus is expected.
• Volatile anesthetics have been shown to depress baroreflex control of heart rate in a
concentration-dependant manner and continue to exert depressive effects after emergence
from general anesthesia (5).
• Prolonged nitroprusside infusion as well as sevoflurane anesthesia can lead to a shift in the
baroreceptor reflex resting set point such that perturbations of the carotid sinus result in
smaller fluctuations of hemodynamics (6).
• Surgery for CSS may include “adventitial stripping,” whereby the proximal carotid artery is
opened and the sinus is denervated over an area of at least 3 cm. Postoperative monitoring
is mandatory since wide variations in heart rate and BP can occur (6).
REFERENCES
1. The parasympathetic nervous system is fully functional at birth in the neonate, including
the baroreceptor reflex. In contrast, the sympathetic nervous system is not complete until
4–6 months of age. As a result, certain noxious stimuli may cause bradycardia in neonates.
During general anesthesia, the responsiveness of the baroreceptor reflex may be reduced by
volatile anesthetics.
2. Gianaros PJ, Jennings JR, Olafsson GB, et al. Greater intima-media thickness in the carotid
bulb is associated with reduced baroreflex sensitivity. Am J Hypertens. 2002;15(6):486–
491.
3. Toorop RJ, Scheltinga MR, Moll FL, et al. Anatomy of the carotid sinus nerve and surgical
implications in carotid sinus syndrome. J Vasc Surg. 2009;50(1):177–182.
4. Tordoir J, Scheffers I, Schmidli J, et al. An implantable carotid sinus baroreflex activating
system: Surgical technique and short-term outcome from a multi-center feasibility trial for
the treatment of resistant hypertension. Eur J Vasc Endovasc Surg. 2007;33(4):414–421.
5. Mourikis D, Chatoupis K, Katsenis K, et al. Percutaneous injection of lidocaine within the
carotid body area in carotid artery stenting: An “old-new” technique. Cardiovasc Intervent
Radiol. 2008;31(4):709–712.
6. Umehara S, Tanaka M, Nishikawa T. Effects of sevoflurane anesthesia on carotid-cardiac
baroreflex responses in humans. Anesth Analg. 2006;102(1):38–44.
7. Toorop RJ, Scheltinga MR, Moll FL. Adventitial stripping for carotid sinus syndrome. Ann
Vasc Surg. 2009;23(4):538–547.
ADDITIONAL READING
• Hines, R, Marschall K. Stoelting’s Anesthesia and Co-Existing Disease, 5th Ed. Philadelphia,
PA: Churchill Livingstone Elsevier; 2008:252.
• Carotid body
• Heart transplant
CLINICAL PEARLS
• Increased arterial wall tension or external pressure on the carotid sinus (i.e., carotid
massage) induces hypotension and bradycardia via a baroreceptor-mediated reflex.
• Atropine can be given to attenuate the effects of the carotid sinus baroreflex when
manipulation is anticipated in normal hearts.
• The transplanted heart is parasympathetically denervated; therefore, atropine and
baroreceptor-mediated reflexes are ineffective.
CATARACT EXTRACTION
BASICS
DESCRIPTION
General
• A cataract is an opacity in the lens of the eye that can cause partial or total blindness. It
results from changes to the crystalline lens fibers that can accompany aging and disease
processes: Increased density, clumping, and formation of opacities.
• Eye drops are administered to dilate the pupils. The surgical area is exposed with a lid
speculum that prevents blinking.
• An incision in the anterior capsule is made to gain access. The cataract is emulsified (broken
up) either by phacofracture or phacoemulsification (phaco) (1).
– Phacofracture is an extracapsular cataract extraction (ECCE) technique. It is utilized more
commonly in developing countries, for very hard cataracts, and for weak epithelial tissue
in the cornea. After an incision is made, a circular tear in the front of the lens capsule is
made. Instruments are inserted to remove the lens intact or be mechanically broken up
(and suctioned). An air bubble or viscoelastic material may be injected into the empty lens
capsule to maintain its shape during the lens insertion.
– Phaco is the preferred method for extraction. It involves the insertion of a tiny, hollowed
instrument that utilizes ultrasonic vibrations (high frequency 40,000 Hz) to emulsify the
cataract. The same tip may be utilized to suction out the lens.
• An intraocular lens implant is inserted to replace the cloudy lens that was removed. A
variety of options are available that are beyond the scope of this chapter.
• If viscoelastic material is injected, it is typically removed after the lens is in place.
Position
Supine
Incision
• Anterior capsulotomy
• Phaco involves a small, 2–3 mm incision that is typically self-sealing (without suturing).
• ECCE requires a larger, 5–12 mm incision that requires suturing; may be performed via a
microincision technique (<1.5 mm).
Approximate Time
15–60 minutes
EBL Expected
Minimal
Hospital Stay
Outpatient procedure
• Microscope
• Intraocular lens implant
• Ultrasonic machine
EPIDEMIOLOGY
Incidence
• US in 2005: Approximately 2,790,000 cataract surgeries were performed (2).
• US: 1 in 50 will have a cataract removed (2).
• The number of people in the US affected by cataracts is estimated to rise to 30.1 million
people in the next 20 years (an increase of 50%) (2).
• Cataracts are responsible for blindness in 19,000,000 people worldwide (50% of all cases of
blindness) (3).
• Women are almost 40% more likely to develop cataracts than men (3).
Prevalence
• Increases with age
• It is estimated that 20.5 million (17.2%) of Americans aged 40 years and above have a
cataract in either eye (3).
Morbidity
Surgical complications include posterior capsular tear, retinal detachment, infection, and
glaucoma.
Mortality
Negligible
• Although this is a quick, simple, and hemodynamically stable procedure that can be
performed without sedation, the anesthesia provider may be asked to provide care due to
significant comorbidities (Parkinson’s disease, dementia, pulmonary cripples, uncontrolled
hypertension, anxiety, or other mental disorders), pediatric cases, or when a retrobulbar
block is utilized.
• The need for a cardiac workup may arise based on the patient’s history, signs and
symptoms, or EKG. It must be weighed against the minimal hemodynamic effects and
American Heart Association (AHA) “low-risk” surgical procedure classification, on an
individual basis. Patients with acute ischemia should clearly be delayed for cardiac
treatment; however, those with nonspecific but suggestive symptoms can pose a conundrum
to the anesthesia care provider.
• The surgical location precludes easy access to the airway. Supplemental oxygen via nasal
cannula is advisable, and all sedatives should be carefully titrated.
SYMPTOMS
Blurry vision
History
Patients requiring anesthesia often have significant comorbidities, which need to be carefully
assessed and evaluated.
Signs/Physical Exam
• Visual deficits
• Check for signs and symptoms of cardiac and pulmonary decompensation.
• Attention to positioning issues in patients with severe scoliosis and orthopnea.
MEDICATIONS
• Alpha blockers may result in intraoperative floppy iris syndrome.
• Topical steroid use; has very minimal systemic absorption.
Labs/Studies
• No routine screening tests have been shown to improve outcomes. Tests are based on the
patient’s other comorbidities.
• Although 12-lead EKGs are commonly ordered on patients within this age group, delaying
the procedure to attain the test may not be warranted. It is often deemed appropriate,
however, in patients with a pacemaker or defibrillator, significant cardiac history, or signs
and symptoms of acute ischemia.
• Pulmonary disease
• Dementia
TREATMENT
Premedications
• Anxiolysis may be warranted, but may cause confusion, dysphoria, and prolonged sedation
in the elderly. If administered, the use of midazolam, a short-acting agent, is preferred.
• Narcotic, as needed, to assist with lying flat. Again, the use of a short-acting agent, such as
fentanyl or alfentanil, is preferred.
If performed as a monitored anesthesia care (MAC) technique, patient and family should be
made aware of reasonable sedation goals and the potential for some recall of intraoperative
events.
Topical
INTRAOPERATIVE CARE
• MAC in conjunction with topical local anesthetic or retrobulbar block is most commonly
provided. It avoids unnecessary hemodynamic swings, airway instrumentation, and
postoperative cognitive dysfunction that may be associated with a general anesthetic in this
patient population.
– Topical anesthesia provides a safe, comfortable, expedient, and cost-effective mechanism
of pain relief. It avoids the risks of local anesthetic systemic toxicity or total spinal.
– Retrobulbar block. Provides anesthesia as well as akinesia (prevents movement). It is
typically performed by the ophthalmologist with a needle inserted in the inferior orbital
rim and advanced at a caudal angle to a depth of ∼1.5–2 cm. After careful aspiration, 2–3
mL of local anesthetic is injected.
– Peribulbar block. Typically performed by the ophthalmologist through the lower lid.
• General anesthesia is considered in certain situations such as in pediatrics, demented, or
violent patients.
Monitors
• MAC
– Supplemental oxygen; typically with a nasal cannula to avoid invasion of the surgical
field.
– Judicious titration of anxiolytics, sedatives, and/or opioids (potential for compounded
sedative or respiratory depressant effects).
– Backup airway equipment should be available.
– Although a laryngeal mask airway may be utilized, it is less secure than an endotracheal
tube (shared space and head of bed position) and may not be appropriate.
– Induction may result in wide swings in blood pressure; a slow, controlled induction should
be performed.
– Succinylcholine may be contraindicated; consider not utilizing nondepolarizing
neuromuscular blocking drugs if the procedure is expected to be quick (duration of action
may preclude reversibility in a timely manner).
Maintenance
• MAC
– Agitation may be one of the first signs of hypoxia or hypercarbia. Be cautious about
“giving more” before ruling out hypoxia and hypercarbia (especially in a patient that was
previously cooperative).
– Sedation should be titrated to patient comfort and the ability to communicate.
– Volatile or total intravenous anesthetic
– Minimal opioid administration, as a local anesthetic block is commonly performed to
reduce postoperative pain.
• MAC
– Reorient patient as needed
– Consider deep extubation to avoid coughing and bucking. However, in the event of
difficult mask ventilation, this may not be appropriate. Airway should trump all other
considerations. Consider intravenous lidocaine 2–3 minutes prior to extubation (or topical
lidocaine at the time of intubation).
POSTOPERATIVE CARE
BED ACUITY
• Outpatient surgery and discharge criteria should be met.
• Patients should not be allowed to drive themselves home.
ANALGESIA
Often not needed; consider acetaminophen
COMPLICATIONS
• Puncture site hematoma
• Retrobulbar blocks: Retrobulbar hemorrhage, local anesthetic systemic toxicity (the
proximity to the brain decreases the toxic dose required), globe perforation, optic nerve
damage, and total spinal.
• Peribulbar blocks: May need to be repeated, as they have a longer time to onset.
REFERENCES
1. Thomas R, Kuriakose T. Surgical techniques for a good outcome in cataract surgery:
Personal perspectives. J Comm Eye Health. 2000;13(35):38–39.
2. National Eye Institute (NEI). Are you at risk for cataract? Publication No 94-3463.
3. Congdon N, Vingerling JR, Klein BE, et al. Prevalence of cataract and
pseudophakia/aphakia among adults in the United States. Arch Ophthalmol.
2004;122(4):487–494.
ADDITIONAL READING
• Emmanuel N, Philippe C. Anesthesia for cataract surgery. Drugs Aging. 2010;27(1):21–38.
• Oculocardiac reflex
• Total spinal
CODES
ICD9
366.9 Unspecified cataract
ICD10
H26.9 Unspecified cataract
CLINICAL PEARLS
• Anesthesia providers are often asked to provide care for patients with significant
comorbidities. The need for efficiency and speed, combined with the low cardiac risk of the
procedure, should not preclude proper patient management.
• General anesthesia may be required in certain situations, such as in pediatric, demented, or
violent patients, but this carries an increased risk.
• MAC must implement judicious titration of medications that can cause respiratory
depression; the patient’s head is shared with the surgeon and makes easy access somewhat
challenging.
CAUDAL EPIDURALS
Peter K. Yi, MD
BASICS
DESCRIPTION
• Caudal epidurals can be used as an alternate form of intraoperative or postoperative pain
control, as well as provide intraoperative muscle relaxation and reduce anesthetic
requirements.
• Caudal epidurals are performed for:
– Surgical procedures with sacral and lower lumbar innervation
Inguinal and femoral herniorrhaphy
Cystoscopy and urethral surgery
Hemorrhoidectomy and anal dilation
Gynecologic procedures
Surgery on the penis or scrotum
– Pediatric patients for the above-mentioned surgical procedures, as well as for desired
lumbar and thoracic epidural coverage (catheter can be threaded for single shot and
removed, or remain indwelling). Entry in the epidural space at this level, as opposed to
higher in the spine, has a decreased incidence of accidental subarachnoid injection since
children have a lower lying dural sac. Additionally, the anatomy is more easily
appreciated; the sacral cornua and ligaments thicken with age.
– Chronic back pain with a radicular component. The injection of corticosteroids and local
anesthetics is usually performed with fluoroscopic guidance. In general, caudals are not
done for complex regional pain syndrome (CRPS) or cancer pain.
– Patients with prior lumbar spinal surgery that would benefit from an epidural injection; a
catheter can be threaded to the appropriate level to increase the likelihood of medications
reaching the targeted nerves.
Injectate. Because caudal epidurals are placed at the terminus of the spinal canal, an
increased volume is used to achieve appropriate anesthesia or analgesia. In addition to
volume, the patient’s age and weight can affect the epidural spread of medications.
• Pediatrics. Volumes of 0.7–1.0 mL/kg have been suggested to reach an analgesic level of
∼T10.
• Adults. Volumes of 10–25 mL are typically injected.
• Caution must be taken with the amount of volume used since loculation of the injectate can
occur and thus compromise blood supply to the spinal cord. This phenomenon can be seen
in patients who have scar tissue from previous spinal surgery.
ANATOMY
• Performing a caudal epidural requires understanding of the sacral anatomy. The anatomy is
typically easier to palpate in children; hence it is more readily used in this population.
– The sacrum is a fusion of the five sacral vertebral bodies.
– The sacral hiatus is the failure of the laminae of S5 and part of S4 to fuse together. It takes
on a variable form among individuals but is usually an inverted “V” shape.
– The sacrococcygeal ligament is the extension of the ligamentum flavum. It overlies the
sacral hiatus between the sacral cornua.
• The dural sac terminates around S3–4 in children and around S1–2 in adults, (usually at the
level of the posterior superior iliac spine). The spinal cord, however, ends around L3 in
infants and at L1–L2 in adults.
• Epidural fat is more fluid in children and thus can allow an increased range of spread. In
adults, the fat is more densely packed and limits the spread of medications.
• Chronic back pain. Caudal epidurals have been shown to have moderate levels of efficacy in
appropriately selected patients (2). Corticosteroids reduce inflammation and inhibit the
further release of pro-inflammatory mediators.
• Potential complications of caudal epidurals include:
– Infection (epidural abscess, meningitis)
– Bleeding (epidural hematoma)
– Dural puncture and associated postdural puncture headache
– Patchy spread of local anesthetic
– Nerve injury
– Local anesthetic systemic toxicity (increased vasculature compared to lumbar or thoracic
epidural spaces) from vascular absorption.
– Inadvertent subdural or intravascular injection
– Pneumocephalus, air embolism
– Back pain
– Sheared or knotted epidural catheters
• Positioning
– Children: Commonly placed in the lateral position after induction (or sedation for MAC
cases) with the knees pulled towards the abdomen
– Adults: Can be performed in the lateral or prone position while the patient is awake or
mildly sedated
• Landmarks
– Children: The sacral hiatus and cornu are typically located with palpation
– Adults: The sacral cornua and ligaments thicken with age and are not readily identified by
palpation. After identifying the posterior superior iliac spine, an imaginary line is drawn
towards the coccyx to approximate the sacral hiatus. These lines form an equilateral
triangle with the sacral hiatus located at the bottom corner.
FIGURE 1. Landmark Identification. The sacral hiatus is located at the bottom corner of an equilateral triangle formed by
lines from the posterior iliac spines.
• Preparation. As with any procedure, appropriate prep and drape as well as sterile technique
should be maintained.
• Needles
– Children: Single shot local anesthetic and/or opioid administration is commonly
performed with a 20 or 22 gauge needle. Appropriately sized epidural needles are utilized
when placement of an indwelling catheter is desired.
– Adults: The skin and subcutaneous tissue of the sacral hiatus can be infiltrated with 1–2
mL of 1% lidocaine prior to insertion. A Tuohy needle is utilized for catheter placement. A
20 or 22 gauge needle is typically used for steroid/local anesthetic injection for chronic
pain procedures
• Needle insertion: A decrease in resistance should be felt as the needle passes into the caudal
canal; it is advanced until bone is contacted. The needle is then withdrawn slightly and
redirected at an angle more parallel to the skin. Another loss of resistance is encountered as
the needle passes through the sacrococcygeal ligament and is then advanced another 1–2
cm.
• Confirming proper placement in adults:
– A syringe is attached to the needle and aspirated. If aspiration is negative for "heme" and
cerebrospinal fluid, a test dose can be administered (typically ~3 mL of lidocaine 1.5%
with 1:200,000 epinephrine). Look for signs of intrathecal (sensory/motor block within
minutes) and intravascular (increased heart rate, palpitations, hypertension) injection.
– The Whoosh test involves injection of 2 mL of air through the needle while listening with
a stethoscope placed at the thoracolumbar spine. If a “whoosh" is heard, this can indicate
that the needle is in the caudal epidural space (5).
• Local anesthetics
– Bupivacaine 0.25% or ropivacaine 0.2% can be used and provides analgesia for 6–8 hours.
– As previously mentioned, volumes are dependent on the level of anesthesia/analgesia
required for a particular case. The following can also be used as general guidelines for
dosing local anesthetics in adults:
Sacral dermatomes: 0.5 mL/kg
Sacral and lumbar dermatomes: 1.0 mL/kg
Midthoracic dermatomes: 1.25 mL/kg (increased risk of rostral spread)
• Adjuncts. The addition of epinephrine can prolong the duration of action (vasoconstriction
decreases systemic absorption and increases the duration that the local anesthetic will
remain in the epidural space).
• Indwelling catheters are placed for continuous infusion or repeat bolusing. Care should be
taken since securing and preventing catheter migration can be difficult in the sacral region.
Catheters may also be utilized when local anesthetic delivery to a higher level is desired,
but where placement of an intralaminar or transforaminal epidural injection may be
difficult. However, this is usually limited due to scar formation from prior instrumentation.
The spread and distribution of the medication can be tracked with fluoroscopy after 1–2 mL
of contrast dye is injected through the catheter
REFERENCES
1. ggarwal A, Kaur H, Batra YK, et al. Anatomic consideration of caudal epidural space: A
cadaver study. Clin Anat. 2009;22(6):730–737.
2. bdi S, Datta S, Trescot AM, et al. Epidural steroids in the management of chronic spinal
pain: a systematic review. Pain Physician. 2007;10(1):185–212.
3. Armitage EN. Regional anaesthesia in paediatrics. Clin Anesthesiol. 1985;3:553–558.
4. Barham G, Hilton A. Caudal epidurals: The accuracy of blind needle placement and the
value of a confirmatory epidurogram. Eur Spine J. 2010;19(9):1479–1483.
5. Eastwood D, Williams C, Buchan I. Caudal epidurals: The whoosh test. Anaesthesia.
1998;53(3):305–307.
6. Manchikanti L, Pampati V, Boswell MV, et al. Analysis of the growth of epidural injections
and costs in the Medicare population: A comparative evaluation of 1997, 2002, and 2006
data. Pain Physician. 2010;13(3):199–212.
7. Thomas ML, Roebuck D, Yule C, et al. The effect of volume of local anesthetic on the
anatomic spread of caudal block in children aged 1–7 years. Paediatric Anaesthesia.
2010;20(11):1017–1021.
8. Rathmell J. Atlas of Image Guided Intervention in Regional Anesthesia and Pain Medicine.
Philadelphia: Lippincott Williams Wilkins; 2006.
• American Society of Anesthesiologists Taskforce on Pain Management. Practice guidelines
for chronic pain management: An updated report by the American Society of
Anesthesiologists Task Force on Chronic Pain Management and the American Society of
Regional Anesthesia and Pain Medicine. Anesthesiology. 2010;112(4):810–833.
• Epidural
• Postdural puncture headache
• Local anesthetic toxicity
CLINICAL PEARLS
• Single shot caudal epidurals can be useful in children undergoing surgeries below the
umbilicus (e.g., inguinal or genital procedures); it can decrease the amount of general
anesthesia to be used. This can be significantly beneficial in neonates where volatile agents
can cause postoperative apnea.
• For patients on anticoagulation therapy, the general precautions apply when performing a
caudal epidural as with any other neuraxial procedure.
CELIAC PLEXUS BLOCK
BASICS
DESCRIPTION
• Celiac plexus block (CPB) is commonly used for blockade or neurolysis of visceral afferent
pain fibers to treat upper abdominal pain. The most common indication is pancreatic
cancer; however, it is also used for other abdominal cancers and occasionally for benign
conditions such as acute or chronic pancreatitis.
• In one study, good to complete pain relief at 1 week reached 85%; continued relief at 3
months was seen in 50–90% of these patients (1)[B]. Duration of the neurolytic block can
be hindered by aggressive tumors that invade the peritoneum and surrounding organs, as
well as by regeneration of new pain pathways.
• The celiac plexus is an aggregate of ganglia and a dense network of nerve fibers that
innervates most of the digestive tract.
• It contains autonomic efferent nerves that innervate the upper abdominal viscera and
visceral afferent fibers from the distal esophagus to transverse colon. Afferent fibers travel
along sympathetic nerves.
ANATOMY
• Located in the abdomen at approximately the L1 level, anterior to the aorta, and below the
crus of the diaphragm.
• Surrounds the celiac artery and root of the superior mesenteric artery.
• The plexus has several ganglia components that have the appearance of lymph nodes. The
celiac ganglia comprise the “middle” of the plexus, and vary in number (1–5), size (0.5–4.5
cm), and position relative to the vertebral column (bottom of T12 to middle of L2). The
upper portions of the celiac ganglia are joined by the greater splanchnic nerves
(sympathetic chains) after they pierce through the diaphragmatic crura, while the lower
portions receive the lesser splanchnic nerves. In addition to sympathetic fibers, it also
receives some fibers from the right vagal nerve (parasympathetic).
• Secondary plexuses arise from or connect with the celiac plexus: Phrenic, hepatic, lineal,
superior gastric, suprarenal, renal, superior mesenteric, abdominal aortic, inferior
mesenteric.
• Pancreatic cancer remains the most common indication for CPB. Tumors of the pancreas can
cause pain by invasion or stretching of nerves, involvement of viscera or organs, and
blockage of the pancreatic ducts (2)[B]. Neurolysis has been shown to be more effective
when the tumor involves the head of the pancreas. Patients with advanced tumor
proliferation and metastasis showed less favorable results. The limited therapeutic options,
short life expectancy, and opioid limitations of pancreatic cancer make CPB a potentially
effective component of a multimodal treatment regimen.
• Other abdominal malignances such as gastric, esophageal, colorectal, and gallbladder
cancer, as well as liver metastasis and cholangiocarcinoma (3)[A] may be indications for a
CPB. As with pancreatic cancer, new pain pathways, or growing tumor, can limit long-term
efficacy.
• Chronic and acute pancreatitis. CPBs are controversial for this indication; opponents state
that the lack of long-term pain reduction and potential adverse effects limit its use.
Advocates, however, assert that the improvement in quality of life (amelioration of food
intolerance, weight loss, and opioid use), even if temporary, justifies the procedure (4).
• Complications
– Hypotension. Sympatholysis of the splanchnic vasculature causes pooling of blood in this
large capacitance, vascular bed (common and transient). Prophylaxis with prehydration
(500–1000 mL crystalloid), appropriate monitoring (during and after the procedure), and
treatment can alleviate the effects and consequences. Elderly, debilitated, and acutely or
chronically dehydrated patients may be at a greater risk for hypotension (5)[A].
– Nerve injury/paraplegia. May occur from the spread of neurolytic agent to somatic nerves
(6)[B], spinal cord ischemia due to radicular artery spasm, or needle injury to the spinal
cord. Manifestations are multitudinous, transient and permanent, and of varying severity
(loss of sensation over anterior abdominal wall to paraplegia).
– Pneumothorax can occur in up to 1% of CPB blocks secondary to passing the percutaneous
needle through the pleura of the lungs. A high index of suspicion should exist in the
setting of reduced pulse oximetry, dyspnea, or tachypnea.
– Diarrhea results from unopposed parasympathetic activity (sympathetic block). Up to 60%
of patients encounter self-limited diarrhea for 36–48 hours (5)[B].
– Failed block from poor placement of the needle, alternative pain pathways, anatomic
variations, insufficient volume of neurolytic agent, or the inability to inject the agent
secondary to tumor or scar tissue encasement of the aorta in the region of the celiac
plexus. Additionally, distorted anatomical relationships (ascites, organomegaly, tumor
bulk, obesity), postradiation changes, postsurgical changes, peritoneal seeding, and
surgical clip interference may also reduce successful neurolysis. Long-term failure may be
seen when local extension of the tumor involves structures with other pain fiber
pathways.
• Anticoagulation must be discontinued with documentation of normal PT/INR and PTT if
suspicion of clotting dysfunction exists.
• Monitoring. Standard ASA monitoring. If sedative or opioid administration is given,
supplemental oxygen such as a nasal cannula or facemask should be applied. Avoid
oversedation in the prone position; oversedation also prevents assessing the effectiveness of
the local anesthetic injection prior to neurolysis.
• Imaging. Radiologic guidance is considered the standard of care to identify the needle tip
location as it is advanced, as well as the final needle position with radiocontrast before
injection of neurolytic material; most frequently performed with x-ray, fluoroscopy, or CT
assistance.
• Local anesthetic. Prior to neurolysis with permanent agents, a local anesthetic block is
performed for diagnostic and prognostic purposes to confirm that the pain is part of a
viscerally mediated pathway. Most practitioners perform this in two stages on the same day,
without moving the confirmed needle placement. Both lidocaine 0.5–2% (10–15 mL) and
bupivacaine 0.125–0.25% (10–15 mL) can be used.
• Posterior approach. There are two described techniques: The deep splanchnic nerve block
(SNB) or true CPB. The clinical effect and potential complications between the two
techniques are virtually indistinguishable. Although they both utilize percutaneous needles
introduced at the T12 level, the needle tip in relation to the diaphragmatic crura differs
(retrocrural for SNB and antecrural for CPB). The decision between the two techniques may
depend on the indication as well as potential for complications. The CPB may be more
useful for visceral abdominal pain secondary to pancreatic masses where the celiac plexus
anatomy may be distorted; it also has the benefit of being unilateral, requiring less
neurolytic agent, and possibly a more contained spread in the preaortic area. The SNB may
predispose to complications including paraplegia, resulting from diffusion of neurolytic
agents to the nerve roots, pneumothorax, or damage to the liver or kidney.
– Retrocrural SNB. After identifying the L1 spinous process, bilaterally mark points 7–8 cm
from the midline and place a skin wheal with local anesthetic. Begin on one side by
inserting a 20 or 22 g 10–15 cm needle at a 45–60% angle from the table. The needle tip
should be advanced to a final position anterior to the body of L1. In the anteroposterior
view, the needle tip should be close to the midline, overlying the same vertebral body.
This is repeated on the other side.
– Antecrural SNB (CPB). The antecrural, or true CPB, involves unilateral needle placement
anterior to the diaphragmatic crura. The right side may be preferred to avoid the aorta.
After identifying the L1 spinous process, create a skin wheal on one side 5–6 cm from the
midline. A 20 or 22 g 10–15 cm needle is inserted at a 45–60% angle from the table. The
needle tip should be advanced to a final needle position that is anterior to the vertebral
body, typically 10–13 cm of needle insertion.
– Aspiration is performed prior to injection of radiocontrast, local anesthetic, or neurolytic
agent in order to rule out CSF, urine, and blood.
• Anterior approach. Typically performed by surgeons when performing open
splanchnicectomies; or percutaneously with CT, MRI, and ultrasound imaging modalities
using “skinny needles.” Advocates of the anterior approach cite a low complication rate,
avoidance of the prone position (recent abdominal surgery, pain, pulmonary compromise
from ascites, etc.), and one puncture (less discomfort, procedure time, and volume of
neurolytic agent). Potential disadvantages include damage to the visceral organs that the
needle passes through, peritonitis and intra-abdominal abscess, hemorrhage and fistula
formation.
• Neurolytic agents. The volume injected depends on the localization of the needle and ease of
flow in the injected area. The volume of injectate is usually 25 mL through each needle,
because the needle tip is placed directly into the plexus; the anterior approach typically uses
a smaller injectate of 15–30 mL. The two available options are alcohol and phenol; studies
have not clearly delineated a benefit with one over the other.
– Alcohol. Mechanism of action involves the extraction of cholesterol and phospholipid from
the neural membrane and the precipitation of lipoproteins and mucoproteins.
Concentrations range from 50% to 100%. Benefits include the possibility of more intense
nerve destruction compared to phenol. Drawbacks include the potential for severe,
transient pain on injection; the addition of local anesthetic can reduce the discomfort.
– Phenol. Mechanism of action involves protein coagulation and necrosis of the neural
structures. Concentrations range from 6 to 10%. Benefits include less pain with injection
(has an immediate local anesthetic effect). Drawbacks include a slightly slower onset of
action, less efficacy, shorter duration, and increased viscosity that makes it difficult to
inject (6% is often preferred to the 10%).
• Radiofrequency lesioning. A “neurodestructive” procedure that lesions the nerve plexus with
temperatures that exceed 45°C. Advocates cite the benefit of a circumscribed and controlled
lesion, compared to neurolysis. The proximal and distal spread of the lesion beyond the
uninsulated tip of the probe is only 1 mm, with the cross-sectional lesion diameter 5–6 mm.
There is little or no possibility of nerve root damage or destructive damage of the epidural
and subarachnoid structures. Sensory and motor stimulation are often performed, in order
to ensure that there is no break in the insulation.
GRAPHS/FIGURES
REFERENCES
1. Firdousi FH, Sharma D, Raina VK. Palliation of celiac plexus block for upper abdominal
visceral cancer pain. Trop Doct. 2002;32(4):224–226.
2. Nakagawa T, Mori K, Nakano T, et al. Perineural invasion of carcinoma of the pancreas and
biliary tract. Br J Surg. 1993;80(5):619–621.
3. Eisesnberg E, Carr DB, Chalmers TC. Neurolytic celiac plexus block in varying locations of
pancreatic cancer: Influence of pain relief. Anesthesiology. 2000;92(2):347054.
4. Mercadante S. Celiac plexus block: A reappraisal. Reg Anesth Pain Med. 1998;23(1):37–48.
5. Raj PP. Celiac plexus/splanchnic nerve blocks. Tech Reg Anesth Pain Manag.
2001;5(3):102–115.
6. Wong GY, Brown DL. Celiac plexus block for cancer pain. Tech Reg Anesth Pain Manage.
1997;1(1):18–26.
7. Romanelli DF, Beckmann CF, Heiss FW. Celiac plexus block: Efficacy and safety of the
anterior approach. Am J Roentigenol. 1993;160(3):497–500.
8. att RB. Peripheral neurolysis. In: Patt RB ed. Cancer Pain. 1st ed. Philadelphia: J.B.
Lippincott, 1993:359–337.
ADDITIONAL READING
• Chauhan S, Forsmark CE. Pain management in chronic pancreatitis: A treatment algorithm.
Best Pract Res Clin Gastroenterol. 2010;24(3):323–335.
• World Health Organization. Cancer Pain Relief. 2nd ed. 1996.
• Singh ND. Celiac plexus blocks. In: Interventional Pain Management, Gupta A (Ed.). New
York, NY: Oxford University Press.
Autonomic nervous system
CLINICAL PEARLS
• The celiac plexus is an aggregate of ganglia and a dense network of nerve fibers uniting,
crossing through, and surrounding the ganglia that innervates most of the digestive tract.
• The two principal techniques performed via the posterior approach are the deep SNB or true
CPB. Although the CPB and SNB are anatomically different procedures, their clinical effect
and potential complications are virtually indistinguishable.
• The antecrural, or true celiac plexus block, involves needle placement anterior to the
diaphragmatic crura. Theoretical advantages of this technique are that it can be done
unilaterally, requires less total neurolytic injectate, and minimizes neurologic complications
by limiting the spread of neurolytic agent (exclusive preaortic spread), although this has not
been proven in studies.
• Radiological imaging is considered the standard of care to identify the needle tip location
while it is advanced, as well as assess final needle position with radiocontrast before
injection of neurolytic material.
• The physician must understand the potential complications in order to balance the potential
risks with the benefits of the procedure, enhance optimal patient selection, reduce the
incidence of complications, as well as maintain a high index of suspicion should they occur.
Risks include hypotension, nerve injury, diarrhea, and pneumothorax.
• Alcohol and phenol are neurolytic agents commonly used. Studies have not shown a strong
benefit of one over the other in clinical practice.
CELL MEMBRANE
Dorothea Rosenberger Parravano, MD, PhD
BASICS
DESCRIPTION
• A lipid cell membrane surrounds the cell and the majority of its intracellular organelles. Its
primary function is to control passage of substances to establish and maintain intracellular
homeostasis.
• Cell membranes can be excitable (neurons and muscle cells) and nonexcitable (tubular or
cutaneous cells).
• Cell membranes are also involved in cell-to-cell adhesion, storage of molecules, receptor
binding, cellular signaling, and intercellular communication processes.
• Active and passive transport are mechanisms for ion, molecule, and protein transfer through
the cell membrane.
– Passive transport involves movement of either particles or charge from high concentration
to low concentration (diffusion).
Ion flow through cell membranes is based on the electrochemical gradient for that
specific ion and its physical properties. The “Nernst Equation” defines the voltage
gradient at which intra- and extracellular equilibrium for a single ion is reached.
– Active transport requires energy (adenosine triphosphate, ATP) to transport against a
gradient where passive transport (diffusion) occurs along the concentration gradient.
Primary active transport mechanisms obtain energy directly from ATP hydrolysis.
Released phosphate is available for phosphorylation of carriers. Na+–K+–ATPase is an
active transporter of Na+ and K+ ions against their concentration gradient to maintain a
transmembrane, electrochemical potential/gradient.
Secondary active transport involves a carrier that has binding sites for a specific ion and
another substance to be carried along with the ion. The co-transported substance can
travel in the same or the opposite direction of the ion. An example of this is Na+-glucose
transporters in the intestinal mucosa.
Endo- and exocytosis are active transport mechanisms involving formation of membrane-
bound vesicles for uptake and release of extracellular and intracellular macromolecules.
Transport vesicles are formed by invagination of the membrane. Examples of this
include: Acetylcholine in the motor end-plate is excreted out of synaptic vesicles via
exocytosis and the uptake of cholesterol occurs through receptor-mediated endocytosis.
• Membrane receptors and channels
– Cell membrane receptors are required for intracellular uptake of amino acids,
catecholamines, peptides, and complex molecules or pharmaceuticals.
– Receptors and channels can be ligand-, voltage-, or mechanically gated.
– Ligand-gated ion channels are controlled by chemical messengers (e.g., acetylcholine).
– Voltage-gated receptors require electrical conformation changes and are controlled by
changes in membrane potential. Voltage-gated Na+ channels and K+ channels are found
in membranes of electrically excitable nerve or muscle cells.
– Mechanically gated or metabotropic receptors have G protein-mediated effects.
G proteins can control the release of second messengers that have stimulatory or
inhibitory effects.
Several G proteins may be activated by a single receptor and are capable of amplifying a
signal through several effector proteins associated with one specific G protein.
G protein receptors regulate neurotransmitter release in the sympathetic and
parasympathetic nervous system.
• Electrical membrane potentials
– The resting potential of all living cells is called the membrane potential.
– Generation of an action potential is the ability of a nerve or muscle cell to greatly change
the ion conductance of their membrane in response to a stimulus, leading to impulse
propagation along the neuron (sensory qualities such as pain) or resulting in contraction
and relaxation of skeletal and smooth muscle cells.
ANATOMY
• Cell membranes consist of a double layer of phospholipids, cholesterol, and glycolipids
(Figure 1).
FIGURE 1. Cell membrane, lipid bilayer with integral membrane proteins.

• The lipid bilayer determines the basic structure of the cell membrane and separates the cell
interior from the extracellular space. Fluidity of the bilayer allows individual lipid
molecules to diffuse rapidly within their monolayer. However, the bilayer is highly
impermeable for most polar molecules.
• Inner and outer membrane layers have variable amounts of lipids, reflecting different
functions of the specific cell membrane.
• Phospholipids and their fragments are involved in intracellular signaling pathways. They are
amphipathic with a polar and a nonpolar end. Polar ends are oriented outward, nonpolar
ends inward.
• Cholesterol helps maintain membrane integrity, plays a role in cell signaling, and maintains
membrane fluidity (separates the phospholipids so that the fatty acid chains do not come
together and crystallize). It may comprise up to half of the cell membrane.
• Glycolipids are only found in the outer cell membrane.
• Polysaccharide chains (glycocalyx) coat the extracellular surface of membrane proteins. The
glycocalyx protects the cell surface from chemical and mechanical damage and are part of
the extracellular matrix.
• Proteins are embedded within the bilayer; they can also interrupt the bilayer.
• Integral membrane proteins interrupt the bilayer. Ion channels, adhesion molecules, carrier
proteins, second messengers, and G proteins are integral membrane proteins involved in
transmembrane transport of substances.
• Cerebrum: The blood–brain barrier is formed by tight junctions around cerebral capillaries
to separate blood from cerebrospinal fluid. The barrier maintains concentrations of glucose,
neurotransmitters, and other essential substances at different levels from the rest of the
body, and prevents many pathogens from entering the brain. It is usually impermeable to
large or polar molecules, and only variably permeable to ions and small hydrophilic
nonelectrolytes. Barbiturates, propofol, etomidate, and benzodiazepines can cross the
blood–brain barrier. Whenever the cell-to-cell junctions are disrupted, water, electrolytes,
and large hydrophilic molecules can enter perivascular brain tissue and lead to vasogenic
cerebral edema.
• Cardiac: Electrolyte disorders can lead to disturbed electrical conduction due to changes in
the resting membrane potential. Hyperkalemia increases the resting membrane potential
(less negative; e.g., -90 mV to -80 mV) and increases the speed of repolarization.
• Pulmonary: Oxygen and carbon dioxide move between air and blood by diffusion through
the alveolar–capillary barrier down a partial pressure gradient. Disruption of the basal
membrane can lead to increased protein (colloidal) movement, which creates an oncotic
pressure gradient for water movement (Starling’s equation) into the pulmonary
parenchyma. This disturbance leads to “thickening" of the alveolar-capillary barrier as well
as increases alveolar collapse (decreased FRC); diffusion of oxygen and carbon dioxide can
be markedly affected (noncardiogenic pulmonary edema).
• Intestinal: Gastric parietal cells secrete H+ into the gastric lumen in exchange for K+ by the
H+–K+ ATPase. Acid secretion is stimulated by histamine via H2 receptors (G protein
driven mechanism) as well as acetylcholine via M3 muscarinic receptors (Ca2+ as second
messenger). Overstimulation leads to high gastric acidity and risks disruption of the intact
mucosal barrier, causing tissue ulceration. Pharmacologic agents such as omeprazole block
the H+-K+ pump to decrease gastric acidity.
• Renal: Filtration, absorption, concentration, and excretion of urine depend on receptors,
carriers, channels, and pores in tubular cells and the nephron. Increased permeability of
tubular cells leads to influx of proteins into the urine, a first sign of renal insufficiency.
Defects in the renal countercurrent transporter impair its concentrating ability and can
manifest as polyuria or anuria. Aminoglycoside antibiotics can damage tubular epithelium
and disrupt cellular fluidity and Na+-K+ ATPases, potentially causing renal failure.
• Endocrine:
– Iodine uptake into the thyroidal cell depends on a secondary active Na+/I cotransporter.
Nitrates or perchlorates compete with iodine for intracellular uptake on the transporter
resulting in decreased iodine uptake. This leads to a decline in circulating thyroid
hormones, increased TSH, and goiter formation.
– Glucose enters the cell via facilitated diffusion or by secondary active transport with Na+.
Glucose transporters are potential targets for novel antidiabetic drugs.
• Anaphylaxis: A trigger substance induces mainly IgE-related pathways. IgE is produced in
response to allergen exposure, and binds to a high-affinity IgE membrane receptor on mast
cells and basophils. Activation leads to release of various inflammatory mediators (e.g.,
histamine, tryptase, prostaglandin, and leukotrienes) affecting integumentary, respiratory,
GI, cardiovascular, and central nervous systems. Hypotension, tachycardia, and edema are
clinical symptoms of disrupted cell membrane integrity and binding of mediators to cellular
membrane receptors.
• Benzodiazepines bind to GABA receptors and enhance GABA neurotransmitter binding with
resultant chloride ion transport into the cell (hyperpolarizes the membrane resting
potential).
• Local anesthetics inhibit fast Na+ channels that are responsible for Phase 0 depolarization.
Perioperatively, they are used to disrupt sensory, motor, and autonomic nerve conduction.
Effects have variable duration, depending on the receptor affinity and the degradation,
distribution, and metabolism of the substance and its byproducts.
• Opioids bind to μ, kappa, ORL1, and NMDA receptors in the cerebrum, spinal cord, and
several peripheral tissues, leading to pain relief, respiratory depression, sedation, itching,
and constipation.
• Propofol, etomidate, and ketamine bind to GABA and NMDA receptors, inducing reversible
loss of consciousness and sensation. Different affinities to GABA receptors, their subtypes,
and specific subunits determine the action, duration, and side effects of these induction
agents.
– Propofol binds to GABA-A receptors. Propofol also blocks Na+ channels and might have
an effect on various endogenous opioid receptors.
– Etomidate binds also to GABA-A receptors.
– Ketamine is an antagonist at the NMDA receptor and also binds to dopamine and opioid
receptors depending on the given dose.
• Neuromuscular blocking drugs can be used to facilitate intubation, surgical procedures, and
mechanical ventilation.
– Nondepolarizing agents (e.g., pancuronium) are nicotinic receptor competitive
antagonists; they prevent acetylcholine binding.
– Depolarizing agents (e.g., succinylcholine) mimic acetylcholine at the cell receptor. They
bind to the receptor and depolarize the muscle cell (causing contraction), and then
prevent acetylcholine from binding to the receptor until they detach.
• Inhalational agents have sedative and hypnotic effects that are thought to be caused by
binding to NMDA receptors (acting as receptor blocking) and GABA receptors (inhibiting
effects enhanced). However, most of the cellular mechanisms are still unknown.
EQUATIONS
• Nernst Equation: Determines ion flux across the membrane. Flux is dependent on the
gradient between intra- and extracellular ion concentration.
REFERENCES
1. Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell, 5th ed. New York:
Garland Science, 2008.
2. anong, WF. Review of Medical Physiology, 22nd ed. New York: McGraw Hill
Medical/Lange, 2008.
• Diffusion
• Blood–brain barrier
• PaO2
• PaCO2
• Hyperkalemia
CLINICAL PEARLS
Malignant hyperthermia (MH): The combination of volatile anesthetics and/or
succinylcholine in individuals with inherited defects at the ryanodine receptor can lead to a
life-threatening hypercatabolic state. About 6 gene loci have been identified to be responsible
for this reaction, along with at least 25 possible mutations in the gene expressing ryanodine
receptor protein in the sarcoplasmatic reticulum (SR). Specific gene loci are responsible for
forming Ca2+ channels that control Ca2+ flux intra- and extracellularly from the SR. Drastic
increases in Ca2+ lead to muscle rigidity, a leading symptom of MH. Other symptoms include
a high end-tidal carbon dioxide, temperature increase, tachycardia, hyperkalemia,
respiratory, and metabolic acidosis and rhabdomyolysis. Dantrolene, a muscle relaxant itself,
can block further Ca2+ excretion from the SR and is the only know effective antidote for an
MH crisis.
CELL SALVAGE
Alan Ashworth, MBChB, FRCA, FFICM
Andrew A. Klein, MD
BASICS
DESCRIPTION
• Autologous transfusion describes returning the patient’s own blood to them, whereas
allogeneic transfusion describes transfusing someone else’s blood to a patient. Autologous
transfusion potentially avoids many of the adverse effects associated with allogeneic
transfusion.
• Cell salvage, commonly referred to as “cell saver,” involves suctioning, washing, and
filtering blood from the surgical field, then returning it to the patient. This is the most
common autologous transfusion technique.
• It is commonly (but not exclusively) used in cardiac, neurologic, hepatic, vascular, and
orthopaedic surgery where expected blood loss is significant enough to merit the cost.
• History of cell salvage. First used in the 18th century when managing patients with
postpartum hemorrhage. Blood-soaked swabs were washed in saline and then the mixture
was reinfused; not surprisingly, this was associated with a high mortality. Throughout the
19th century, experimentation with cell salvage and autologous transfusion continued. In
1931, blood salvaged from hemothoraces was directly reinfused into patients. The first cell
salvage autotransfusion device was developed in 1943 by straining suctioned blood through
a cheese cloth, which forms the basis of modern cell salvage machines.
• The process of cell salvage can be separated into collection, washing, and reinfusion.
• Collection. A dedicated double-lumen suction device allows collection of red blood cells
(RBCs) from the operative field. One lumen suctions blood from the operative field and the
other lumen adds a predetermined volume of anticoagulant flush to the salvaged blood.
Heparinized saline flush is commonly used; its composition depends on manufacturer
guidelines, and typically consists of 30,000 U of heparin in 1,000 mL of 0.9% saline. Some
centers substitute this with a citrate solution. The anticoagulated blood passes through a
filter to remove debris and is then collected in a reservoir.
• Washing. Centrifugation separates the components of blood into RBCs and plasma. The
washed RBCs are then filtered across a semipermeable membrane, which removes free
hemoglobin, plasma, platelets, white blood cells, and heparin.
• Reinfusion. Salvaged RBCs are then suspended in normal saline at which point they can be
reinfused via any peripheral or central venous catheter. The salvaged RBCs may be
transfused immediately or within 6 hours (1). The solution has a hematocrit of 50–70%,
depending on the cell saver machine. In practice, however, some heparin (up to 5%) is not
removed, and a variable quantity of other substances such as leukotrienes and complement
may also be mixed with the red cells. Plasma containing clotting factors and platelets are
removed and wasted during the washing process.
• The use of cell salvage in obstetrics and cases of malignancy or microbiological
contamination remains controversial.
• Obstetrics. There exists a theoretical risk of precipitating amniotic fluid embolus (AFE) if
amniotic fluid is not completely removed by the washing process. Recent evidence has
shown that reinfusion of RBCs salvaged during elective Caesarean section is not associated
with an increase in the incidence of AFE (2).
• Malignancy. Previously, was an absolute contraindication due to the theoretical risk of
disseminating tumor cells. However, studies in patients with urological malignancy have
showed that cell salvage and autologous transfusion were not associated with an increase in
biochemical recurrence rates of prostate cancer and was effective at reducing allogeneic
blood transfusion requirements (3). Therefore, certain cases may merit the use of cell
salvage during surgery for malignancy, provided the risks and benefits are discussed with
the surgeon and patient.
• Infection. In cases where there is potential contamination of salvaged blood with bowel
contents or purulent material, the use of cell salvage is contraindicated by the
manufacturers. However, there is some evidence that cell salvage in combination with a
leucocyte depletion filter (LDF) may be safe. Therefore, infection or enteric content should
no longer be considered an absolute contraindication. In cases where there is gross enteric
content contamination, the surgeons should avoid suctioning the most contaminated areas,
broad spectrum antibiotics should be administered, and the volume of saline wash should
be increased. Risks and benefits of cell salvage use should be discussed with the surgeon and
patient preoperatively.
• The aim of cell salvage is to reduce or eliminate the need for allogeneic blood transfusion. A
recent meta-analysis found that cell salvage was efficacious in reducing the need for
allogeneic blood transfusion in adult elective surgery by 39%, with an average saving of 0.7
units per patient (4). This could
– Reduce the risks of infectious and noninfectious complications of allogeneic blood
transfusions.
– Increase the mean erythrocyte viability compared to autologous blood. Salvaged RBCs
maintain their normal biconcave disk shape, whereas allogeneic blood assumes an
echinocyte shape (after 14 days), which is thought to impair its ability to flow through the
capillary beds.
– Increase 2,3-diphosphoglycerate (2,3-DPG) compared to autologous blood, which
improves oxygen-carrying capacity and tissue oxygen delivery.
– Increase patient survival. Studies have shown that following an esophagectomy, there is
increased survival, which may be due to the lack of immunomodulatory effects of
salvaged blood compared to allogeneic blood.
– Have immunostimulatory effects that may reduce postoperative infections.
• Cell salvage should be considered in advance for cases where blood loss may exceed 1000
mL in adults and 10 mL/kg in pediatrics.
• If unsure about blood loss, consider setting up cell salvage as backup. This means prepare
the reservoir, suction tubing, and heparinized saline flush (inexpensive and quick). If blood
loss (after subtracting heparinized saline and any other wash fluids) occurs, the machine
can then be set up to process the blood. If blood loss is minimal, this can then be discarded.
Such a policy would generate considerable savings in terms of allogeneic blood, and
potentially in healthcare costs.
• Cell salvage complications. The literature shows that complications associated with the use
of cell salvage are rare. In cases where patients are autotransfused large volumes of
processed RBCs, this may be accompanied by coagulopathy because of the loss of clotting
factors and platelets (see above).
– In cases where the volume of blood washed is less than 30% of the patient’s total blood
volume, studies have shown that there is no increase in perioperative bleeding, and that
no coagulopathy can be detected (5).
– The point at which coagulopathy associated with cell salvage becomes clinically relevant
varies between patients, but it is not likely until >50% of the patient’s blood volume has
been washed (around 3,000 mL in the average sized adult).
– If the patient is actively bleeding, thromboelastography, prothrombin time, fibrinogen,
and platelet counts should be performed.
– Blood product replacement with plasma, cryoprecipitate, and/or platelets should be
performed.
• Allogeneic blood transfusions have been affiliated with the following risks:
– Tumor recurrence
– Postoperative infections
– Acute lung injury
– Perioperative myocardial infarction
– Postoperative low-output cardiac failure
– Increased morbidity and 5-year mortality
– Immunomodulation is dose dependent; transfusion of allogeneic blood is associated with
decreased transplant rejection.
• Developing abnormal antibodies. Exposure to multiple units of allogeneic blood makes
future cross-matching more difficult and time consuming.
REFERENCES
1. shworth A, Klein AA. Cell salvage as part of a blood conservation strategy in anaesthesia.
Br J Anaesth. 2010;105:401–416.
2. Geoghegan J, Daniels JP, Moore PAS, et al. Cell salvage at caesarean section: The need for
an evidence-based approach. Br J Obstet Gynaecol. 2009;116:743–747.
3. Nieder AM, Carmack AJK, Sved PD, et al. Intraoperative cell salvage during radical
prostatectomy is not associated with greater biochemical recurrence rate. Urology.
2004;65:730–734.
4. Carless PA, Henry DA, Moxey AJ, et al. Cell salvage for minimizing perioperative
allogeneic blood transfusion. Cochrane Database Syst Rev. 2006;4:CD001888.
5. Klein AA, Nashef SAM, Sharples L, et al. A randomized controlled trial of cell salvage in
cardiac surgery. Anesth Analg. 2008;107:1487–1495.
• Transfusion infections
CLINICAL PEARLS
• Cell salvage (“Cell Saver”) is the most common form of autologous blood transfusion. RBCs
are isolated and purified from suctioned blood, resuspended in saline, and reinfused in the
patient.
• In elective cases, cell salvage has been shown to increase erythrocyte viability, oxygen-
carrying capacity, possibly reduce infection, and increase survivability compared to
allogeneic transfusion.
• Cell salvage has generally been contraindicated in cases where reinfusion could theoretically
spread pathology (obstetrics, malignancy, cases involving infection). However, studies have
not supported this finding and certain cases may merit its use after careful discussion with
the surgeon and patient.
CEMENT IMPLANTATION SYNDROME
Valbona Kanarek, MD
BASICS
DESCRIPTION
• Cement implantation syndrome (CIS) is a rare and potentially fatal complication in patients
undergoing cemented total hip arthroplasty (THA).
• Methylmethacrylate (MMA), or bone cement, is utilized to secure the implant to the joint. It
can result in peripheral vasodilatory effects, fat and marrow embolism, and activation of the
clotting cascade in the lungs.
• CIS occurs around the time of prosthetic insertion and is characterized by a constellation of
clinical features:
– Hypoxia
– Decreased systemic vascular resistance (SVR)
– Increased pulmonary vascular resistance (PVR)
– Confusion
– Cardiac arrhythmias, or arrest
EPIDEMIOLOGY
Prevalence
• True incidence is unknown, likely from underreporting and/or a wide variety of clinical
presentations.
• Hypotension during THA: 2% as defined as a reduction in SBP>30% (1)[C]
• Desaturation of more than 5%: 17% (2)[C]
• CIS has been associated with other procedures (vertebroplasty, total knee arthroplasty, hip
hemiarthroplasty) where bone cement is used.
Mortality
• Intraoperative mortality due to cardiopulmonary complications in patients undergoing
cemented THA: 0.11% (0% for those with uncemented THA) (2)[C].
• Cemented THA for pathological bone fractures: 4.3% (1)[C].
• Increased in elderly patients and those with impaired cardiopulmonary function (2)[B].
• Injection of pressurized bone cement intramedullarily
• Increased age
• Poor preexisting physical reserve
• Pulmonary hypertension
• Impaired cardiopulmonary function
• Bone metastases with pathologic hip fractures, femoral fractures
• Patent foramen ovale (PFO): increased risk for paradoxical emboli and neurological sequela
• A previously uninstrumented femur increases the risk for CIS since there may be more
potential embolic material, and a previously cemented inner surface of the femur becomes a
less permeable surface.
• Bone cement is utilized to improve femoral contact surface area with the prosthesis.
• The exact pathogenesis of CIS is not well understood. Several models have been suggested to
account for the hemodynamic and pulmonary changes and involve either mechanical
and/or chemical causes.
• The MMA monomer model suggests a chemical-mediated pathogenesis with circulating
MMA particles causing worsening pulmonary artery pressure (PAP) or reducing SVR (3)[A]
(1)[B]. These monomers have been linked to histamine and IgE release (possible
complement activation) with resultant:
– Pulmonary artery vasoconstriction
– Increased microvascular permeability and noncardiogenic pulmonary edema
– Bronchospasm
– V/Q mismatch (due to decreased ventilation and shunting of nonoxygenated blood to the
systemic circulation)
– Hypoxia
• The embolization model suggests a mechanical and chemical model. Bone marrow, fat,
fibrin, and platelet debris emboli are seen with transesophageal echo (TEE) in the right
atrium during preparation of the femoral canal, prosthesis insertion, and cement placement
(4)[A]. This can result in
– Direct mechanical obstruction of the pulmonary vasculature causing V/Q mismatch (dead
space: Ventilating but not perfusing) and increased afterload to the right ventricle (RV)
with subsequent RV dysfunction (increased central venous pressure, CVP, increased JVD)
– Chemical endothelial damage of the pulmonary vasculature from vasoactive substances
such as thrombin, platelet activating factor, and endothelin-1
Increased shunt
Increased PVR
Increased RV afterload
Decreased cardiac output (CO) and decreased SV (4)[B] with resultant cerebral and
cardiac ischemia (tachyarrhythmias, ST changes).
Tissue thromboplastin and adenine nucleotides cause profound reductions in SVR with
worsening cerebral hypoperfusion leading to confusion, or loss of consciousness.
• Multimodal model. CIS is most likely a constellation of the above processes (1,5)[B].
However, the extent to which each of the above models contributes to the clinical
presentation of the patient will depend on the patients preexisting cardiovascular function.
The impact of mechanical insult (fat, marrow, platelet debris) and chemical insult
(vasoactive substances from pulmonary endothelial damage) on SVR, PVR, cardiac function,
and V/Q mismatch (increase shunt and increase dead space) varies in severity among
patients.
• Paradoxical embolization of marrow debris occurs in the presence of a PFO. The debris
bypasses the lungs and spills into the systemic, cerebral, or coronary arteries which can lead
to embolic strokes and acute coronary ischemia. Embolization is not always associated with
these hemodynamic changes and the degree of embolization does not correlate with the
severity of hypotension or hypoxemia (6[A].
• Anesthetic strategies to minimize the occurrence of CIS:
– Maintain euvolemia
– Increase FIO2 prior to cementing.
– Avoid nitrous oxide in high risk patients; it can increase the size of air emboli as well as
increase PVR.
• Surgical strategies to decrease the occurrence of CIS:
– Drill a vent hole in the femur prior to prosthesis insertion; this decreases the risk of
intramedullary hypertension and emboli formation (5)[B].
– Utilize a cementless prosthesis. This has the added benefit of lasting longer, but requires
that the patient has good bone growth (younger population) and can increase recovery
time.
• ETCO2 decreases are sensitive indicators of worsening dead space. CIS can result in
microemboli that can lodge in the pulmonary vasculature as well as decreased cardiac
output. Carbon dioxide continues to be produced by tissues, but in both circumstances,
cannot reach alveolar capillaries for exhalation from alveoli (PaCO2 increases).
• In addition to standard anesthetic monitoring, invasive hemodynamic monitoring is
recommended for high-risk patients.
• CVP monitoring to guide:
– Fluid management
– Right atrial filling pressures
– Inotrope administration
– However, this is not a reliable monitor for left ventricular function
• Arterial pressure monitoring can provide
– Beat-to-beat blood pressure monitoring
– PaO2 measurements can detect changes in oxygen partial pressure despite the pulse
oximetry reading 100%
• Pulmonary artery catheter (PAC) can provide
– CVPs
– PAPs
– Left ventricular end-diastolic pressures
– CO
– Mixed venous oxygen saturation
– SVR
• TEE for high-risk patients to monitor for
– Large emboli
– Segmental wall motion abnormalities
– Cardiac function
• Acute coronary syndrome
• Pulmonary embolus
• Cerebrovascular accident
TREATMENT
• 100% inspired oxygen to optimize oxygen delivery to ischemic areas.

• RV hemodynamic support with ephedrine, epinephrine, or milrinone. Milrinone is a
phosphodiesterase inhibitor that increases contractility while decreasing afterload (in this
case PVR).
• SVR support with norepinephrine, ephedrine, or epinephrine.
• Cardiopulmonary resuscitation with compressions in the event of PEA.
FOLLOW-UP
If hemodynamic stability is achieved, consider continuing the surgical procedure.
REFERENCES
1. Donaldson AJ, Thomson HE, Harper NJ, et al. Bone cement implantation syndrome. B J
Anaesth. 2009;102:12–22.
2. Parvizi J, Holliday AD, Ereth MH, et al. Sudden death during primary hip arthroplasty. Clin
Orthop Relat Res. 1999;369:39–48.
3. Ereth MH, Weber JG, et al. Cemented vs. non-cemented THA, embolism, hemodynamics
and intrapulmonary shunting. Mayo Clinic Proc. 1992; 67:1066–1074.
4. Urban M, Sheppard R, Gordon M, et al. Right ventricular function during revision total hip
arthroplasty. Anesthesia Analgesia. 1996;82:1225–1229.
5. Christie J, Robinson C, Singer B, et al. Medullary lavage reduces embolic phenomena and
cardiopulmonary changes during cemented hemiarthroplasty. J Bone Joint Surg. 1995;77-
B:456–459.
• Fat embolism syndrome
• Dead space
• Pulmonary artery catheter
• Transesophageal echocardiogram
• Atrial septal defect
CLINICAL PEARLS
• Vigilance to physiologic parameters during cementing.
• Intravenous fluid repletion, invasive monitoring in patients with poor reserve.
CENTRAL LINES
Edna Ma, MD
BASICS
DESCRIPTION
General
• Central venous catheter (CVC) placement involves cannulization of a large vein of the neck
(internal jugular or external jugular vein), the chest (subclavian vein), or groin (femoral
vein).
• CVC is used for the administration of
– Medications: Vasoactive drugs, hyperosmolar medications, chemotherapeutic agents, long-
term antibiotic use
– Cardiovascular (CV) measurements: Central venous pressure
– Venous access for frequent blood tests: Including mixed venous oxygenation saturation
– Cardiac pacing
– Hemodialysis
– Nutrition: Total parenteral nutrition (TPN)
• Surgical placement of central lines are often performed in the operating room, entail larger
bores, provide longer-term access, and have the option of utilizing an open approach.
• Tunneled catheters are inserted in the operating room into either the internal jugular or
subclavian veins via an open approach or “cut-down.” The distal end of the catheter is
passed under the skin and emerges at a site separate from the insertion site; it is connected
to either a subcutaneous port or a port that emerges through the skin for direct access. IV
contrast dye may be injected to confirm vascular placement.
– The advantages to having a tunneled catheter include patient comfort, stability, and
prevention of infection. An implantable port lies completely under the skin so patients can
swim and bathe normally.
– An implantable port is a reservoir that can be filled and releases medication into the
patient’s bloodstream; it is accessed with a special noncoring (Huber) needle that will not
damage the ports rubber septum.
– An example of a tunneled catheter with an implanted port is the “Port-a-cath,” and is used
for chemotherapy or TPN.
• Nontunneled catheters. Typically performed percutaneously with the catheter and its ports
fixed in place at the site of insertion.
– Frequently performed at the patient’s bedside
– Examples include triple- or double-lumen catheters placed in the internal jugular or
subclavian veins; as well as Quinton catheters, which are used for temporary access for
dialysis.
• PICC lines: peripherally inserted central catheters. Typically inserted through one of the
veins (e.g., cephalic, basilic, and brachial vein) in the upper extremity. The catheter is
inserted through a peripheral vein and threaded so its tip rests in the distal superior vena
cava or cavoatrial junction.
– Typically inserted outside of the operating room, with the assistance of an ultrasound
device, by doctors, physician assistants, or certified nurses.
Position
• Trendelenburg; improves vein “engorgement” and prevents air entrainment into the
intravascular space.
• Lateral rotation of the patient’s head can improve access to the subclavian and internal
jugular veins.
Incision
• A hollow bored needle, with continuous negative pressure, is introduced through the skin
until blood is aspirated.
• The entry site may be enlarged using a dilator or small skin incision for catheter placement.
• The catheter can be tunneled under the skin and connects to a subcutaneous port.
Approximate Time
10–30 minutes
EBL Expected
<10 mL
Hospital Stay
• Depends on the CVC indication
• Outpatient procedure for long-term antibiotic therapy or chemotherapy.
• Ultrasound guidance device
• Fluoroscopy and IV contrast dye
• Postprocedure chest x-ray
EPIDEMIOLOGY
Prevalence
>5 million are inserted every year in the US (1)
Morbidity
Greater than 15% have complications (2), including
• Pneumothorax
• Vascular injury
• Infection
• Thrombus
• Venous air embolus
• Hemorrhage
• Hematoma
• Arrhythmias
• Loss of guidewire
• Valvular or cardiac perforation
Mortality
Associated with
• Catheter or wire embolism
• Vascular injury; hemothorax, hydrothorax, carotid artery injury, subclavian artery injury,
pulmonary artery rupture (3)
• The anaesthetist has the option of minimal to no sedation or a general anesthetic with a
laryngeal mask airway (LMA) or endotracheal tube (ETT). The decision is based on the
patient’s comorbidities and ability to lie still in the Trendelenburg position as well as the
surgical provider’s preference.
• The two requisites of a venous air embolism (VAE) are direct communication between an air
source and vasculature in addition to a pressure gradient that favors passage of air into the
circulation. CVC equipment allows direct access to the vein, and when the patient is
spontaneously ventilating, or obstructing, a negative pressure breath can provide the
driving force.
SYMPTOMS
• Chemotherapy access patients could include treatment for breast or colon cancer or
lymphomas.
• Hemodialysis access patients could include uremia symptoms, anemia, acidosis, and volume
overload.
• PICC line access patient could include those in need for long-term antibiotic or
chemotherapy.
History
Requires an assessment of the indication and underlying disease.
Signs/Physical Exam
Variable
MEDICATIONS
Peripheral nutrition infusion may be held during the procedure.
Labs/Studies
• Coagulation studies
• Potassium value may be performed; however, the access is often placed in order to dialyze
and regain electrolyte homeostasis.
Variable
TREATMENT
Premedications
Anxiolysis as appropriate
When performing under sedation, a discussion with the patient and family should include
realistic goals and the possibility of recollection of certain events. Additionally, the patient
should be aware that they may be asked to “breath hold” during cannulation.
Skin organisms; a third-generation cephalosporin such as cefazolin may be indicated.
INTRAOPERATIVE CARE
• Local with only lidocaine for subcutaneous anesthesia
• Sedation
• General anesthesia is often chosen for pediatric, uncooperative, demented, or anxious
patients; as well as patients who cannot tolerate head-down position due to comorbidities
(risk for aspiration, reduced functional residual capacity, and pulmonary edema).
– LMA may be considered when aspiration is unlikely.
– ETT placement should be considered if there is a potential for aspiration or a difficult
airway (prior neck radiation or obesity).
Monitors
• Sedation: Anesthetic goals should include patient comfort for positioning (e.g.,
Trendelenburg, tunneling of catheter, and arms tucked) and subcutaneous infiltration of
local anesthetic.
• General anesthesia: ETT insertion may be improved with the assistance of muscle relaxation.
If needed, consider succinylcholine for its short duration; however, it may be precluded
given comorbidities (patients presenting for dialysis who have hyperkalemia). If a
nondepolarizing agent is utilized, its duration of action/ability to be reversed may exceed
the duration of the procedure.
Maintenance
• Sedation should be titrated cautiously. Oversedation can result in obstruction and may
increase the potential for VAE during instrumentation and tunneling.
• General can be maintained with volatile or IV agents.
• Sedation: Reorient patient that the procedure is complete.
• General: Standard extubation criteria apply.
FOLLOW-UP
BED ACUITY
Postprocedure upright chest x-ray to confirm placement and rule out complications.
ANALGESIA
Minimal to none. Soreness at the site may be treated with acetaminophen.
COMPLICATIONS
• VAE
– The awake patient may present with acute dyspnea, continuous cough, gasp reflex,
lightheadedness, and vertigo. Cardiac manifestations (in awake and asleep patients)
include dysrhythmias, peaked P waves, ST segment changes, JVD, right heart failure, low
BP, and CV collapse.
– Preventive measures include Trendelenburg position and occlusion of the needle and hub
during placement and removal, avoidance of deep inspiration when the patient is SV
(avoids negative pressure/suction effect), and PEEP when positive pressure ventilation
(PPV) is being administered.
– When Trendelenburg is contraindicated (increased ICP), consider temporary positioning
during insertion of the guidewire or catheter, or raising the legs to increase venous return
and pressure in the right atrium.
• Pneumothorax may be diagnosed by physical exam (absent breath sounds on ipsilateral side
of chest +/– hypotension) and/or chest x-ray. Incidence may be minimized by the use of
ultrasound guidance. Treatment typically involves chest tube placement to evacuate the
pleura air and re-expand the lung.
• Hemothorax; diagnosis and treatment are similar to pneumothorax.
REFERENCES
1. aad I. Intravascular-catheter–related infections. Lancet. 1998;351:893–898.
2. Sznajder JI, Zveibil FR, Bitterman H, et al. Central vein catheterization: Failure and
complication rates by three percutaneous approaches. Arch Intern Med. 1986;146:259–
261.
3. Bowdle TA. Central line complications from the ASA closed claims project: an update. ASA
Newsletter. 2002;66(6):11–12 & 25.
• Pneumothorax
• End-stage renal disease
CLINICAL PEARLS
• The anesthesia provider may be called on to provide care to patients requiring tunneled
central line access in the operating room in the form of no sedation, sedation, or general
anesthesia.
• Additionally, the anesthesia provider frequently place central lines via the percutaneous
approach for intraoperative or postoperative care.
• VAE, pneumothorax, and hemothorax are serious and potentially fatal complications of CVC
placement; efforts should be made to reduce the incidence, and treatment should be
aggressive.
CEREBRAL ARTERIOVENOUS MALFORMATION
Joseph R. Whiteley, DO
Thomas I. Epperson III, MD
BASICS
DESCRIPTION
• Brain arteriovenous malformations (BAVM) are abnormal tangles of dilated arteries and
veins, known as an arteriovenous nidus, that directly shunt blood between the arterial and
venous circulations without a true capillary bed.
• The harmful effects of BAVMs can be the result of a mass effect, rupture (intracranial
hemorrhage), ischemia to surrounding brain tissue, and the ability to incite seizure activity.
• Following a BAVM rupture, surgery may be delayed until the patient has recovered from the
effects of the bleed, unless the hematoma is causing clinical deterioration.
• Procedures to treat brain AVMs include preparatory and therapeutic embolization, surgical
resection, and stereotactic radiosurgery.
EPIDEMIOLOGY
Prevalence
Approximately 1 per 100,000 adults per year are newly diagnosed. Children comprise 3–19%
of all AVM patients.
Prevalence
Estimated at ∼0.01% of the general population, with reported rates from 0.001% to 0.52%
Morbidity
• Accounts for 1–2% of all strokes; in young adults, it is responsible for 4% of all strokes and
9% of subarachnoid hemorrhages.
• Of AVM hemorrhages, 30–50% result in permanent neurologic deficits.
Mortality
Hemorrhage risk 2–4% per year, with 5–10% of hemorrhages resulting in death.
• Cause remains unknown. Two hypotheses for AVM pathogenesis are embryonic agenesis of
the capillary system and retention of primordial vascular connections between arteries and
veins. However, intrauterine and neonatal ultrasonography do not support this assertion.
• Current thought is a multifactorial etiology, with contributions from
– Genetic polymorphisms: Active angiogenic and inflammatory phenotypes, such as
overexpression of vascular endothelial growth factor-A and matrix metalloproteinase.
– Environmental exposures, while lacking strong evidence, may include unremarkable
episodes of trauma, infection, and inflammation.
• Vast majority are sporadic, not familial.
• AVMS are high-flow, low resistance shunts that lack a true capillary bed. Pathologic
consequences can result from:
– Diversion of blood from surrounding tissue can result in inadequate perfusion and
ischemia.
– Rupture of a feeding artery in a small AVM, or more commonly, from the eventual rupture
of dilated veins exposed to high arterial pressures. Normally, veins receive low pressure
blood from capillary beds; whereas with AVMs, the thin, nonmuscular walls of veins face
abnormally high transmural pressures.
• AVMs are dynamically changing vascular pathologies; they can enlarge or shrink over time.
Growth, remodeling, and/or regression of brain AVMs are thought to be due to a
combination of factors: both molecular (growth factors and extracellular proteins) and
physiologic (arterial and venous blood flow forces).
• For both open craniotomy resection and interventional embolization procedures, the goals
of anesthesia are to provide a motionless field, maintain cerebral perfusion pressure (CPP),
provide brain relaxation and optimize the surgical field through controlled ventilation
and/or diuretics, and to decrease brain tissue oxygen demand by lowering cerebral
metabolic rate with anesthetic agents.
• Rapid and controlled emergence with tight hemodynamic control and early postoperative
neurologic exam.
• In the setting of rupture: hypotension is induced; cerebral protection is maximized with
varying combinations of barbiturates, propofol, or volatile agents to decrease cerebral
metabolic rate; and hyperglycemia and hyperthermia are avoided.
SYMPTOMS
• Headaches (specifically migraines)
• Vertigo/dizziness
• Dysarthria or apraxia
• Numbness and tingling
• Bruit – audible to patient
History
Most commonly discovered in young adults aged 20–40 who present with hemorrhage or
seizure.
Signs/Physical Exam
• Seizures
• Neurologic deficits
• Intracranial hemorrhage, most common presenting sign (20–50% of patients).
TREATMENT HISTORY
• Surgical resection (craniotomy, microsurgical) for low-grade lesions (Spetzler–Martin
grading scale I–III); high-grade lesions require multimodal treatment. Most commonly used
in pediatric cases.
• Embolization (minimally invasive) may be therapeutic; or can be used to obliterate fistulas
and feeding arteries to decrease blood flow in preparation for surgery.
• Stereotactic radiosurgery (noninvasive) for lesions <2 cm and in deep locations not easily
approachable by microsurgical or endovascular techniques.
• Observant management may be indicated in older patients with comorbid conditions.
MEDICATIONS
• Antiepileptics: Phenytoin, levetiracetam, carbamazepine
• Antihypertensives
– Direct-acting vasodilators: Sodium nitroprusside, hydralazine
– Adrenoreceptor antagonists: Labetalol, esmolol
– Calcium channel blockers: Nimodipine, nicardipine, clevidipine
• Osmotic agents (mannitol, hypertonic saline) following an intracranial bleed may be
administered to create an osmolar gradient across an intact blood–brain barrier. This results
in brain relaxation and decreases intracranial pressure (ICP).
Labs/Studies
• CT: Sensitive for detecting acute hemorrhage
• Computed tomographic angiography (CTA): Allows visualization of AVM vascular detail.
• MRI or magnetic resonance angiography (MRA): Allows visualization of the AVM and
surrounding structures.
• Digital subtraction angiography (DSA): The gold standard to evaluate AVM. Detects
associated aneurysms, venous outflow obstruction, and patterns of venous drainage.
• Superselective WADA testing (intracarotid sodium amobarbital procedure). One hemisphere
of the brain is briefly anesthetized and the patient undergoes a series of language and
memory-related tests. Determines hemisphere dominance and whether surgery will affect
language and memory.
• Functional MRI helps assess the relationship between brain function and cerebral
hemodynamics. The imaging reflects task-related local changes in the vascular response of
brain tissue. It serves as an indirect measure of neural activity and is used to plan surgery of
motor and language areas.
Cerebral aneurysms found in 3–20% of patients with AVMs
Delay AVM surgery in the setting of acute intracranial hemorrhage unless the hematoma is
causing deterioration in neurologic function through increased ICP.
CLASSIFICATIONS
Spetzler–Martin grading scale for AVMs: The higher the grade, the greater the surgical risk.
Grade I–III are typically offered surgical resection; Grade III and higher are typically offered
surgery after embolization and/or radiotherapy.
See Table
TREATMENT
Premedications
Premedication with benzodiazepines if no existing neurologic deficits. Avoid when there is a
depressed level of consciousness (LOC).
In patients who are present with hemorrhage or cerebral ischemia, the resultant aphasia,
dysphasia, or depressed LOC can make communication difficult.
INTRAOPERATIVE CARE
Monitors
• Arterial line (embolization and surgical) for continuous, direct BP monitoring and blood
sampling; consider placing preinduction.
• Central venous access may be considered for surgical resection of large AVMs that have the
potential for large blood loss.
• Neurophysiologic monitoring is often used during AVM surgery. EEG monitoring can be
used intraoperatively to detect ischemia and also to guide barbiturate titration during “burst
suppression.”
• Somatosensory-evoked potentials (SSEPs) can be used to monitor perfusion of the sensory
cortex and brainstem.
• A smooth controlled induction should be performed to maintain adequate CPP. Hypotension
should be avoided due to a risk of ischemia to hypoperfused regions that are adjacent to the
arteriovenous nidus.
• Attenuate hypertensive responses to laryngoscopy, intubation, and placement of pins for
head fixation. Techniques include brief laryngoscopy, deepening anesthetic, and/or
administering short-acting antihypertensives such as sodium nitroprusside or esmolol.
Maintenance
• Volatile, intravenous, or mixed technique may be used. Total intravenous anesthesia can
optimize SSEPs and motor-evoked potentials (MEPs).
• For craniotomies, adequate brain relaxation and ICP control can decrease ischemia from
retractors and facilitate surgical access. Techniques include the “head up” position (15%),
diuretics/osmotherapy, cerebrospinal fluid drainage, mild hypocapnia, and avoidance of
cerebral dilating anesthetics.
• Barbiturates can be used to achieve “burst suppression” of the EEG. Barbiturate loading
results in delayed emergence. Animal data suggests propofol is an effective alternative agent
if thiopental not available.
• Fluids are usually isotonic, nonglucose containing solutions.
• Severe bleeding during AVM resection most commonly occurs due to inadequate occlusion
of feeding arteries; hypertension-induced rupture is very rare. Induced hypotension may be
useful when this occurs (especially with large AVMs that have a deep arterial blood supply).
• Smooth controlled emergence.
• Avoid hypertension and coughing or bucking. Treat with rapidly acting agents such as
lidocaine, sodium nitroprusside, nitroglycerin, esmolol, and nicardipine/clevidipine.
• Early neurologic examination to detect surgical complications and hematoma formation.
FOLLOW-UP
BED ACUITY
Intensive care unit (ICU)
COMPLICATIONS
• Rupture, 1–2%
• Hyperemic complications: Increased blood flow
• “Normal-perfusion pressure breakthrough” describes brain swelling and hemorrhage
following AVM resection or embolization. It is believed that normal blood flow
autoregulation is impaired due to longstanding hypoperfusion. AVM resection results in
shunting of blood to hypoperfused regions; resumption of normal arterial pressures causes
hyperperfusion, edema, and bleeding.
• Occlusive hyperemia results from venous outflow obstruction caused by surgical ligation of
veins in adjacent normal tissue.
REFERENCES
1. riedlander RM. Clinical practice. Arteriovenous malformations of the brain. N Engl J Med.
2007;356(26):2704–2712.
2. Inoue HK, Negishi M, Hirato M, et al. Treatment of unruptured arteriovenous
malformations in the brain. J Clin Neurosc. 1998;5Suppl:61–64.
3. Hudspith MJ, Popham PA. The anaesthetic management of intracranial haemorrhage from
arteriovenous malformations during pregnancy: Three cases. Int J Obstet Anesth.
1996;5(3):189–193.
4. Hashimoto N, Nozaki K, Takagi Y, et al. Surgery of cerebral arteriovenous malformations.
Neurosurgery. 2007;61(1):SHC-375–SHC-389.
5. endo AA. Intracranial vascular surgery. Anesthesiology Clin N Am. 2002;20(2):377–388.
• Burst suppression
• Craniotomy for intracranial hemorrhage
• Somatosensory- and motor evoked potentials
• Intracranial hypertension
CODES
ICD9
747.81 Anomalies of cerebrovascular system
ICD10
Q28.2 Arteriovenous malformation of cerebral vessels
CLINICAL PEARLS
• Pregnant patients with AVMs should avoid strenuous and painful labor; epidural and/or
elective C-section is recommended. In the setting of intracranial hemorrhage, pregnant
patients receive the same neurosurgical management as the nonpregnant patient. Anesthetic
techniques in the pregnant patient should include considerations for the developing fetus;
avoiding certain medications such as mannitol (to avoid fetal dehydration, instead use a
loop diuretic such as furosemide), beta-blockers (to minimize fetal bradycardia, use a
combined beta and alpha blocker such as labetalol), sodium nitroprusside (fetal cyanide
toxicity), and benzodiazepines (although only long-term use has possible teratogenic effect).
Additionally, limit profound hyperventilation so as not to impair fetal oxygen delivery from
alkalosis/hyperventilation-induced umbilical artery constriction, decreased uteroplacental
perfusion, and by a leftward shift of the maternal oxygen–hemoglobin dissociation curve.
CEREBRAL BLOOD FLOW
Jayson T. Maynes, MD, PhD
BASICS
DESCRIPTION
• Although the brain comprises only 2% of the body’s mass, it accounts for ∼20% of the
body’s metabolic requirements and receives 14% of the cardiac output.
• Regional differences of cerebral blood flow (CBF) exist and reflect the metabolic
requirements (cerebral metabolic rate of oxygen, CMRO2). CBF in:
– Gray matter is 80 mL/100 g/min (CMRO2 of 6 mL/100 g/min).
– White matter is 20 mL/100 g/min (CMRO2 of 2 mL/100 g/min).
– Global average is 50 mL/100 g/min (CMRO2 of 3.2 mL/100 g/min).
• Demographics and CBF. In addition, CBF is higher in females than males and also decreases
with age.
• The brain requires a constant supply of a substrate and oxidizer in order to meet the high
metabolic requirements.
– Glucose is the main metabolic precursor with a consumption of ∼5 mg/100 g/min;
∼90% is metabolized aerobically. When unavailable, secondary metabolic precursors
include acetoacetate and beta-hydroxybutyrate.
– There is no adenosine triphosphate (ATP) storage mechanism in the brain. Thus, in the
event that the oxygen supply is lost, ATP levels will fall to zero within 7 minutes.
– 40% of the brain’s energy is used for basal function (membrane potential, “housekeeping"
activities) and the remainder 60% is used for functional activity (signal transmission).
• Cerebral oxygen extraction is high compared to the systemic circulation. Hemoglobin
saturations measured at the jugular vein (SjO2) range from 45–60%, compared to normal
mixed venous saturations (SvO2) of 55–70%.
• Regional flow. CBF lacks global control. Instead, areas of the brain act in an independent
fashion to control flow via heterogeneous and homeostatic control mechanisms.
Homeostatic mechanisms of CBF control include metabolism, temperature, metabolic
products, PaCO2, PaO2, blood viscosity, and autoregulation.
– Metabolism. Blood flow-metabolism coupling is the most important mediator of the
cerebral circulation and is maintained during sleep and general anesthesia. The CMRO2
varies regionally in the brain. Under normal circumstances, its main determinants are
sleep or wakefulness, temperature, age, and degree of neuronal activity (e.g., seizures).
– Hypothermia reduces CMRO2 (and therefore CBF) by 5–7% for every degree Celsius drop
in body temperature (functional and basal energy requirements). The Q10 for CBF in
humans is 2 (represents the factor by which the reaction rate decreases when the
temperature is decreased by ten degrees; it is a unitless quantity). Complete suppression of
metabolic activity occurs at 18–20%C.
– Metabolic products. Mediators of cerebral vasodilation and flow-metabolism coupling
include glutamate (indirectly by causing release of vasodilators, a feed-forward
mechanism), arachidonate derivatives, nitric oxide (NO), prostaglandin E2 (PGE2)
adenosine, potassium, vasoactive intestinal peptide, lactate, and carbon dioxide (CO2).
– PaCO2. CO2 crosses the blood–brain barrier (BBB) and changes the pH of the CSF. CBF
increases linearly by 2–4% (1–2 mL/100 g/min) per 1 mm Hg increase in PaCO2 (when
the PaCO2 is in the range of 25–75 mm Hg). The change begins within seconds, and fully
equilibrates within 2 minutes. Conditions that cause a reduction in CO2 reactivity include
severe carotid artery stenosis, head injury, subarachnoid hemorrhage, hypotension,
cardiac failure, female gender, and age (>40 years). Acids and protons themselves cannot
cross the BBB (1,2)[A].
– PaO2. A PaO2 <60 mm Hg will increase CBF and takes 6 minutes to equilibrate (2)[A].
– Viscosity. Blood viscosity is primarily determined by hematocrit and temperature. As
viscosity decreases, the CBF increases due to changes in blood rheology. The effect that
this has on the microvascular circulation is not consistent and depends on local factors.
Therefore, the generalization that a lower hematocrit improves microcirculatory flow
cannot be made. Additionally, a lower viscosity may increase intracranial pressure (ICP).
– CBF autoregulation. Under normal conditions, there is minimal change in the CBF with
mean arterial pressure (MAP) changes between 60 and 160 mm Hg. Both arterioles
(smooth muscle in vessel wall) and capillaries (pericytes that encircle the capillary) dilate
or constrict in response to perfusion pressure, in order to maintain a constant blood flow.
However, larger arteries and the venous system do not play a role in dynamic flow
changes. It should be noted that there is significant individual variation in the range of
autoregulation, based on a person’s baseline BP.
• Global and regional blood flow can be measured by nitrous oxide washout and Xenon CT
scanning/Xe clearance. Neither is done routinely.
ANATOMY
• Generally, branches of the common carotid arteries supply the cerebrum and branches of the
vertebral arteries supply the cerebellum.
• All areas supplied by the carotid arteries have good collateral circulation except for the
middle cerebral artery. This area is most prone to ischemia.
• The classical Circle of Willis for collateral circulation is present in only 50% of people.
• The superior sympathetic ganglion provides sympathetic stimulation to the cerebral
vasculature, and plays a role in cerebral vasospasm following injury and stroke.
• The fixed volume of the intracranial vault consists of brain tissue (80%), blood (12%), and
CSF (8%). ICPs above 30 mm Hg generally produce pathological changes in CBF (with 15
mm Hg being defined as an elevated ICP). CBF at this point becomes strictly flow dependent
(entirely reliant on the MAP being greater than the ICP) (3)[A].
• Cushing’s response: A physiologic phenomenon resulting from increased ICP and subsequent
cerebral ischemia. It consists of
– Hypertension (to increase the cerebral perfusion pressure, or CPP)
– Bradycardia (an inappropriate reflex to the hypertension)
– Irregular respirations (from pressure on the brain stem); not always observable
• Cerebral autoregulation is impaired by
– Trauma or traumatic brain injury
– Hypoxemia
– Hypercapnia (PaCO2 >60 mm Hg)
– High-dose volatile anesthetics
– Subarachnoid hemorrhage
– Ischemic cerebrovascular disease
• Ischemia. Because of regional differences, CBF in one area does not correlate with blood
flow in another ischemia-prone area.
– Normal CPP is 80–100 mm Hg in adults.
– CPP <50 mm Hg manifests as EEG slowing.
– CPP <25–40 mm Hg will produce a flat EEG.
– CBF <15–20 mL/100 g/min shows an isoelectric EEG signal.
– CBF <5 mL/100 g/min produces irreversible damage (1)[A].
• Moyamoya: Creation of a web of collateral vessels to deeper brain structures as a result of
longstanding stenosis/malformation of the internal carotid arteries. Pathology of the blood
vessels shows intimal hyperplasia and elastic fiber formation with sparing of the media and
adventitia. This is likely from an elevation of basic fibroblast growth factor. The Moya-Moya
regions have decreased responsiveness to CO2 and are dependent on CPP alone to avoid
underperfusion (ischemia) and overperfusion (rupture). Brain areas around the stenosed
vessels show a decreased CMRO2 and regional blood flow with an increased oxygen
extraction ratio (signs of inadequate blood supply). There is a bimodal age of presentation
in the 1st and 4th decades of life. Pediatric patients commonly present with signs of
ischemia (∼80%), whereas adults predominantly present with a rupture (40–65%, usually
basal ganglia). Symptoms may be elicited by maneuvers that lower the PaCO2, causing
vasoconstriction and focal ischemia (coughing, crying, straining, hyperventilation). During
anesthesia, it is vitally important to preserve blood flow to areas with a tenuous supply.
This is achieved with preoperative volume restitution (preadmittance with IV fluids),
avoidance of cerebral vasoconstriction (avoid crying and hyperventilation before induction),
intraoperative EEG with or without cerebral oximetry, frequent blood gases to avoid both
hypocapnea (watershed ischemia), and hypercapnea (steal of blood from the Moya-Moya
regions by dilated cerebral vessels). Efforts should be made to minimize intraoperative
CMRO2 (avoid pain intraoperatively with adequate opiates/anesthesia and avoid
hyperthermia). Steal may also occur with the return to normocarbia after a period of
hypocarbia and the EEG may take time to normalize (3,4)[A and C].
• Carotid stenosis/carotid endarterectomy (CEA). Stenosis can impair CBF and perfusion
pressures, resulting in syncopal episodes, ischemia, and stroke; repair is undertaken in order
to restore flow. Intraoperatively, the MAP (and therefore the CPP) can change rapidly with
increases and decreases in pressures, catecholamine release from manipulation of the
carotid sinus, and bradycardia from vagus nerve clamping. Postoperatively, hyperperfusion
syndrome may result; its etiology is not clear, but is related to postoperative hypertension to
previously underperfused areas and usually does not occur until several hours after surgery.
• Ruptured cerebral aneurysms/subarachnoid hemorrhage. Inadequate regional blood flow or
ischemia is experienced in the area of the aneurysm. Extravascular hemoglobin can cause
cerebral vasospasm, exacerbating the ischemia.
• Vasospasm can be treated with nimodipine or “Triple H Therapy”: Hemodilution,
hypervolemia, and hypertension.
• Anesthetic agents decrease the neuronal functional energy expenditure, but do not change
the basal energy expenditure. Thus, all volatile agents, propofol, and barbiturates can
reduce the CMRO2 to a flat EEG reflecting electrical silence, but can act no further (unlike
hypothermia).
– Regional differences. Propofol and barbiturates produce a larger overall reduction in
CMRO2 than inhalational anesthetics; this is of unknown benefit. Additionally, this
decrease is not uniform across the brain; propofol and barbiturates produce a larger
reduction in the cerebellum and deep structures, whereas volatile agents produce a
greater reduction in the neocortex.
– Direct effects. Propofol and barbiturates have minimal effect on cerebrovascular tone but
may decrease the CPP by lowering the MAP. Propofol has slight cerebral vasoconstrictive
properties. Opiates have the least direct effect on CBF (if the MAP is maintained);
exceptions include the ability of alfentanil and normeperidine to induce seizure foci,
resulting in a focal increase in CMRO2 in the seizure area. Ketamine increases CMRO2 in
focal areas and therefore CBF. It also dilates cerebral vasculature, increasing the ICP, and
can induce seizure activity.
– Autoregulation. Volatile agents dilate the cerebral vessels but do not abolish
autoregulation. The effect is transitory and, within 5 hours, blood flow returns to normal.
• CBF in chronic hypertensives. The autoregulation region is right-shifted and vessels are
narrower, thus patients can experience ischemia at moderately low blood pressures
compared to normotensives. Perioperatively, patients should have their BP maintained at a
higher pressure to compensate and avoid ischemia. Generally, a change of less than 30%
from baseline is recommended.
• Perioperative stroke. The rate of postoperative stroke is small (0.08–0.4%) but is slightly
higher in patients with known cerebrovascular disease (0.4–3.3%). It is highest in patients
having open cardiac surgery (4%). Documenting preoperative neurological deficits is
imperative in identifying brain regions susceptible to ischemia, to document changes
postoperatively, and to identify patients at risk of difficult extubations (cranial nerve
involvement or cognitive problems). The mortality after postoperative stroke is high (26%).
• EEG. The absolute EEG frequencies are less important than sudden changes or trends during
intraoperative occurrences or surgical events (e.g., carotid clamping during a CEA in order
to decide whether to create an arterial shunt).
• Cerebral vessel anatomy. For relevant surgeries, the patency of the Circle of Willis and
presence of collateral blood flow can be tested preoperatively using cerebral angiography.
This may aid with estimating the chances of cerebral ischemia.
EQUATIONS
CPP = MAP – (CVP or ICP); the greater of the two values is utilized. CPP is cerebral
perfusion pressure, MAP is mean arterial pressure, CVP is central venous pressure, and ICP is
intracranial pressure.
REFERENCES
1. Curley G, Laffey JG, Kavanagh BP. Bench-to-bedside review: Carbon dioxide. Crit Care.
2010;14(2):220–226.
2. Curley G, Kavanagh BP, Laffey JG. Hypocapnia and the injured brain: More harm than
benefit. Crit Care Med. 2010;38(5):1348–1359.
3. Vavilala M, Lee L, Lam, AM. Cerebral blood flow and vascular physiology. Anesthesiology
Clin N Am. 2002;20:247–264.
4. Parray T, Martin TW, Siddiqui S. Moyamoya disease: A review of the disease and
anesthetic management. J Neurosurg Anesthesiol Epub ahead of print.
ADDITIONAL READING
• Carney NA, Ghajar J. Guidelines for the management of severe traumatic brain injury. J
Neurotrauma. 2007;24(Suppl 1):S1–2.
• Patel PM, Drummond JC. “Cerebral physiology and the effects of anesthetics and
techniques”, in Miller’s anesthesia Sixth Edition, ed. D. Miller (Philadelphia: Elsevier, 2005)
pp. 813–857.
• Cerebral metabolic rate
• Craniotomy, cerebral aneurysm clipping
• Circle of Willis
CLINICAL PEARLS
• Intraoperative shunting of blood may be done to increase CBF in cases such as CEA and in
the repair of a proximal thoracic aortic aneurysm.
• Desflurane and sevoflurane maintain flow metabolism coupling to a higher degree than
isoflurane.
• Propofol has a slight vasoconstrictive property and will not increase cerebral blood volume
or ICP but may lower the CPP secondary to lowering of the systemic BP.
• Dynamic cerebral autoregulation can be tested by inflating bilateral thigh BP cuffs for 3
minutes and measuring CBF changes with transcranial Doppler while quickly deflating both
cuffs.
• Cerebral vasospasm can be partially avoided with nimodipine, but if the vasospasm has
already occurred, nimodipine will be less effective.
• Ketamine should be avoided in any patient with an increased ICP, increased intraocular
pressure, or a prior history of seizures.
CEREBRAL EMBOLIZATION
Keren Ziv, MD
BASICS
DESCRIPTION
General
• Cerebral embolization is performed in the neuroradiology suite for the treatment of cerebral
aneurysms, arteriovenous malformations (AVM), and in preparation for intracranial tumor
resections.
• Patients presenting for embolization range from being very healthy with unruptured
aneurysms (Hunt and Hess classification grade 1, survival >70%) to comatose and
moribund (Hunt and Hess grade 5, survival <10%).
• These procedures can be lengthy and uncomfortable for patients and hence will either
require monitored anesthesia care or general anesthesia.
• Vascular sheaths are introduced into the femoral arteries, through which catheters are
passed. Fluoroscopy is used to advance and position the catheters near the level of the
aneurysm. Microcatheters with detachable coils are then threaded through the catheter and
deployed at the site of the aneurysm. Coils are typically made of soft platinum wires with a
diameter smaller than a strand of hair; they come in varying diameters and lengths. They
are flexible and can conform to the aneurysm shape.
• The body eventually forms blood clots around the coils and blocks blood flow into the bulge
or passageway to keep the vessel from rupturing or leaking; this decreases transluminal
pressure against the aneurysmal wall.
• Coils are not the only choice for embolization. Cyanoacrylates, onyx embolic material,
gelfoam, polyvinyl alcohol, and others are also used.
Position
• Supine
• Bilateral groins are prepped and draped for vascular access.
• Limited access to the patient due to fluoroscopy equipment (particularly if 3D images are
obtained).
Incision
Bilateral percutaneous punctures are made in the groin to access femoral vessels.
Approximate Time
Simple cases will be accomplished in 1–2 hours, while complex cases can take many hours.
EBL Expected
• Usually minimal, on the order of 50–100 cc.
• In the event of aneurysm or AVM rupture during the procedure, there may be some blood
loss, which has little hemodynamic consequences, but dire effects on the CNS. This may
require emergent ventricular drain placement or even craniotomy for evacuation of
hematoma and clipping of the aneurysm or AVM.
• There is a small risk of hidden retroperitoneal hematomas, which can become
hemodynamically significant.
Hospital Stay
Patients are typically discharged home on postoperative day one after coiling for unruptured
lesions. Others may require multiple-day hospitalizations as dictated by the patient’s
condition.
• Comprehensive fluoroscopy equipment with 3D capabilities and computer processing
• IV contrast dye
• Detachable coils or other embolization material
EPIDEMIOLOGY
Incidence
• Incidence of subarachnoid hemorrhage (SAH) is 9 per 100,000 people annually.
• Up to 85% of cases of spontaneous SAH are due to ruptured aneurysms.
• Other causes of SAH are AVMs (~10%), cerebral hemorrhage (~10%), and others (e.g.,
tumors).
• Risk increases with age, family history, hypertension, heavy alcohol consumption, and
smoking
• Most hemorrhages are from small aneurysms, although risk of rupture increases with
increasing size.
Prevalence
About 1–2% of the population has at least one cerebral aneurysm.
Morbidity
• If the early course after aneurysm rupture is survived, 25% of patients will have significant
restrictions in their lifestyle, and only 20% will have no residual symptoms.
• Other problems include long-term cognitive impairment, depression, fatigue, headache,
PTSD, and hypopituitarism.
Mortality
• Following a SAH, mortality can approach 50%.
• Unruptured aneurysms or AVMs who undergo uncomplicated procedures, generally do very
well.
• During induction of anesthesia and stimulating parts of the procedure, tight BP control is
essential to prevent rupture or rebleeding.
• For ruptured aneurysms, prevention of vasospasm and management of increased intracranial
pressure (ICP).
• Limited access to the patient requires optimizing monitor location and having adequate
extensions for the breathing circuit and other catheters.
SYMPTOMS
For hemorrhage: increased ICP such as headache, nausea, vomiting, altered sensorium, or
focal neurologic finding.
History
• Healthy patients for elective coiling need no special workup.
• A detailed history as to the presence of hypertension is sought.
• Contrast or shellfish allergy is elicited given the large amounts of contrast used.
• Heparin and protamine allergies should be noted.
Signs/Physical Exam
A thorough neurologic exam needs to be performed to assess the baseline status of the patient
so it can be compared to the postprocedure exam. In this fashion, subtle changes can be
picked up; allowing for further diagnostics and therapeutics to be pursued in a timely fashion.
MEDICATIONS
Patients presenting to the interventional radiology suite for urgent embolization may have
been given mannitol, furosemide, or 3% saline to manage intracranial hypertension; calcium
channel blockers to prevent vasospasm; other medications to control BP.
Labs/Studies
• Hg/Hct to assess hemodilution during triple H therapy (hypertension, hemodilution,
hypervolemia).
• Chemistry panel to assess for cerebral salt-wasting (hyponatremia and hypokalemia) due to
the release of brain and atrial natriuretic hormone and SIADH.
• SAH can produce EKG changes including QT prolongation, Q waves, cardiac dysrhythmias,
and signs consistent with acute ischemia.
• Rhythm disturbances will occur in up to 90% of patients with SAH.
• A small percentage of patients with SAH will develop ischemic cardiomyopathy due to
vasospasm and high catecholamine state. This needs to be addressed in the same manner as
ischemia from coronary artery disease secondary to arthrosclerosis would be treated.
Usually this ischemia is reversible and patients recover.
TREATMENT
Premedications
• Healthy patients may be given premedication in usual fashion, with the caveat that heavy
premedication and short cases may lead to delayed emergence and neurological assessment.
• Patients with altered sensorium or with increased ICP should be premedicated very
carefully, if at all, as small changes in CO2 tension can lead to large changes in ICP and
obtundation.
Patients need to understand that there may be a need for prolonged intubation and the
possibility for emergent craniotomy.
Usually no antibiotics are given.
INTRAOPERATIVE CARE
• Local only, monitored anesthesia care, or general anesthesia may be appropriate.
• Local cases may be appropriate for otherwise healthy and very motivated patients with
minimal risk for cerebral ischemia requiring emergent intubation.
• Monitored anesthesia care, again, should be reserved for healthy motivated patients.
Sedation should be kept very light as to allow for patient communication and cooperation.
• General anesthesia (with endotracheal intubation) is chosen in most cases. Benefits include a
motionless field, full airway control, control of hemodynamics and ICP, and control during
complications (acute rupture, induction of barbiturate coma, treatment of seizures, and
emergent craniotomy).
Monitors
• Foley catheter
• There should be a low threshold for placing an arterial line in patients with SAH from a
ruptured aneurysm or AVM; if difficult to access, the operating physician can often provide
access via the groin line.
• EEG monitoring and evoked potentials are not the standard of care, but should be
considered in cases of giant and wide neck aneurysms, aneurysm in close proximity to other
vessels, high ICP, large SAH, or who are otherwise at risk for cerebral ischemia.
• Management of ICP, BP, cerebral perfusion pressure (CPP), and the airway are the main
concerns during induction.
• Patients with unruptured aneurysms and AVMs rarely have high ICP. Maintaining a stable
BP with minimal variation is more important than an absolute number. Patients with
recently ruptured aneurysms or AVMs should have their BP controlled at, or slightly below,
normal levels to avoid rebleeding. If the ICP is increased, a drop in BP can cause CPP to
become marginal. Intracranial hypertension may be controlled with mannitol,
hyperventilation, furosemide, and decreasing or discontinuing volatile anesthetics (convert
to a propofol, dexmedetomidine, and/or opioid technique).
• Patients at risk for vasospasm on “triple H (hypertension, hemodilution, hypervolemia)"
therapy need to have their BP maintained in the high normal range to avoid cerebral
ischemia. This is accomplished with a combination of pressors and volume.
Maintenance
• Unless ICP cannot be controlled with the methods described, a balanced anesthetic with low
levels of volatile anesthetics can be employed.
• There is no evidence that any particular anesthetic is superior to another for uncomplicated
cases.
• Movement must be avoided utilizing either deep anesthesia or paralysis, especially during
critical coil positioning and deployment. Coil positioning and deployment is usually not
painful, but when work is performed close to the dura, thalamus, or certain parts of the
brainstem (e.g., during AVM embolization), the patient may move.
• Coagulation management with heparin and other agents may be required to prevent
intraoperative thromboembolic events; this may need to be reversed at the conclusion of the
case. Protamine reversal is often done with a small “test dose” to assess for allergic or
anaphylactic reactions followed by slow titration to avoid hypotension.
• Naturally, emergence should be smooth.
• Endotracheal lidocaine may be administered at the beginning of the case during
laryngoscopy. Alternatively, IV lidocaine may be given at the end to reduce tracheal
reflexes.
• Aggressive multimodal emesis prophylaxis.
POSTOPERATIVE CARE
BED ACUITY
Almost all patients, even those presenting electively, will require overnight ICU or step-down
care for frequent neurological assessments. Continued higher level of care is dictated by the
patients’ condition.
ANALGESIA
• Usually, patients will have very little postoperative pain. Local anesthesia at the site of
puncture should be administered intraoperatively.
• Some patients (especially those with AVMs) may experience strong headaches due to venous
congestion. They can be given small doses of opioids. Head elevation may also help.
COMPLICATIONS
• Rare (about 3%) and include hemorrhage (aneurysm perforation, vessel injury, dissection)
or occlusion (thromboembolic, coil displacement, vasospasm)
• Contrast reaction/nephropathy
• Hemorrhage at the puncture site
• Retroperitoneal hematoma
• Infection
PROGNOSIS
• The International Subarachnoid Aneurysm Trial has shown that endovascular coiling of
simple aneurysms is superior to surgical clipping if measured as survival and development
of seizures at 1 year, but the risk of rebleeding is higher in the coiling group.
• Even for complex aneurysms, aneurysm coiling is at least as efficacious as clipping.
REFERENCES
1. Molyneux A, Kerr R, Stratton I, et al. International subarachnoid aneurysm trial (ISAT) of
neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured
intracranial aneurysms: A randomised trial. Lancet. 2002;360:1267–1274.
2. Van der Schaaf I, Algra A, Werner M, et al. Endovascular coiling versus neurosurgical
clipping for patients with aneurysmal subarachnoid hemorrhage. Cochrane Database Sys
Rev. 2005: CD003085.
3. Lui AY, Lopez JR, Do HM, et al. Neurophysiological monitoring in the endovascular
therapy of aneurysms. Anesth Analg. 2007;105:887–888.
ADDITIONAL READING
• Nadjat-Haiem C, Ziv K, Osborn I. Anesthesia for cerebrovascular procedures in
Interventional Neuroradiology. IAC. 2009;47(2):29–43.
• Varma MK, Price K, Jayakrishnan V, et al. Anesthetic considerations for interventional
radiology. Br J Anesth. 2007;25:391–412.
• Craniotomy for cerebral aneurysm clipping
• Craniotomy for intracranial hemorrhage
CLINICAL PEARLS
• Use same standards and vigilance as during a craniotomy. Be prepared to look for signs of
hemorrhage (e.g., Cushing’s response) and be prepared to change venue (CT scanner,
operating room).
• Avoid movement during critical parts of the procedure and be aware of what the procedurist
is doing. Good communication between the neurointerventionalist and anesthesiologist is
crucial, especially if complications arise (prompt decisions can be made regarding further
treatment).
CEREBRAL METABOLIC RATE
BASICS
DESCRIPTION
• Cerebral metabolic rate of oxygen (CMRO2) is described as the milliliters of oxygen
consumed by 100 g of brain tissue per minute.
• Local differences exist for the CMRO2 (gray versus white matter, type of cell). In the adult,
the averaged value over all areas is 3–3.5 mL/100 g/minute.
• The neuroanesthetist must balance the CMRO2 with oxygen delivery. However, despite the
importance, there are no readily available techniques within the operating room that can
directly measure tissue oxygen metabolism.
• The adult human brain weighs ∼2% of the total body weight. However, it
– Receives ∼12–15% of the cardiac output; and is considered a high perfusion organ.
– Comprises ∼20% of total body oxygen consumption. This high rate is required primarily
for the maintenance of depolarization and repolarization activity as well as for cellular
homeostasis.
• CMRO2 and cerebral blood flow (CBF) are “coupled.” Increases in oxygen consumption are
met by an increase in blood flow. The mechanism is not completely understood; however, it
is believed that local factors and nitric oxide (NO) contribute to changes in vascular tone
and CBF based on electrical and metabolic oxygen demands.
– Normal CBF is ∼45–55 mL/100 g/minute and autoregulation maintains a relatively
constant CBF over a wide range of mean arterial pressures (MAPs), between 70 and 150
mm Hg.
– Increases in CMRO2 result in parallel increases in CBF, whereas decreases in CMRO2 result
in parallel decreases in CBF.
– Consequently, increases in neuronal activity result in a “superfluous” increase in CBF
compared to the CMRO2 (provides a cushion) (1).
• Regional differences of CMRO2 (and hence CBF) are as follows (2):
– Gray matter is four times that of white matter.
– Neurons are greater than glial cells.
– Lowest in the spinal cord and increases cephaladly through the medulla, midbrain,
thalamus, cerebellum, and cerebral cortex.
• Factors affecting CMRO2 (and hence CBF).
– Sleep. Non-rapid eye movement (Stages 2 and 3) is associated with a 23% reduction across
the entire brain (regional variations exist). However, certain areas (basal forebrain,
hypothalamus, amygdala, hippocampus) have an increase in glucose utilization likely
from homeostatic regulation and mnemonic processing.
– Aging results in neuronal loss and can also progressively lower CMRO2 (3).
ANATOMY
• Gray matter comprises ∼40% of the brain’s mass and consists of neuronal cell bodies,
dendrites, and glial cells. Mostly present in the outer portions.
• White matter comprises ∼60% of the brain’s mass and consists of myelinated axons and is
mostly present in the inner portions.
• Seizure activity describes uncontrolled and chaotic electrical activity that is accompanied by
significant increases in CMRO2. With status epilepticus, values can increase by 200–300%
(4).
• Oxygen delivery
– Decreases that are secondary to impaired CBF (stroke, hypotension) are accompanied by
decreased glucose delivery and increased partial pressure of carbon dioxide (PaCO2).
Initially, the brain tissue increases oxygen extraction to compensate, and CMRO2 remains
stable. However, when the reduction in CBF exhausts the compensatory increase in
oxygen extraction, the CMRO2 decreases.
– Decreased blood oxygen content is accompanied by the normal delivery of glucose and
does not affect carbon dioxide removal. Normal arterial partial pressures are ∼100 mm
Hg. At values of 30 mm Hg, there is a significant decrease in the CMRO2 that is
accompanied by a ∼50% increase in CBF (5).
• Carbon dioxide. Increases in the PaCO2 result in vasodilation and increased CBF (pH
mediated mechanism). However, its effects on the CMRO2 are poorly understood and lack
consensus. At this time, it is believed that mild increases appear to have a negligible effect
on global CMRO2.
• The neuroanesthetist is often called on to manipulate the CMRO2 and optimize oxygenation.
– Decreases in electrical activity can be attained with both IV and volatile agents. The
electroencephalogram may be utilized to assess electrical activity (not cellular
homeostasis). The term burst suppression describes a periodic pattern of high-amplitude
complexes that are interspersed by low-voltage amplitude complexes. This represents a
state of maximal electrical activity suppression (recall that this comprises the majority of
CMRO2) (6).
– Cellular homeostasis (“basic housekeeping”) may be decreased by lowering the
temperature. Hypothermia lowers the CMRO2 that is associated with providing energy
(e.g., adenosine triphosphate [ATP] to maintain transmembrane ion gradients) that is
essential for neuronal viability and other basic functions of cellular upkeep (e.g., protein
synthesis). For each degree celsius decrease, there is a corresponding CMRO2 decrease of
∼7%. To that extent, deep circulatory arrest can theoretically approach a CMRO2 of zero.
• IV medications, in general, maintain coupling of CMRO2 and CBF.
– Barbiturates. Dose-dependent reduction in CBF and CMRO2. Tolerance to this effect can
develop rapidly. Animal studies have demonstrated improved outcome for focal, but not
global, ischemia.
– Propofol. Appears to have a similar dose-dependent reduction in CBF and CMRO2 as
barbiturates. Its shorter duration of action compared to barbiturates can decrease the need
for postoperative intubation and delays in performing a neurological exam.
– Etomidate. Appears to have a similar profile to barbiturates. Because it maintains MAP
well, it can effectively reduce intracranial pressure (ICP) without reductions in cerebral
perfusion pressures (CPP) with tumors and closed head injuries (CHI). It is not routinely
used to induce or maintain burst suppression, however, due to its ability to cause
adrenocortical suppression and renal injury with repeat, routine, or continuous use.
– Ketamine. The only IV anesthetic agent that can cause an increase in the CMRO2 and
hence CBF (elevation in ICP). These effects can be blunted by coadministration of volatile
agents or benzodiazepines.
– Benzodiazepines. Decreases CMRO2 and CBF.
– Flumazenil (in some studies) has been shown to increase CBF and ICP.
– Lidocaine can decrease CMRO2 in a dose-dependent fashion. A bolus dose has been
advocated as an adjunct for acute elevated ICP. However, CNS toxicity can cause seizures
that will increase the CMRO2.
– Narcotics. It appears that CBF and CMRO2 are relatively unaffected. However, the
information has inconsistencies and varies depending on the narcotic. When an effect was
found, usually it showed a decrease in CMRO2 and CBF.
– Epinephrine and norepinephrine. Increase CMRO2 and CBF regardless of whether or not
there is an intact blood–brain barrier (BBB).
– Dobutamine. Can increase CMRO2 and CBF by up to 30%.
– Beta-blockers. Studies show that they appear to reduce or have no effect on CMRO2 or
CBF.
– Alpha 2-agonists (dexmedetomidine). Reduces CBF with no effect on CMRO2.
– Nondepolarizing muscle relaxants. Do not directly affect CMRO2. However, the histamine
release associated with atracurium can increase ICP.
– Succinylcholine. Does not directly affect CMRO2. However, histamine release can cause a
rapid increase in ICP.
• Volatile agents decrease the CMRO2; however, CBF does not decrease in parallel; this is
known as “uncoupling.” The cerebral vasculature vasodilates due to smooth muscle
relaxation in response to the volatile agent. This increases the CBF to CMRO2 ratio with
resultant “luxury” perfusion.
– Order of CMRO2 suppression (measured in terms of equal MAC concentrations):
Isoflurane, enflurane, desflurane, sevoflurane>halothane.
– Order of vasodilating potency: Halothane>>enflurane>isoflurane = sevoflurane =
desflurane. After initially increasing the CBF, there is a substantial fall in CBF until a
steady state is reached (usually after 2.5–5 hours after exposure).
– Therapeutic use: Decreases in CMRO2 can develop quickly.
– Carbon dioxide responsiveness remains well maintained.
• Nitrous oxide (N2O). Results have been mixed; however, it is generally accepted that the
CMRO2, CBF, and ICP increase, likely from sympatho-adrenal-stimulating effects.
GRAPHS/FIGURES
See Table
See Table
REFERENCES
1. Uludag K, Dubowitz DJ, Yoder EJ, et al. Coupling of cerebral blood flow and oxygen
consumption during physiological activation and deactivation measured with fMRI.
Neuroimag. 2004;23:148–155.
2. Jain V, Langham MC, Floyd TF, et al. Rapid magnetic resonance measurement of global
cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia. J
Cereb Blood Flow Metab. 2011;31(7):1504–1512.
3. Nofzinger EA, Buysse DJ, Miewald JM, et al. Human regional cerebral glucose metabolism
during non-rapid eye movement sleep in relation to waking. Brain. 2002;125(Pt 5):1105–
1115.
4. Ingvar M. Cerebral blood flow and metabolic rate during seizures. Relationship to epileptic
brain damage. Ann N Y Acad Sci. 1986;462:194–206.
5. An H, Liu Q, Chen Y, Lin W, et al. Evaluation of MR-derived cerebral oxygen metabolic
index in experimental hyperoxic hypercapnia, hypoxia, and ischemia. Stroke.
2009;40:2165–2172.
6. Nemoto EM, Klementavicius R, Melick JA, et al. Suppression of cerebral metabolic rate for
oxygen (CMRO2) by mild hypothermia compared with thiopental. J Neurosurg Anesthesiol.
1996;8(1):52–59.
CLINICAL PEARLS
• Increases in CMRO2 can have detrimental effects, possibly resulting in intracranial
hypertension from increased CBF as well as ischemia from an imbalance in oxygen supply
and demand.
• Most IV anesthetics cause a decrease in both CBF and CMRO2, except ketamine that can
cause an increase in both.
• Volatile agents “uncouple” CBF and CMRO2. In other words, while CMR decreases, CBF does
not (can increase or remain the same).
• For every degree (celsius) decrease, the CMRO2 falls ∼6–7%.
CEREBRAL PALSY
BASICS
DESCRIPTION
• Cerebral palsy (CP) is a term used to describe a large and diverse group of neurological
disorders that result from injury to the developing fetal or infant nervous system.
• It is associated with varying degrees of motor, sensory, and intellectual impairment. In mild
cases, the patient can be almost completely functional and in severe cases patients can have
profound morbidity and mortality even in childhood.
• Nonprogressive condition; does not have an evolving neurologic clinical deterioration.
EPIDEMIOLOGY
Prevalence
1:450 live births in developed countries
Prevalence
1:350 children and adults in the US
Morbidity
Although CP is often manifested as problems with posture and movement, the more severe
forms affect neurologic, respiratory, GI, musculoskeletal, and genitourinary systems.
• Congenital CP (80% of cases)
– Prematurity (10 to 50-fold increase)
– Neonatal asphyxia
– Male gender
– Chorioamnionitis
– Preeclampsia
– Peripartum hemorrhage
– Advanced maternal age
– Multiparous birth
– Initial low Apgar score
– Prenatal infection (toxoplasmosis, rubella, cytomegalovirus, herpes)
– Vascular maldevelopments
– Metabolic disorders
– Intrauterine growth retardation
– Trauma to fetus
– Breech birth
– Maternal hypothyroidism
– Fetal alcohol syndrome
• Acquired CP (20%) within first 2 years of life
– Intracerebral hemorrhage
– Bacterial meningitis
– Hyperbilirubinemia
– Viral encephalitis
– Brain injury
– Neonatal seizures
• Clinical presentation may result from neurologic injury that occurs in the prenatal,
perinatal, or postnatal periods. The injury may be due to toxins, infections, hypoxia,
vascular insufficiency, trauma, or complications associated with prematurity.
• Injury may occur at different points in brain development, therefore resulting in a wide
spectrum of clinical presentations.
• CP due to prematurity is most likely associated with the physical stress that the premature
neonate brain is unable to compensate for. This results in cerebral white matter
hypoperfusion, which can lead to varying degrees in subependymal and germinal matrix
hemorrhage and/or leukomalacia. Because these areas carry fibers responsible for motor
control to the lower extremities, the patient suffers from lower extremity weakness and
spasticity.
• If hemorrhagic lesions extend outward from the lateral ventricles toward the descending
fibers of the motor cortex (centrum semiovale and corona radiata), then the upper
extremities will be affected along with the lower extremities.
• CP due to hyperbilirubinemia or hypoxic ischemic injury perinatally result in
extrapyramidal signs often associated with hypertonicity.
• In summary there is no one cause of CP as is outlined in the risk factors above, and most
cases are likely to have multifactorial causes. By definition, CP is a nonprogressive disorder
in which the injury has occurred and does not have an evolving neurologic clinical
deterioration.
• Assess severity of multiorgan disease
• Assess the patient’s level of cooperation and cognition.
• Optimize pulmonary function, minimize chance of aspiration
• Return to normal regimen of anticonvulsant and antispasmodic medications as soon as
possible so as to avoid adverse events such as withdrawal symptoms and seizures.
SYMPTOMS
Cardiopulmonary symptomatology is difficult to evaluate because these patients will
frequently be immobile, but may have ischemic heart disease, pulmonary hypertension, and
cor pulmonale.
History
• Up to 70% may have intellectual impairment.
• Enlist the help of the parent/guardian to take a thorough history including an evaluation of
previous anesthetics – many of these patients will have had frequent surgical procedures.
• Many patients will have an ASA classification of III or more due to other comorbid
conditions. Assess the multiple organ systems involved.
• Assess fluid status and hydration
• Assess drug regimen and efficacy
• Inquire about intrathecal baclofen pump
• Assess level of cooperation
• Inquire about chronic pain conditions
Signs/Physical Exam
• Muscle contractures, spasticity, and sometimes hypotonia
• Abnormal neck or truncal tone
• Asymmetric posture, strength, or gait
• Temporomandibular joint (TMJ) dislocation
• Scoliosis
MEDICATIONS
• Baclofen (oral or via intrathecal pump): Used to decrease spasticity, especially in lower
extremities. Withdrawal symptoms can include confusion, painful muscle spasms, seizures,
and hemodynamic instability.
• Anticonvulsants: May be on multiple medications for chronic seizure disorder (can increase
metabolism of anesthetic drugs).
• Botulinum: Injections are often used to decrease muscle spasticity and progression to
contractures. Botulinum can also be used to reduce drooling associated with CP.
• Patients may also be on chronic regimens of antidepressants, antibiotics (for recurrent
infections), and analgesics.
Labs/Studies
• Chest Radiograph (CXR) (pneumonia, cardiomegaly, and congestive heart failure)
• Electrocardiogram (right heart failure, ischemic heart disease)
• Complete blood count, electrolytes, urea, and creatinine
• Cardiac: Patients have been reported to have a higher incidence of ischemic heart disease.
• Neurologic: CP often manifests as a motor disorder involving spasticity and contractures.
Most will have cognitive dysfunction and seizure disorders. Also seen are visual, auditory,
and sensory impairments. Neurosis and psychosis can occur.
• Pulmonary: Chronic lung disease is a frequent manifestation due to either chronic aspiration
pneumonia, neonatal respiratory distress syndrome, bronchopulmonary dysplasia,
asthma/reactive airway disease, or scoliosis causing restrictive lung disease.
• Musculoskeletal: Because of chronic immobility, patients can have marked osteopenia and
may be more prone to fracture. Contractures may also make vascular access and positioning
difficult under anesthesia. Patients may have TMJ disorder with poor mouth opening.
• GI: May have poor nutritional status, gastroesophageal reflux disorder (GERD), drooling,
and constipation. Dental caries and poor dentition are also common.
• Immunologic: May be immunosuppressed due to malnutrition.
• Genitourinary: Chronic urinary tract infections due to neuropathic bladder. These patients
are at increased risk of latex allergy due to repeated urinary catheterizations.
• Acute respiratory infection/pneumonia
• Acute baclofen withdrawal
• Acute heart failure
CLASSIFICATIONS
Classified according to resting tone and limb involvement:
• Spastic hemiplegia: Predominantly on one side of the body, with the upper extremity more
involved than the leg.
• Spastic diplegia: Affecting bilateral lower extremities more than upper extremities.
• Spastic quadriplegia: All extremities.
• Athetoid/dyskinetic CP: Associated with mixed muscle tone and extrapyramidal signs.
• Ataxic CP: Caused by damage to cerebellum. Balance while walking is affected.
• Hypotonic CP: Limp musculature.
TREATMENT
Premedications
• Consider anxiolytic medication if appropriate
• In hypotonic patients, sedative premedication is best avoided because it can decrease airway
reflexes.
INTRAOPERATIVE CARE
As the CP patient population can have significant cognitive dysfunction as well as
cardiopulmonary comorbidities, general anesthesia should be considered carefully.
Monitors
• Consider measurement of urine output
• Airway management can be difficult because of TMJ disorder/dislocation and poor
dentition.
• Patients can have reactive airway disease.
• Because of the upregulation of acetylcholine receptors in the neuromuscular junction, the
patient can have decreased sensitivity to nondepolarizing neuromuscular blockers.
However, due to changes in volume of distribution, there may be an increased amount of
medication available at the neuromuscular junction. These changes most likely counteract
each other.
• Succinylcholine is considered safe to use.
• In patients where GERD is a concern, consideration of a rapid sequence induction is
appropriate in patients with intravenous access. However, there is no strong evidence that
this is safer than a well-positioned inhalational induction, so as to minimize passive
regurgitation.
Maintenance
• Keep patients warm as CP patients are prone to hypothermia due to muscle atrophy.
• Minimum alveolar concentration (MAC) and drug clearance may be affected by the use of
anticonvulsants.
• Ensure full reversal if muscle relaxation was used.
• CP patients often have increased secretions so an intact cough reflex is crucial to prevent
postoperative pulmonary complications.
• Consider prophylaxis for postoperative nausea and vomiting.
FOLLOW-UP
BED ACUITY
• Consider monitoring in a high-dependency environment for those with significant
comorbidities, seizure disorder, or the potential for baclofen withdrawal if unable to take
usual therapy.
• Vigilance for respiratory dysfunction, hypothermia, and hypoxia
• Respiratory therapy and incentive spirometry
• Ensure appropriate analgesia as patients will often have difficulty in communicating.
COMPLICATIONS
• Perioperative aspiration: Treat with supportive measures including supplemental oxygen,
chest physiotherapy, and ventilatory support in severe cases.
• Baclofen withdrawal: Can manifest as anxiety, confusion, pain, muscle spasm, seizures, and
autonomic instability. Resume baclofen regimen as soon as appropriate.
• Seizure: May be precipitated by inadequate blood levels of anticonvulsant medication or
electrolyte abnormality. Look for other causes of perioperative lowering of seizure
threshold. Treat with benzodiazepines, supportive care, and resume previous anticonvulsant
regimen as soon as appropriate.
REFERENCES
1. Krigger KW. Cerebral palsy: An overview. Am Fam Physician. 2006;73:91–102.
2. Cans C, De-la-Cruz J, Mermet M-A. Epidemiology of cerebral palsy. Paediatr Child Health.
2008;18:393–398.
3. Prosser D, Sharma N. Cerebral palsy and anaesthesia. Contin Educ Anaesth Crit Care Pain.
2010;10(3):72–76.
4. Jacobsson B, Hagberg G. Antenatal risk factors for cerebral palsy. Best Pract Res Clin
Obstet Gynaecol. 2004;18(3):425–436.
ADDITIONAL READING
• www.aacpdm.org
• American Academy for Cerebral Palsy and Developmental Medicine
• Aspiration
• Asthma
CODES
ICD9
• 343.0 Congenital diplegia
• 343.1 Congenital hemiplegia
• 343.9 Infantile cerebral palsy, unspecified
ICD10
• G80.0 Spastic quadriplegic cerebral palsy
• G80.1 Spastic diplegic cerebral palsy
• G80.9 Cerebral palsy, unspecified
CLINICAL PEARLS
• Assess the severity of disease in order to plan an appropriate anesthetic technique.
• Enlist the help of the parent/guardian as they sometimes have extensive knowledge about
previous surgeries and anesthetics.
• Evaluate cardiopulmonary status as these patients may have extensive comorbidities
including pulmonary hypertension, chronic aspiration, scoliosis, and ischemic heart disease.
• Resume normal anticonvulsants and antispasmodics as soon as possible to prevent seizures
and withdrawal symptoms.
• Ensure patients have adequate pain control postoperatively, as they will often have
difficulty communicating.
CEREBRAL VASOSPASM
Victor Duval, MD
BASICS
• Cerebral vasospasm is defined as the constriction of one or more major cerebral arteries,
usually secondary to subarachnoid hemorrhage (SAH) or craniocerebral trauma.
• The amount of blood in the basal cistern and the presence of intraventricular blood correlate
with the risk of developing clinically significant cerebral vasospasm.
• The diagnosis can be made clinically, angiographically, or by transcranial Doppler (TCD).
• The resulting decrease in cerebral blood flow (CBF) can lead to ischemia and infarction, and
is a main cause of permanent neurologic injury and death after SAH.
• Up to 70% of patients with SAH demonstrate angiographic evidence of vasospasm.
• Clinical symptoms of cerebral ischemia and infarction develop in 30–40% of patients.
Up to 1.2 million patients per year are estimated to have permanent or fatal neurologic injury
as a result of vasospasm following an intracranial bleed.
Morbidity
Vasospasm may be detectable for up to 14 days after SAH. Symptoms can range from subtle
focal deficits to debilitating neurologic injury, and typically peak between 3 and 12 days.
Mortality
The risk of death in patients who develop vasospasm following SAH can reach 3 times that of
patients who do not.
• The cause of vasospasm following SAH is still unknown. It is thought that the presence of
blood in the subarachnoid space can lead to cerebral vasoconstriction. Various components
and breakdown products have been proposed as mediators. Oxyhemoglobin has several
properties that make it one of the most likely candidates.
• The Fisher grade on initial presentation is highly predictive of the development of clinically
significant cerebral vasospasm. The presence of thick blood in the basal cistern and
intraventricular or intraparenchymal hemorrhage is associated with the highest risk of poor
neurologic outcome.
• Although patients > 68 years of age are more likely to develop symptomatic vasospasm,
younger patients are more likely to show angiographic evidence of vasospasm.
• Female gender, hypertension, elevated intracranial pressure (ICP), smoking, and cocaine use
also increase the risk of developing vasospasm.
• Contraction of smooth muscle in the vessel wall leads to lumen narrowing and restricted
blood flow. Cerebrovascular resistance shifts from the penetrating arterioles to the major
branches of the Circle of Willis, which undermines the brain’s ability to autoregulate. BP
then becomes the main determinant of CBF beyond the affected vessels.
• There is also evidence that histological changes occur. These include thickening of all three
vascular layers, periadvential inflammation, and myointimal hyperplasia. However, the
extent of the clinical significance of these findings is unclear.
• Since autoregulation in the brain is impaired, hypotension should be avoided throughout the
perioperative period; flow is pressure dependent.
• Hypertension, hypervolemia, and hemodilution (triple-H therapy) can potentially minimize
the risk of ischemia; however, it is associated with a significant risk of morbidity that must
be carefully weighed against this unproven benefit. Invasive monitoring is recommended.
• Consider avoiding volatile agents. Uncoupling of CBF and cerebral metabolic rate of oxygen
consumption (CMRO2) may lead to lower cerebral vascular resistance in unaffected areas of
the brain. This can decrease perfusion distal to spastic vessels. Intravenous agents such as
propofol have a more favorable profile in the setting of vasospasm.
• Decreased level of consciousness is the most common finding indicative of cerebral
vasospasm.
• Rarely, patients can present with focal neurologic findings without a global decrease in level
of consciousness.
Cerebral vasospasm usually occurs within 2 weeks of SAH. Patients often have comorbid
conditions associated with cerebrovascular disease, such as hypertension and smoking.
Focal neurologic deficits depend on the affected vessels. Associated findings are contralateral
and can involve cranial nerves, motor function, and sensory function. Brainstem function and
coordination are usually intact.
TREATMENT HISTORY
• Patients with cerebral vasospasm may have had an aneurysm surgically clipped or
endovascularly embolized.
• Triple-H therapy is widely used.
MEDICATIONS
• Most patients with symptomatic vasospasm are treated with calcium channel blockers.
Nimodipine has been shown to provide some benefit. Its intravenous equivalent nicardipine,
on the other hand, has demonstrated inconclusive results.
• Other medications that have been experimented with include fibrinolytic therapy, sodium
nitroprusside, magnesium, cyclosporine, erythropoietin, and clazosentan.
• Electrolytes should be checked, especially if the patient is suspect to have developed
cerebral salt wasting syndrome or SIADH.
• CBC
• EKG: “Canyon T-waves" are common. Nonspecific T-wave changes, QT prolongation, ST-
segment depression, and U waves can also occur. The EKG changes usually do not reflect
the degree of myocardial dysfunction, nor do they predict the development of cardiac
failure. The EKG should be monitored for potential lethal dysrhythmias, including Torsades
de Pointes, in the setting of QT prolongation, which can frequently occur in patients with
severe SAH.
• Elevated troponin levels are common but are usually lower than those associated with
cardiac ischemia.
• Cardiovascular
– Cerebral vasospasm may, in and of itself, lead to hypovolemia for unknown reasons.
– Reversible myocardial stunning can occur in the setting of SAH. Its severity is associated
with the degree of neurologic injury.
– Aneurysms occur more frequently in certain genetic conditions such as polycystic kidney
disease, coarctation of the aorta, fibromuscular hyperplasia, and connective tissue
disorders.
• Pulmonary function should be assessed in patients who are smokers. Also, patients with
compromised neurologic status are at an increased risk of aspiration.
• Patients on triple-H therapy are at risk of developing cardiac, pulmonary, and renal
complications.
• Delay in surgical clipping after SAH or interventional radiologic procedures to treat
vasospasm can have severe consequences, including rebleeding and devastating neurologic
injury.
• If ischemic heart disease is suspected, an echocardiogram may be helpful in guiding
intraoperative management.
CLASSIFICATIONS
• The Fisher grade classifies the appearance of SAH on CT scan and correlates it to the risk of
clinically significant vasospasm:
– Grade 1: No hemorrhage evident
– Grade 2: SAH < 1 mm thick
– Grade 3: SAH > 1 mm thick
– Grade 4: SAH of any thickness with intraventricular hemorrhage or parenchymal
extension.
TREATMENT
Premedications
Anxiolytics are seldom necessary and can interfere with neurological exam.
Since vasospasm can affect sensorium, informed consent may not be obtainable from the
patient. It is wise to identify a surrogate decision maker in light of the significant risk of
neurologic complications.
General endotracheal
Monitors
• An arterial line should always be used, and can be most helpful if placed before induction.
• Central line monitoring may be useful to help guide fluid management (especially in elderly
patients) or pressor support, as well as in the setting of myocardial dysfunction.
• Specific anesthetic agents should be selected on a case-by-case basis to fulfill the anesthetic
goals described above.
• Poorly organized clot in the early stages after SAH is particularly prone to rebleeding
secondary to systolic hypertension and tachycardia. A rebleed during induction is often
lethal. It is therefore extremely important to avoid excessive, sustained systolic hypertension
and secure the airway quickly in these patients. On the other hand, prolonged hypotension
should also be avoided to minimize the risk of ischemia.
Maintenance
• Inhaled agents can increase the CBF. This undermines brain relaxation and the ability to
maintain a high cerebral perfusion pressure (CPP); alternatively, propofol has a more
favorable profile.
• Elevation of the mean arterial pressure (MAP) may be achieved with phenylephrine or
dopamine.
• Recent evidence suggests that hyperventilation should be avoided unless absolutely
necessary to temporarily decrease ICP; vasoconstriction can further worsen ischemia.
• The dose and timing of mannitol administration varies per surgeon preference. Usual doses
range between 1 and 2 g/kg, and may be given immediately following induction or on
initial skin incision. Surgeons may also request an additional dose at the time of dural
opening.
Extubation/ Emergence
• The objective is for the patient to be able to participate in a neurological exam yet
comfortable enough to minimize reaction to extubation. Using a relatively low dose of
fentanyl 15–20 minutes before extubation can be highly effective; alternatively a
remifentanil infusion may be considered. Intravenous lidocaine can also be used to suppress
the coughing reflex.
• Hypertension and tachycardia on emergence is common and is usually not related to painful
stimuli. This is usually best treated with beta-blockers.
• Prophylaxis against postoperative nausea and vomitting should be given to decrease the risk
of postoperative bleeding secondary to the sudden and severe rise in ICP associated with
vomiting.
FOLLOW-UP
BED ACUITY
Patients at high risk for vasospasm, based on clinical and radiologic findings post-SAH, should
be monitored at least every 2 hours for neurologic changes. This is usually done in an
intensive care unit (ICU) setting. Lower risk patients can be monitored every 4 hours.
• Patients at risk for cerebral vasospasm are almost always placed on a nicardipine drip. They
may further be placed on a pressor such as norepinephrine to maintain MAPs that are 10–
20% above baseline.
• Daily labs should include CBC, chemistry panel, and measures of urine function.
• TCD can be a useful screening tool but is fraught with technical limitations. Magnetic
resonance angiography (MRA) is more reliable. Cerebral angiography is the gold standard
for diagnosis.
• Consults should be obtained as clinically indicated if cardiac, pulmonary, or renal
complications are detected.
• One should be prepared for the risk of significant bleeding intraoperatively. This can lead to
malignant brain swelling with devastating consequences. Brain protection and brain
relaxation techniques should be immediately instituted in such an event.
• As with any neurosurgical procedure, there is risk of intracranial hemorrhage. Patients
should be monitored closely for changes in neurological function for at least 24 hours
postoperatively.
• There is also the potential for developing an intraoperative infarct, especially if hypotension
is maintained. This may present in the postoperative period as delayed emergence, altered
mental status, or focal neurologic deficits.
• Any of the above complications resulting in neurologic injury can lead to compromised
airway reflexes, which puts the patient at risk for aspiration.
• Triple-H therapy can lead to additional complications, such as cerebral edema, cardiac
ischemia, pulmonary edema, and hyponatremia. Patients should be closely monitored in an
ICU. Central venous pressure monitoring is recommended.
REFERENCES
1. Alaraj A, Charbel FT, Amin-Hanjani S. Peri-operative measures for treatment and
prevention of cerebral vasospasm following subarachnoid hemorrhage. Neurol Res.
2009;31(6):651–659.
2. Lee KH, Lukovits T, Friedman JA. “Triple-H” therapy for cerebral vasospasm following
subarachnoid hemorrhage. Neurocrit Care. 2006;4:68–76.
CODES
ICD9
435.9 Unspecified transient cerebral ischemia
ICD10
G45.9 Transient cerebral ischemic attack, unspecified
CLINICAL PEARLS
• The extent of SAH and the patient’s subsequent neurologic status can predict the likelihood
of developing cerebral vasospasm.
• A change in the level of consciousness after SAH or postaneurysm clipping should always be
investigated for the possibility of vasospasm in the first 2 weeks.
• It is important to avoid prolonged periods of hypotension in order to minimize the risk of
ischemia.
• The benefit of triple-H therapy has yet to be proven; additionally, it can lead to significant
complications, especially if the patient is not monitored closely.
CEREBROSPINAL FLUID
BASICS
DESCRIPTION
Cerebrospinal fluid (CSF) is a clear, colorless fluid surrounding the central nervous system
(CNS) that provides physical protection and a chemically stable environment.
• CSF is a direct extension of the extracellular fluid compartment of the CNS.
– The volume of CSF in an adult is ∼150 mL and in infants 50 mL.
– It is secreted and absorbed continuously throughout the day, with daily production in
adults ∼500–600 mL.
– Absorption is pressure dependent and linear over a wide range.
• CSF provides nourishment to the brain as well as assists in removing by-products of
neuronal metabolism.
• Electrolyte composition
– Differs from that of plasma due to the blood–CSF barrier, which allows free diffusion of
water, gases, and lipid-soluble compounds but requires active or passive transport of
glucose, amino acids, and ions.
– CSF is composed primarily of sodium, chloride, and bicarbonate.
– Proteins are largely excluded from CSF. See Table 1 for comparison of CSF to plasma (1).
Table 1 Composition of CSF: Plasma
• A decrease in plasma pH results in a similar decrease in CSF pH due to the ability of carbon
dioxide to easily cross the blood–brain barrier.
ANATOMY
• Site of production. Ninety percent of CSF is formed from blood in the choroid plexus of the
lateral, 3rd, and 4th ventricles. The remaining 10% is formed from brain substance.
• Nutrients reach neurons and glial cells either by
– Crossing the blood–CSF barrier that is regulated by the choroid plexus or,
– Crossing the blood–brain barrier of cerebral capillaries.
• The blood–CSF barrier is formed by impermeable “tight junctions” between epithelial cells
that regulate the diffusion of certain molecules.
• Once molecules enter the CSF, they travel to the interstitial fluid surrounding neurons and
glial cells by diffusing through a “leaky” ependymal layer.
• Arachnoid villi (granulations) in the superior sagittal, transverse, and other venous sinuses
absorb the majority of CSF. The rest is absorbed by veins in the cranial and spinal
subarachnoid spaces and lymphatic vessels of the cranial and spinal nerves.
• Normal intracranial pressure (ICP) is usually 5–15 mm Hg and is comprised of
– Intracranial CSF
– Brain tissue
– Intracranial blood (arterial and venous)
• Compensation. An increase in any one component of intracranial volume must be offset by a
decrease in another component to prevent an increase in ICP. Initially, as the intracranial
volume increases, CSF is shifted from the cranium to the spinal subarachnoid space, in order
to prevent an increase in ICP.
• Increased ICP. If the intracranial volume continues to increase beyond the ability of the CSF
to translocate, then an exponential rise in ICP is likely with associated clinical symptoms.
• Nonobstructive hydrocephalus is a condition of increased production or decreased
absorption of CSF. Obstructive or noncommunicating hydrocephalus occurs when there is a
blockage anywhere along the path of CSF flow (e.g., tumor, congenital structural
abnormalities, infection, and trauma). Treatment depends on the etiology of the
hydrocephalus. In certain situations, the placement of a CSF shunt is indicated in order to
translocate CSF and lower the ICP, thereby maintaining cerebral perfusion (CPP = MAP −
ICP, where CPP is cerebral perfusion pressure, MAP is mean arterial pressure).
• CSF leak. Leakage of CSF into the nasal, oral, ear, or dermal sinus cavities can result from
trauma, intracranial surgical procedures, infection, hydrocephalus, congenital
malformations, or neoplasms. Interruption of the anterior cranial fossa floor allows leaks of
CSF through the cribriform plate. It most commonly presents as otorrhea or rhinorrhea and
is exacerbated by a Valsalva-type maneuver (coughing, sneezing, bending, heavy lifting, and
straining).
• Postdural puncture headache (PDPH) occurs most frequently after a “wet tap” and is a
phenomenon related to the spontaneous loss of CSF from the subarachnoid to the epidural
space.
– Most common complication of neuraxial anesthesia due to a knick in the dura from a
relatively large sized needle.
– Manifests as pain or stiffness in the neck, nausea or emesis, diplopia due to unilateral or
bilateral sixth nerve palsy, dizziness, changes in hearing, visual blurring, photophobia,
intrascapular pain, facial numbness or weakness, galactorrhea, and/or radicular upper
limb symptoms.
– Debate exists over the timing and use of epidural blood patches in the treatment of
PDPHs. Current literature does not support prophylactic epidural blood patches over other
treatments because there are too few trial participants to allow reliable conclusions to be
drawn. However, therapeutic epidural blood patch showed a benefit over conservative
treatment based on available evidence (2)[A].
• Neuraxial anesthesia involves the injection of local anesthetics and/or narcotics either into
the intrathecal space where CSF bathes the spinal cord (spinal anesthesia) or into the
epidural space where the nerves exit the spinal cord through the dura. Neuraxial anesthesia
is used primarily in surgeries involving the lower extremities, abdomen, and/or pelvis.
Potential benefits of neuraxial techniques include reduced blood loss, blood clots, incisional
pain with respiration, atelectasis, pneumonia, and need for narcotics; as well as a quicker
return of bowel function, ambulation, and patient satisfaction (3)[A]. For Cesarean section,
it is considered advantageous over a general anesthetic in regard to the simplicity of the
technique, reduced risk of systemic toxicity to mother and fetus, and maternal satisfaction.
There is no difference between epidural and spinal anesthesia shown with respect to failure
rate, need for additional intraoperative analgesia, conversion to general anesthesia
intraoperatively, maternal satisfaction, and neonatal intervention (4)[A].
• Neuraxial local anesthetics used for spinal anesthesia are characterized according to their
baricity (e.g., hypobaric, isobaric, or hyperbaric), which is the ratio of the density of the
solution at a specified temperature compared to the density of CSF (1.0001–1.0005 at 37°C)
(5).
– Hypobaric solutions (density <0.9998) “float" upward.
– Hyperbaric solutions (density >1.0008) “sink" downward.
– Isobaric solutions (density between 0.9998 and 1.0008) “stay" at the point of injection.
• Neuraxial opioids work on opioid receptors (primarily mu receptors) in the substantia
gelatinosa of the spinal cord.
– Analgesia is better for visceral rather than somatic pain.
– An advantage of neuraxial opioids compared to local anesthetics is that analgesia is
produced without sympathetic nervous system denervation, skeletal muscle weakness, or
loss of proprioception.
– Onset of analgesia, duration of action, and cephalad movement in the intrathecal space
depend on lipid solubility. Poorly lipid-soluble opioids, such as morphine, have a slower
onset, longer duration of action, and remain in the CSF longer for transfer to more
cephalad locations than highly lipid-soluble opioids, such as fentanyl.
– Coughing or straining can also affect opioid movement in the CSF. However, body position
does not usually affect opioid movement.
– Vascular absorption after intrathecal administration of opioids is minimal; however
increased with lipid-soluble drugs.
– Side effects of neuraxial opioids are dose dependent and include pruritus, nausea and
vomiting, urinary retention, and respiratory depression.
– Cephalad migration of morphine in the CSF can lead to respiratory depression 6–12 hours
after neuraxial administration due to an interaction with opioid receptors in the ventral
medulla.
• “Wet tap.” Accidental dural puncture is possible during epidural anesthesia. It is recognized
by the appearance of warm CSF (versus cold saline used to identify loss of resistance) at the
hub of the epidural needle during placement. When this happens, a postdural puncture
headache is likely due to the large hole created in the dura by the epidural needle, allowing
the leakage of CSF from the intrathecal space to the epidural space.
• Ventriculostomy: Aseptic placement of a pressure transducer into the subdural space
(subdural bolt), brain parenchyma, or ventricle that allows ICP monitoring as well as the
withdrawal of CSF. One major benefit of such a drainage system is that it can be organized
to only drain CSF when the ICP rises above a selected value. Another benefit is that CSF can
be easily obtained for lab analysis.
• Lumbar subarachnoid catheter (lumbar drain): CSF can be withdrawn or allowed to
passively drain.
– Utilized in thoracoabdominal aortic aneurysm surgery at some institutions. Purpose is to
reduce the CSF pressure, improve blood flow to the spinal cord, and reduce the risk of
ischemic spinal cord injury. However, current available evidence does not fully establish
CSF drainage as a method of protection (6)[A].
– Lumbar CSF pressure may not accurately reflect ICP secondary to compartmentalization.
– There is a risk of tonsillar herniation with the drainage of CSF via lumbar subarachnoid
catheters in certain patients (i.e., brain tumor).
• Decreased pH in the CSF. Occurs with respiratory acidosis and stimulates ventilation via the
medullary chemoreceptors located in the fourth cerebral ventricle. Over time, the pH is
restored to normal by the active transport of bicarbonate ions into the CSF. Conversely, in
respiratory alkalosis, bicarbonate ions are actively transported out of the CSF (7).
REFERENCES
1. Modified from Table 27-2, Anesthesia for Neurosurgery. In Barash PG, Cullen BF, Stoelting
RK (Eds.), Clinical Anesthesia, 5th ed., p. 750. Philadelphia, Lippincott Williams and
Wilkins, 2006. As adapted with permission from Artru AA: Cerebrospinal Fluid. In Cottrell
JE, Smith DS (Eds), Anesthesia and Neurosurgery, p. 95. St Louis, CV Mosby, 1994.
2. oonmak P, Boonmak S. Epidural blood patching for preventing and treating post-dural
puncture headache. Cochrane Database Syst Rev. 2010;1:CD001791.
3. arbosa FT, Cavalcante JC, Jucá MJ, et al. Neuraxial anaesthesia for lower-limb
revascularization. Cochrane Database Syst Rev. 2010;1:CD007083.
4. g KW, Parsons J, Cyna AM, et al. Spinal versus epidural anaesthesia for caesarean section.
5. rnst A. In vitro changes of osmolality and density of spinal anesthetic solutions.
Anesthesiology. 1968;29:104.
6. itchell RA, Singer MM. Respiration and cerebrospinal fluid pH in metabolic acidosis. J Appl
Physiol. 1965;20:905–911.
7. Khan SN, Stansby GP. Cerebrospinal fluid drainage for thoracic and thoracoabdominal
aortic aneurysm surgery. Cochrane Database Syst Rev. 2004;1:CD003635.
ADDITIONAL READING
• Covino BG, Scott DB, Lambert DH. Cerebral Spinal Fluid. Handbook of Spinal Anaesthesia
and Analgesia. WB Saunders Company. 1994:46–47.
• Barash PG, Cullen BF, Stoelting RK (Eds.). Anesthesia for neurosurgery. In: Clinical
Anesthesia, 5th ed. Lippincott Williams and Wilkins. 2006: 749–750.
• Epidural
• Ventriculo-peritoneal shunt
CLINICAL PEARLS
• PDPH is the most common complication of neuraxial anesthesia and is related to the loss of
CSF from intrathecal to epidural space.
• CSF is a component of ICP and can be drained in certain situations to decrease ICP and help
improve CPP temporarily.
CERVICAL PLEXUS BLOCK
Maged N. Guirguis, MD
Sherif Zaky, MD, PhD
BASICS
DESCRIPTION
• Deep and superficial cervical plexus blocks can provide anesthesia to the neck and upper
shoulders.
– Superficial cervical plexus block can be used alone for many superficial neck surgeries or
in conjunction with a deep cervical block for more invasive procedures, including
thyroidectomy or carotid endarterectomy (CEA).
– If a superficial cervical plexus is used alone, local anesthetic supplementation from the
surgeon might be required for deeper structures.
• Postoperative analgesia; can last up to 8 hours after the time of the block, depending on the
local anesthetic chosen.
• Indications
– CEA; allows for an awake patient and continuous neurological assessment.
– Thyroid operations; when general anesthesia poses high risk, especially in patients with
significant cardiac history.
– Superficial neck surgeries; such as lymph node dissection and excision of thyroglossal or
branchial cysts.
• Contraindications
– Absolute: Patient refusal
– Relative
Infection at the site of injection
Sepsis
Coagulopathy
Preexisting central or peripheral nervous system disorders
Allergy to local anesthetics
• Advanced pulmonary disease. Deep cervical blocks will also result in blockade of C3, C4,
and C5 (diaphragmatic innervation); this may result in pulmonary embarrassment.
Alternatively, a superficial cervical plexus block with local anesthetic supplementation from
the surgeon should be considered.
• Cutaneous innervations to the head and neck. Innervation by the trigeminal and cervical
nerves can be delineated by a straight line from the vertex of the head to the ear to the chin
(e.g., the “vertex-ear-chin line”). The trigeminal nerve provides sensory innervations above
this line, whereas the upper cervical nerves provide sensory innervations below. The
cervical plexus is formed from the ventral rami of the upper four cervical nerves (C1–C4). It
supplies sensation to the neck, upper shoulders, and chest, as well as motor branches to the
diaphragm and some neck muscles.
– The cervical plexus lies on the anterior surface of the levator ani scapulae and scalenus
medius muscles, covered by the sternocleidomastoid muscle. The plexus at this plane gives
origin to both superficial and deep branches. Superficial branches (superficial cervical
plexus) give rise to cutaneous nerves of the skin and superficial structures of the head,
neck, and shoulders.
– Deep branches (deep cervical plexus) give rise to motor and communicating branches of
the anterior neck muscles and diaphragm (C3, C4, components).
• Superficial cervical block. A technique that blocks the superficial branches of the cervical
plexus nerves at the posterior border of the sternocleidomastoid. In high-risk patients (e.g.,
significant pulmonary disease), superficial cervical plexus block alone can be used with
local anesthetic supplementation by the surgeon.
• Deep cervical block. A technique that blocks the nerves at the paravertebral level near the
vertebral foramina. This blocks C2–C4 prior to forming the plexus.
ANATOMY
• Cervical plexus. The dorsal and ventral roots of C2, C3, and C4 combine to form spinal
nerves after exiting their respective foramina. They subsequently form ascending and
descending branches that come together to form the cervical plexus. The cervical plexus
divides into superficial and deep cervical branches that emerge from the posterior triangle,
midway on the posterior border of the sternocleidomastoid.
• Superficial or cutaneous branches
– Lesser occipital nerve (ascending branch) is a direct branch of C2.
– Greater auricular (ascending) nerve arises from C2 and C3.
– Transverse cervical nerve arises from C2 and C3.
– Supraclavicular nerves (descending) are three nerves that receive innervations from C3
and C4. They innervate regions of the suprascapularis, shoulder, and upper thoracic
region.
• Deep branches
– C1 is mostly a motor nerve that is not blocked by superficial or deep techniques.
– C2 provides a branch to the sternocleidomastoid.
– C3 and C4 may send a sensory branch to the spinal accessory nerve or deep surface of the
trapezius.
• Nerve branches from C2 to C4 that branch out prior to the cervical plexus.
– C3, C4 contribute to the phrenic motor nerve.
– C4 can also send a branch caudally and join C5, thus functioning as part of the brachial
plexus.
• Landmarks
– Mastoid process
– Transverse process of the sixth cervical vertebra (Chassaignac’s tubercle)
– Posterior border of the sternocleidomastoid muscle
• Phrenic nerve blocks can lead to respiratory distress in patients with underlying pulmonary
disease. In healthy patients, unilateral phrenic nerve block is usually asymptomatic due to
respiratory reserve and an intact contralateral phrenic nerve.
• Underlying bleeding disorder or patients taking anticoagulants. Bleeding in this area is
problematic; hematoma may occur if the needle enters a large blood vessel and might
compromise the airway.
• There are case reports of deterioration or worsening of pre-existing neurological disorders,
such as diabetic neuropathy or multiple sclerosis.
• Local anesthetic systemic toxicity. The vertebral artery directly supplies the brain; it is also
in close proximity to the site of injection and very small amounts of intravascular injection
can result in CNS effects.
• Inadvertent subarachnoid or epidural anesthesia can result due to the proximity to the
spinal foramina. It can lead to total spinal anesthesia and respiratory arrest.
• Infection is possible, but very low risk.
• Deep cervical block
– Position. The patient should be positioned supine with the neck slightly extended and the
head rotated away from the side of the block.
– Landmarks to identify the location of C2–C4 as they emerge from the foramina.
A line connecting the mastoid process and the transverse process of C6 is drawn, while
the nondominant hand palpates behind the posterior border of the sternocleidomastoid
muscle.
Label C2, C3, and C4 levels 2, 4, and 6 cm, respectively, from the line starting caudal to
the mastoid process.
– Prep
Supplemental oxygen is usually applied with a nasal cannula, facemask, or blow-by
while avoiding straps in the sterile field.
The skin is cleaned and prepped in usual sterile fashion
Subcutaneous infiltration of local anesthetic is administered along the line over the
transverse processes; this allows the anaesthetist to move the needle caudally and
cephaladly to block each level.
– Needle insertion
A 1 ½ inch, 22 gauge, short-beveled needle (connected to a 20 cc syringe of local
anesthetic, typically with extension tubing) is inserted between palpating fingers and
advanced perpendicular to the skin plane with a slightly caudal angulation.
Advance slowly until the transverse process is contacted, typically at a depth of 2–3 cm.
Withdraw the needle 1–2 mm.
Aspirate to rule out blood or cerebrospinal fluid.
Local anesthetic (3–5 mL) is slowly injected with frequent intermittent aspiration.
Remove the needle and repeat the block at the next level.
Alternatively, some practitioners inject 15 mL at the C3 level only to avoid repeated
passes (3).
• Superficial cervical plexus block
– Landmarks. A line connecting the mastoid process to the C6 transverse process is drawn.
– Prep. As above; usual sterile prep. Subcutaneous infiltration should occur at the midpoint
of the line.
– Needle insertion
A 1 ½ inch, 25 gauge, short-beveled needle (connected to 20 cc syringe of local
anesthetic, typically with extension tubing) is introduced through the numbed area and
passed inferiorly and superiorly along the posterior border of the sternocleidomastoid.
A total of 10–15 mL of local anesthetic should be injected in both directions.
• Local anesthetic (3). The potential toxicity of a particular drug and concentration must be
weighed against the benefits of using that drug. The length of the surgery must also be
taken into account, as different local anesthetics have different durations of action. The
following have been used and described in the literature:
– 1.5% Mepivacaine
– 2% Lidocaine
– 0.5% Ropivacaine
– 0.25% Bupivacaine
• Ultrasound guided deep cervical plexus block: Multiple techniques have been described. One
easy approach involves a single injection of local anesthetic under the carotid artery using
15–20 ml of local anesthetic to block the roots of the cervical plexus. This is usually done
using a high frequency ultrasound probe to obtain a short axis (cross section) view of the
carotid artery while the needle is inserted in plane with the probe from its lateral end. Local
anesthetic will be injected deep to the carotid artery at around the C6 transverse process.
• Signs of a successful block. Sensory block within cutaneous segments of the lesser occipital,
greater auricular, transverse cervical, and supraclavicular nerves, as well as relaxation of
the ipsilateral neck muscles. Ipsilateral ptosis, hyperemic conjunctiva with warm sensation
of the face, and nasal obstruction are also common due to associated block of the
sympathetic fibers.
• CEA (1,2)
– Pros: Allows for an awake neurological exam and avoids hemodynamic shifts. Shunts are
less commonly utilized.
– Cons: Patient interference, lack of anesthetic medications with neuroprotective qualities,
and the need to secure the airway in the event of stroke, hemorrhage, seizure, agitation,
or hypoxia.
– Cervical plexus blockade for CEA also can be effectively performed with a single injection
at C3 level. However, studies have not shown significant difference in quality of
anesthesia during surgery compared to the classic method described above.
• Combined deep and superficial cervical blocks are usually done together for neck surgeries.
• Combined versus superficial plexus blocks for minimally invasive neck surgeries (e.g.,
parathyroidectomy). Some studies suggest that there is no difference in onset of block or
pain scores (4).
GRAPHS/FIGURES
REFERENCES
1. Fiorani P, Sbarigia E, Speziale F, et al. General anaesthesia versus cervical block and
perioperative complications in carotid artery surgery. Eur J Vasc Endovasc Surg.
1997;13:37–42.
2. Merle JC, Mazoit JX, Desgranges P, et al. A comparison of two techniques for cervical
plexus blockade: Evaluation of efficacy and systemic toxicity. Anesth Analg.
1999;89:1366–1370.
3. Gratz I, Deal E, Larijani GE, et al. The number of injections does not influence absorption
of bupivacaine after cervical plexus block for carotid endarterectomy. J Clin Anesth.
2005;17(4):263–266.
4. Pintaric TS. A prospective, randomized comparison between combined (deep and
superficial) and superficial cervical plexus block with levobupivacaine for minimally
invasive parathyroidectomy. Anesth Analg. 2007;105(4):1160–1163.
5. Usui Y, Kobayashi T, Kakinuma H, et al. An anatomical basis for blocking of the deep
cervical plexus and cervical sympathetic tract using an ultrasound-guided technique.
Anesth Analg. 2010;110:964–968. www.nysora.org
• Parathyroidectomy
• Thyroidectomy
• Total spinal
CLINICAL PEARLS
• Branching of spinal nerves. C2–C4 spinal cord→ dorsal and ventral root (before exiting
foramina)→ spinal nerves (after exiting foramina)→ ascending and descending branches →
CERVICAL PLEXUS → superficial and deep cervical branches →individual nerves or
contributions to other nerves.
CHEST TUBES
BASICS
DESCRIPTION
• Tube thoracostomy is performed to drain collections of fluid or air in the pleural space. If
the collection is compressing the lung, removal can result in re-expansion and improved
V/Q matching. If the air collection is under pressure (e.g., tension pneumothorax), removal
can be life saving.
• Tube thoracostomy was initially introduced in the early 1870s; however, there is evidence
that Hippocrates (circa 400 BC) initially considered drainage of the pleural compartment.
• The pleural space is a potential space between the parietal pleura on the inside of the chest
wall and the visceral pleura that lines the outside of the lungs (pleura are thin layers of
tissue). The space contains a small amount of serous fluid to “lubricate” movement.
• The pleural space’s negative pressure bestows function. Because parietal pleura adheres to
the inside of the stiff chest wall space, the negative pressure in the pleural space serves to
“draw" or “pull" the visceral pleura (along with the adherent lung tissue) outward. This
prevents lung collapse.
• Fluid and air collections in the pleural space are pathologic; they prevent adequate lung
expansion (ventilation/perfusion mismatch) and create tension (positive pressure capable of
shifting the mediastinum).
• The chest tube (a.k.a. tube thoracostomy), provides a conduit for the removal of air and
fluid collections from the pleural space. By attaching to a drainage system (typically
comprised of 3 chamber compartments), “one-way" flow out of the pleural space can be
established.
• The system works by combining the following physiologic principles: positive pressure
within the thoracic cavity facilitates extrusion of air and fluid; gravity facilitates drainage of
fluid; air rises in a fluid column; suction facilitates flow of air and fluid out of the pleural
cavity.
• Positive pressure. During spontaneous ventilation (SV), thoracic cavity pressure is positive
on exhalation and negative during inhalation (downward movement of diaphragm and
outward expansion of rib cage). Therefore, air and fluid are extruded out of the pleural
cavity when the patient exhales. During positive pressure ventilation, thoracic cavity
pressure is positive during inhalation, but negative/reduced during exhalation. Therefore,
air and fluid are extruded out of the pleural cavity during inhalation.
• Chest tubes. Clear plastic of varying internal diameter (8F, 12F, 16F, 20F, 24F, 28F, 32F,
36F) that is inserted into the patient’s pleural cavity and connects to the drainage system.
The portion within the pleural cavity contains multiple orifices that improve drainage.
Smaller diameter tubes may be placed via the Seldinger technique; however, they are more
prone to clotting from blood or fluid and therefore may be more appropriate for air
collections. Additionally, a radiopaque line facilitates visualization on chest radiography.
• Drainage system (collection chamber, water seal chamber, suction control chamber)
– Collection chamber. Connects to the chest tube; air and fluid empty directly into this
chamber via gravity, suction, and positive pressure within the chest wall. The chambers
are calibrated, allowing for fluid measurement. Fluid remains here and does not enter the
other chambers, or flow back into the pleural space as long as the gravitational gradient is
maintained. Because air rises in a fluid column, the chambers are set up such that air
enters at the bottom of a fluid-filled chamber and can only move upward (creates one-way
flow).
– Water seal chamber. Middle chamber; partially filled with water. Air from the collection
chamber enters the bottom of this chamber and bubbles upward. Reentry of air cannot
occur (air cannot move down a fluid column) and one-way flow is established. This is
critical, because air would otherwise be able to reenter the pleural cavity.
Air leak: Describes bubbling in the water seal chamber which indicates that air is present
in the pleural space.
Air leak meter: Allows for a qualitative measurement of the air leak (not quantitative;
increased or decreased)
Calibrated manometer: Allows measurement of the negative pressure in the pleural
cavity. As intrapleural pressures become negative, the water level rises. Once negative
pleural pressures are re-established, “Tidaling” occurs. Tidaling describes the rising and
falling water level that corresponds with negative and positive pressures in the pleural
cavity, respectively (SV: Rises with inhalation, falls with exhalation).
High negativity float valve and relief chamber: Safety features that safeguard ill-effects of
high negative pressures that may occur with coughing, chest tube stripping, or
disconnected suction.
– Suction control chamber. The most distal chamber and connects the suction source to the
water seal chamber. Serves to control the level of suction, thereby protecting the pleural
cavity from excessive negative pressures. Water in this chamber serves as a barrier or
buffer between the suction source and patient (allows for a more “gentle” suction and
helps safeguard against the ill-effects of accidental excessive suction). Thus, the height of
water in this chamber determines the amount of suction transmitted to the pleural cavity.
ANATOMY
• Placement occurs with the patient supine, with the head slightly raised (30°). Expose the
axilla by raising and abducting the arm, or placing the hand behind the head.
• Chest tube insertion point is performed between the 3rd and 5th intercostals space at the
midaxillary line.
• A scalpel is used to make a superficial incision that follows the orientation of the ribs,
followed by blunt dissection through subcutaneous tissue with a curved hemostat. Following
identification of the parietal pleura (adheres to the inside of the ribs), the pleural tissue is
punctured to enter the pleural space (rush of air or fluid occurs). The tract is dilated with
the proceduralist’s finger and adhesions are swept away. The chest tube is introduced with a
hemostat in the direction of the air or fluid collection to a distance sufficient for all drainage
holes to be within the chest. Once in situ, the chest tube is secured at the skin with a
mattress suture, occlusively dressed, and connected in a sterile fashion to a drainage system.
When smaller chest tubes are placed, a Seldinger technique may be used to guide the chest
tube.
• Correct positioning is often confirmed with a chest radiograph following chest tube
placement.
• Relative contraindications (or concerns) to chest tube placement include bleeding diatheses,
infection over the chest tube insertion site, pulmonary bullae, or lung densely adherent to
the chest wall throughout the hemithorax.
• Placement of a chest tube has a complication rate ranging from 3% to 16% and includes
improper placement resulting in an inability to drain the desired air/fluid collection;
diaphragm, pulmonary, splenic, hepatic, or gastric laceration; intercostal artery bleeding;
unilateral pulmonary edema following rapid removal of a large pleural effusion or
pneumothorax; thoracic empyema; and persistent air leak.
• Indications for the placement of a chest tube include pneumothorax, hemothorax,
chylothorax, empyema, and pleural effusions.
• Pneumothorax. Air collections can occur from a breach in the pleural tissue, either parietal
or visceral. Causes include trauma, thoracic cavity surgery, pulmonary disease (chronic
obstructive pulmonary disease [COPD], blebs/bullae, adult respiratory distress syndrome
[ARDS], Marfan’s syndrome, multiorgan dysfunction), complications of central line or
peripheral nerve block placement, and bronchopleural fistulas. The effects can range from
subclinical (where a small portion of the visceral pleura becomes detached from the parietal
wall), to life-threatening (tension pneumothorax).
• Fluid collections can result from breaches in the pleural tissue or oncotic/osmotic pressure
pathology. Causes include hemothorax (from surgical or traumatic injury), chylothorax
(lymphatic blockade), and empyema, and pleural effusions (CHF, malignancy, cirrhosis,
nephritic syndrome, lupus). The effects are due to impairment of lung expansion and vary
depending on size and time of accumulation. Unless a breach in the pleural tissue occurs,
they do not necessarily interfere with the negative pressure within the pleural space (thus,
do not necessarily result in complete lung collapse or life-threatening tension scenarios).
• Pulsus paradoxus is an exaggeration of the normal variation of systolic BP during the
inspiratory phase of respiration. Normally, during inhalation the systolic BP will fall <10
mm Hg. In certain disease states where there is an increased intrathoracic pressure, the
systolic pressure will fall >10 mm Hg. These disease states include pneumo/hemothorax,
pleural effusion, hemomediastinum, and COPD.
• Management practices regarding criteria and method of removal as well as monitoring with
chest radiography are variable and depend on the clinician and institution.
• Intensive care unit (ICU) management: Management is centered on daily evaluation
concerning the need to keep the chest tube in situ. Clinical picture, hemodynamic stability,
pleural output, continued bleeding, bronchopleural fistula, and appearance on chest
radiographs are factors that help management
– An air leak can occur if there is a leak in the tubing or if the openings along the lumen of
the tube are outside of the chest wall. It can also occur if there is a bronchopleural fistula
– one of the most feared complications of chest tube placement.
– Volume of chest tube drainage. Studies suggest <2 mL/kg/day or <200 mL/day
(whichever is less) may be appropriate for chest tube removal.
– Removal may be done at end-inspiration or end-expiration. Studies have not shown a
difference in the recurrence of pneumothorax.
– After resolution of air leak/drainage, removal on water seal may result in increased
recurrence, hospital stay, and number of chest radiographs ordered (compared to placing
the patient on suction for 24 hours, and then removing).
– Tube stripping. Conducted by some to prevent clotting (which can create a tension
situation in the chest), however, has the potential to create large negative pressures or
tissue injury to the lung.
– Chest radiography after removal is often performed; however, studies also demonstrate
that clinical exam and judgment may be sufficient.
– Daily chest radiographs may not be indicated
• Management outside of ICU
– Water seal chamber evaluation prior to the procedure is crucial to intraoperative
management. Look to see if there are bubbles – their presence indicates an air leak. If the
bubbles coincide in time to the respiratory cycle, there may also be a bronchopleural
fistula.
– Look for tidaling during the respiratory cycle, this respiratory swing indicates a patent
system.
– A bubbling chest tube should not be clamped. This can lead to accumulation of air and
formation of a tension pneumothorax.
– Unless there are extenuating clinical circumstances, keep the drainage system upright and
below the patient so as to allow drainage of any fluid to gravity. Keep on water seal so as
to prevent flow of air into the pleural space.
– Only attach to suction if there may be an accumulation of fluid/air in the pleural cavity.
– Be prepared to deal with malfunction and even dislodgement of the chest tube. This may
necessitate replacement of the chest tube on an emergent basis.
GRAPHS/FIGURES
REFERENCES
1. Miller KS, Sahn SA. Chest tubes. Indications, technique, management and complications.
Chest. 1987;91:258–264.
2. Laws D, Neville E, Duffy J. BTS guidelines for the insertion of a chest drain. Thorax.
2003;58:ii53–ii59.
3. Paramasivam E, Bodenham A. Air leaks, pneumothorax, and chest drains. Conti Educ
Anaesth Criti Care Pain. 2008;8(6):204–209.
ADDITIONAL READING
• www.surgicalcriticalcare.net/guidelines/chest_tube_2009.pdf
• Pneumothorax
• Central line
CLINICAL PEARLS
• Anaesthetists may need to manage chest tubes perioperatively or in ICU patients.
Additionally, pneumothorax or hemothorax that may occur with regional nerve blocks or
central line placement may require the emergent placement following needle thoracostomy.
• The anesthesia team should understand the pathophysiology, management strategies, and
goals of chest tube drainage for patients who present to the operating room with chest
tubes. Any questions or concerns should be discussed with the primary team.
CHEST X-RAY
James M. Callas, MD
BASICS
DESCRIPTION
• A radiological study that visualizes thoracic structures in a two-dimensional plane.
• Chest x-ray (CXR) is utilized in the preoperative period for examination of cardiopulmonary
processes, detection of pacemakers, and confirmation of lines and tubes. In the
intraoperative period, CXR is used for evaluation of acute pulmonary changes, confirmation
of new line and tube placement, and possibly for evaluation of retained surgical
instruments. In the postoperative period, CXR is used for confirmation of tube and line
placement and evaluation of interval cardiopulmonary changes.
• Intensivists routinely utilize the CXR for monitoring interval pulmonary changes and
checking line and tube placement in critically ill patients.
• Anatomic structures can be visualized by the differential penetration of ionizing radiation.
– Inverse relationship between density of anatomic structures and penetration of ionizing
radiation.
– High-density structures such as bone and fatty tissue attenuate the x-ray beam, and appear
white on film.
– Low-density structures such as air appear black on CXR.
• The orientation of the ionizing radiation can affect the quality of the study.
– Posterior to anterior (PA) orientation of radiation beams can produce a higher quality
study but needs patient cooperation.
– Anterior to posterior (AP) orientation of radiation beams distort anterior thoracic
structures because these structures are further away from the x-ray plate that captures the
image. The heart and pulmonary vessels appear larger on an AP view than its PA
counterpart due to this difference. However, this study can be used more easily on
patients who are otherwise immobile (patients in intensive care unit or operating room)
or uncooperative.
– Lateral films are typically performed in the upright position but can be performed supine.
Lateral decubitus films can help the physician determine if there is layering of pleural
fluid versus a loculated effusion.
ANATOMY
• Technical considerations when ordering and examining CXR
– Markings distinguishing between right and left are always placed by the technologist.
– Incomplete inspiration may be misleading; decreased lung volumes give the illusion of
other anatomic structures appearing larger.
– Technique of film must be taken into account. The technologist uses various settings to
determine energy and timing of radiation dose and this can affect the appearance of
density/contrast on the CXR. It is possible to have two completely different appearing
CXRs on the same patient by simply modifying the radiological technique.
• Cardiovascular
– Relevant anatomy: Heart, superior vena cava (SVC), inferior vena cava, pulmonary
arteries, pulmonary veins, ascending aorta, descending aorta.
– Inspect the contour of the heart; it should have curves corresponding to the aorta, atrium,
and ventricles. A heart devoid of these normal curves is suggestive of pericardial fluid.
– The aorta should be visualized from the 12 o’clock to the 6 o’clock position as it goes from
the left ventricle through the aortic arch and down to the descending aorta.
– The SVC is a vague stripe along the left paratracheum that can be accentuated by the
supine position.
– The aortic knob and apex should be on the left. A right sided aortic knob is suggestive of
situs inversus.
– Heart size should take up 1/3rd or less of the chest cavity.
• Pulmonary
– Relevant anatomy: Trachea, mainstem bronchi, visceral pleura, diaphragm, costophrenic
angle.
– Trachea should be at the midline; assure that the right and left mainstem bronchi are
symmetric (neither elevated nor depressed).
– Lung markings should extend out to the periphery to rule out pneumothorax.
– Pulmonary arteries should be symmetric. Large pulmonary arteries that rapidly taper are
suggestive of pulmonary hypertension.
– The density of both lungs should be the same. Air trapping, mucous plugging, and
pneumothorax can cause hyperlucent lungs.
– Costophrenic angles should be sharp. Pleural fluid, pleural thickening, or pleural-based
mass can blunt these angles.
– Diaphragm contours should be noted; flattening of the diaphragms can be suggestive of
hyperinflation.
• Musculoskeletal
– Relevant anatomy: Ribs, sternum, clavicle, scapula, shoulder girdle.
– Sternum location should be assessed (pectus excavatum).
– Clavicles should be symmetric.
– Rib spacing should be symmetrical bilaterally at the respective levels.
– Lytic or blastic lesions suggest bony destruction.
– Lateral view: Vertebral body heights to exclude compression fractures.
• Gastrointestinal
– Relevant anatomy: Esophagus, stomach.
– An air-fluid level in the mediastinum can result from achalasia or distal esophageal
obstruction from cancer.
– Lateral view: Assess the posterior cardiac shadow for an air-fluid collection which can
represent a hiatal hernia.
– An enlarged esophagus can stretch its outer borders beyond the heart, mimicking a
widened mediastinum.
– Free air beneath the diaphragm. The stomach bubble is on the left and has a normal
appearance of air. Gas in the liver can be suggestive of dead bowel (necrotizing
enterocolitis).
• Chronic obstructive pulmonary disease (COPD)
– Findings: Hyperinflated “black" lungs, large pulmonary arteries that quickly taper,
diminished heart size.
– Lack of pulmonary vascularity in both lungs is due to pulmonary blebs. The relative
hypovascularization creates the black appearance. Asymmetry of the mediastinal contour
can be suggestive of cancer. The heart may appear to be smaller because of increased
intrathoracic pressure.
• Partial pneumothorax
– Findings: Absence of lung markings to the periphery, visceral pleural line demarcating
lung tissue from air, commonly seen in apex.
– In normal lungs, the visceral pleura approximates with the parietal pleura. In a partial
pneumothorax, air comes between the visceral and parietal pleura, allowing the border of
the parietal pleura to be visualized. An upright film is more sensitive than supine in
detecting partial pneumothorax (collects at apex due to gravity).
– The entire clinical picture must be taken into account. Generally, a stable patient with a
small partial pneumothorax can be observed with serial CXR to confirm resolution.
• Tension pneumothorax
– Findings: Complete lucency of the chest with shifting of the mediastinum away from the
affected side, possible lucency in soft tissues of the neck and axilla.
– One-way valve physiology allows air to enter the chest cavity but not escape. The
increasing pressure pushes the trachea and mediastinal structures to the contralateral side.
– Treatment requires emergent needle decompression at the second intercostal space, mid-
axillary line. Do not wait for CXR in an unstable patient.
• Widened mediastinum
– Findings: Mediastinum wider than 8 cm on a standard PA film. Note: a diseased
mediastinum may appear <8 cm due to lung hyperinflation or radiological artifact.
Alternatively, the supine position can produce an engorged SVC that may mimic a
widened mediastinum (if possible, attain an upright CXR to minimize this artifact).
– The differential diagnosis includes: Aortic aneurysm, lymphadenopathy, traumatic aortic
dissection, mediastinal mass. Mediastinal masses can be further divided into superior
(thyroid cancer, lymphoma, teratoma), anterior (thymoma, lymphoma), middle
(carcinoma, lymphoma, esophageal rupture, mediastinal fluid, cardiac tamponade), and
posterior (esophageal cancer, neurogenic tumors, vertebral trauma) locations.
• Lung carcinoma
– Findings: Pulmonary nodule, spiculated mass, multiple masses.
– Multiple masses in lungs suggest metastases or septic pulmonary emboli, especially in
conjunction with cavitation.
– Assess the mediastinum for contour and hilar enlargement.
• Heart failure
– Findings: Pulmonary edema, enlarged pulmonary vasculature, cephalization of blood flow,
increased interstitial markings, enlargement of cardiac silhouette, pulmonary vascular
enlargement, loss of contour of cardiophrenic angle.
• Pulmonary edema
– Findings: Kerley B lines (∼2 cm lines perpendicular to the chest wall), interstitial edema,
cardiomegaly, basilar involvement (gravity causes the lower regions of the lung to receive
higher blood flow), distended SVC.
– It is difficult to distinguish between cardiogenic (hydrostatic) and non-cardiogenic
(permeability) pulmonary edema on CXR.
– Findings: Extensive bilateral opacities and air bronchograms.
– Air bronchograms are pathological conditions that result from increased edema in the
surrounding lung tissue making it appear "whiter" than normal. This causes the border
between air and tissue to appear particularly sharp. Normally, there is a relatively small
difference in contrast between the black appearing air in the conducting airways and the
white appearing surrounding lung tissue.
– Difficult to differentiate between pneumonia, edema, and ARDS; especially with diffuse
lung involvement. Pneumonia is usually lobar and unilateral.
– Therapeutic positive pressure ventilation can give the appearance of improvement on CXR
in ARDS and inaccurately suggest that the patient is ready for weaning off the ventilator.
• Abdominal free air
– Findings: Air beneath the right hemidiaphragm is often suggestive of abdominal free air.
This is best observed on an upright CXR.
• Achalasia
– Findings: Air–fluid level in mediastinum. Prominent esophageal stripe can mimic the
appearance of a widened mediastinum.
• Lung calcifications
– Findings: Almost always an indicator of a benign nodule.
– Previously healed granulomatous disease (histoplasmosis, treated infection, or tumor).
• Aspiration pneumonitis
– Findings: Initially, the CXR appears normal. Hours later a change in density, usually in the
right lower lobe, appears.
• Negative pressure pulmonary edema
– Findings: Extensive bilateral opacities suggesting alveolar fluid.
• Foreign body
– Trachea findings: If a ball valve mechanism is present, will see hyperinflation. If simple
obstruction is present, will see alveolar collapse.
– Esophageal findings: Difficult to see with PA or AP view. Lateral view may provide
additional information.
• Preoperative CXR
– The American Society of Anesthesiologists Task Force recommendations state that chest
radiograph abnormalities may be higher in smokers, patients with recent upper
respiratory infection, COPD, and cardiac disease. However, they assert that extremes in
age, smoking, stable COPD, stable cardiac disease, or resolved recent upper respiratory
infection do not necessarily constitute an indication for CXR (4).
– If a CXR finding is believed to change the management of the anesthetic, it may be
considered.
– Pacemaker or ICD type and presence can be assessed and confirmed. Also, confirm the
absence of a pneumothorax, check the position of the leads to ensure that they are in the
cardiac silhouette (right atrium, right ventricle), and look for fluid collection around the
device.
– Lines and tubes. Follow each line and tube in its entirety. It may be necessary to order
additional radiological studies if the line or tube disappears from the borders of the CXR.
Assess for pneumothorax and hemothorax.
• Intraoperative
– Line and tube placement, acute pulmonary changes.
– Retained surgical instruments: Order radiological study to cover areas of open or
previously open cavities.
• Postoperative CXR
– Line and tube placement, pulmonary status, endotracheal tube (2 cm above carina).
– Atelectasis: Volume loss, with shifting of the mediastinum and bronchus towards the area
of collapse. Changes are often subtle and difficult to appreciate.
Chest radiographs use a relatively low amount of radiation, but the benefits of the study must
be weighed against the risks of ionizing radiation to the embryo or fetus.
REFERENCES
1. Gibbs JM, Chandrasekhar CA, Ferguson EC, et al. Lines and stripes: Where did they go?—
From conventional radiography to CT. Radiographics. 2007;27(1):33–38.
2. Beres RA, Goodman LR. Pneumothorax: Detection with upright versus decubitus
radiography. Radiology. 1993;186:19–22.
3. Lim EHL, Liu EHC. Preoperative chest X-rays and ECGs: A prospective audit. Singapore
Med J. 2003;44(7):340–343.
4. Practice Advisory for Preanesthesia Evaluation. A report by the American Society of
Anesthesiologists Task Force on preanesthesia evaluation. Anesthesiology. 2002;96:485–
496.
ADDITIONAL READING
• Ouelette H, Tetreault.: Clinical Radiology Made Ridiculously Simple (2008).
• Pneumothorax
• Aspiration
CLINICAL PEARLS
• The tip of the central line should ideally sit at the junction of the SVC and right atrium.
• Lateral decubitus films can help the physician determine if there is layering of pleural fluid
versus a loculated infusion.
• Mucous plugging can occur in ventilated patients and appears as a hyperlucency or
complete collapse on the affected side. In experienced clinicians often perceive the normal
side that has a relatively whiter appearance to be diseased.
• Confirmation of pyloric or postpyloric tube for enteral nutrition; make sure the tube is
below the diaphragm and do not confuse nasal or oral gastric tube with a feeding tube.
CHLORIDE
Amy Barulic, BS, MHS
BASICS
DESCRIPTION
• Chloride ions (Cl−) are formed when elemental chlorine accumulates one electron. Chloride
can also be found in compound form by covalent bonds.
• Cl− is an abundant anion found in the intracellular and extracellular compartments. It
functions primarily in the roles of metabolism, acid–base balance, and maintenance of
electroneutrality. Normal blood reference range of chloride for most adults is 95–105
mEq/L.
• Medications and anesthetics (diuretics, gastrointestinal drugs, propofol, etomidate, and
benzodiazepines) that influence Cl− levels are of perioperative concern and relevance.
• Cerebrospinal fluid (CSF). Secretion of fluid into the ventricles by the choroid plexus
depends on active transport of sodium ions (Na+) through the epithelial cells that line the
outside of the plexus. Sodium ions “carry” large amounts of Cl− to maintain
electroneutrality. The two ions, when combined, increase the quantity of osmotically active
ions in the CSF, which in turn causes osmosis of water through the membrane. Less
important transport processes move small amounts of glucose into the CSF while moving
both potassium and bicarbonate ions out, and into the capillaries, thus concentrating Cl−
(the [Cl−] is ∼15% greater in the CSF as compared to the plasma).
• Neuronal resting membrane potential. Cl− is maintained in high concentration in the
extracellular fluid compared to the intracellular environment of the neuron (via the
semipermeable bilayer lipid membrane in combination with active transport processes). The
Cl− gradient (107 mEq/L extracellularly and 8 mEq/L intracellularly) yields a Nernst
potential of –70 mV inside the neuron that is only slightly more negative than the actual
measured value of –65 mV (major contributor).
• GABA (gamma-aminobutyric acid). Functions as a chief inhibitory neurotransmitter in the
CNS to regulate neuronal excitability. GABA receptors are ligand-activated, chloride
channels and bind GABA neurotransmitter and several other drugs (hypnotics,
benzodiazepines, etc.). When an agonist binds, Cl- channels open and ions flow down their
concentration gradient and enter the cell; this results in hyperpolarization (cell becomes
more negative). By further decreasing the membrane resting potential, the ability for an
action potential to be reached is also decreased.
• Stomach. The tubular, oxyntic glands are composed of parietal cells and are located on the
inside surfaces of the body and fundus of the stomach. When stimulated, parietal cells
secrete an acidic solution (at their villus-like projections) that contains 160 mmol/L of HCl,
which is nearly isotonic to body fluid but has a pH of ∼0.8. The rate of formation and
secretion of HCl by the parietal cells is directly related to the amount of histamine secreted
by the enterochromaffin-like cells (ECL cells) that lie in the deep recesses of the oxyntic
glands.
• Kidneys
– Following glomerular filtration, the filtrate enters the proximal convoluted tubule (PCT) of
the nephron. The epithelial cells in the first half of the PCT are highly permeable to most
ions and are responsible for ∼70% of Na+ (via a Na+/K+ ATPase antiporter), as well as
significant water, urea, organic acid, H+, HCO3−, Cl−, and phosphate reabsorption. When
Na+ is reabsorbed, negative ions “follow” to maintain electroneutrality; they passively
diffuse through paracellular pathways and are also reabsorbed via secondary active
transport with Na+ across the luminal membrane.
– The lumen of the nephron in the second half of the PCT has a relatively high
concentration of chloride (∼140 mEq/L) as compared to the early proximal tubule (∼105
mEq/L). This higher concentration favors diffusion of ions through intercellular junctions
and into the renal interstitial fluid.
– As the PCT enters the hyperosmotic medulla, it becomes narrower and eventually forms
the Loop of Henle. Electrolytes are actively transported out of the lumen to create a
concentration gradient in the renal medulla; consequently, the epithelial cells have a high
metabolic rate. Approximately 25% of the filtered load of Cl− is reabsorbed here
• Blood/plasma. Carbonic acid (H2CO3), formed in red blood cells (RBCs), dissociates with
hydrogen (H+) and bicarbonate ions (HCO3−).
– The H+ remains within the RBC and reversibly binds to hemoglobin (Hg) thus, the Hg
molecule functions as an acid–base buffer.
– The HCO3− diffuses out of the RBC and into the plasma, while Cl− diffuses into the cells
to maintain electroneutrality; this occurs via the bicarbonate–chloride carrier protein that
is embedded in the membrane.
– As a consequence, the chloride content of venous RBCs is greater than that of arterial red
cells. This is referred to as “chloride shifting.”
• Sweat secretions. The secretory portion of the sweat gland secretes a fluid called the primary
secretion or precursor secretion; the concentration of the ion constituents is then modified
as the fluid flows through the duct.
– The precursor secretion composition is similar to that of plasma (minus the plasma
proteins), with a Cl− concentration of ∼104 mEq/L.
– As this precursor solution flows through the duct portion of the gland, it is modified by
reabsorption of most of the sodium and Cl−
– The autonomic nervous system, and hence, the rate of sweating, determines the tonicity of
the sweat. A slight stimulation can result in a near complete reabsorption of sodium and
chloride with a resultant concentration as low as 5 mEq/L (hypotonic sweat).
Alternatively, a strong sympathetic stimulation aims to preserve water, and results in a
hypertonic sweat (∼50–60 mEq/L).
• Hyperchloremia is defined as an elevated Cl− plasma concentration (>107–110 mEq/L) and
can result from diarrhea, renal disease, hyperchloremic fluid administration, and as a side
effect of medications. It can result in impaired blood sugar control in diabetics, muscle
weakness, deep and rapid breathing, a nongap metabolic acidosis, and possibly coma.
• Hypochloremia is defined as a low Cl− plasma concentration (<95 mEq/L). It is commonly
seen with hypokalemia from gastrointestinal losses (vomiting, diarrhea, nasogastric
suctioning); potassium binds with chloride (KCl). Hypochloremia may result in muscle
hypertonicity/tetany, shallow and depressed breathing, and metabolic alkalosis.
• Cystic fibrosis (CF) is an autosomal-recessive disease caused by a mutation in the CFTR gene
that impairs Cl− transport and has multiple organ system involvement.
– The primary source of morbidity and mortality is due to the progressive nature of
obstructive pulmonary disease characterized by chronic inflammation, infection, and
destruction of airways.
• Bartter’s syndrome is characterized by the defective transport of Cl− in the thick ascending
Loop of Henle, resulting in salt wasting, metabolic alkalosis, and hypokalemia. It is a rare
genetic condition.
• Iatrogenic fluid administration. The infusion of large amounts of saline-based solutions can
result in hyperchloremia. Normal saline has a [Cl−] of 154 mEq/L; additionally, albumin
and hydroxyethyl starch solutions (Hetastarch) are prepared in a normal saline solution. A
hyperchloremic, nongap, metabolic acidosis can result, initially from dilution of HCO3-.
Ultimately, however, HCO3- anion is eliminated by the kidneys in order to maintain
electroneutrality (increased chloride anion load). Clinical consequences of the metabolic
acidosis are unclear. However, attempts at correcting the abnormality may actually cause
more issues (iatrogenic causes such as administering additional hyperchloremic
crystalloids).
• Mannitol has been shown to reduce the viscosity of mucus in patients with CF and is
currently being examined for the treatment of CF and bronchiectasis. When inhaled as a dry
powder orally, it osmotically draws water into the lungs and thins the mucus. This may also
facilitate coughing as an expectorant during physiotherapy.
• Loop diuretics (furosemide, bumetanide, torsemide) are competitive antagonists at the Cl−
binding site on the luminal surface of the PCT. This results in impaired Na+ reabsorption
and increased urine output (natriuresis). Additionally, the hyperosmotic medulla created by
the countercurrent exchange is hindered.
• Thiazide diuretics (hydrochlorothiazide) are secreted into the PCT from the bloodstream and
selectively inhibit Na+–K+−Cl− transporters in the distal convoluted tubule. This results in
impaired Na+ and Cl− reabsorption and increased urine output (natriuresis).
• Antacids are orally ingested, inorganic salts that release anions on dissolving in acidic
gastric secretions. The anions combine and neutralize hydrochloric acid immediately; they
do not affect gastric pH.
• H2 antagonists are competitive, as well as inverse, antagonists at H2 receptors of gastric
parietal cells. Consequently, they decrease baseline parietal cell acid and volume secretion
as well as blunt the response to normal stimuli, which subsequently inactivates pepsin and
stimulates gastrin release.
• Propofol, etomidate, and benzodiazepines potentiate GABA receptor binding by attaching to
the beta subunit of the GABAA receptor; thus it facilitates an inhibitory response by
hyperpolarizing the cell membrane.
EQUATIONS
Plasma anion gap (mEq/L) = [Na+] – ([HCO3−] + [Cl−])
REFERENCES
1. Base EM, Standl T, Lassnigg A, et al. Efficacy and safety of hydroxyethyl starch 6% 130/0.4
in a balanced electrolyte solution (volulyte) during cardiac surgery. J Cardiothorac Vasc
Anesth. 2011; 25(3):407–414.
2. onhomme V, Demoitie J, Schaub I, et al. Acid–base status and hemodynamic stability
during propofol and sevoflurane-based anesthesia in patients undergoing uncomplicated
intracranial surgery. J Neurosurg Anesthesiol. 2009;21(2):112–119.
3. arcia J, Roure P, Hayem C, et al. Bronchial endoscopy under local anesthesia and pain in
children. The value of a nitrous oxide-oxygen combination. Rev Mal Respir.
1998;15(2):179–183.
4. Kim JY, Lee D, Lee KC, et al. Stewart’s physiochemical approach in neurosurgical patients
with hyperchloremic metabolic acidosis during propofol anesthesia. J Neurosurg
Anesthesiol. 2008;20(1):1–7.
5. Scheingraber S, Rehm M, Sehmisch C, et al. Rapid saline infusion produces hyperchloremic
acidosis in patients undergoing gynecologic surgery. Anesthesiology. 1999;90(5):1265–
1270.
6. Shangraw RE, Winter R, Hromco J, et al. Amelioration of lactic acidosis with
dichloroacetate during liver transplantation in humans. Anesthesiology. 1994;81(5):1127–
1138.
7. Wheeler DW, Thompson AJ, Corletto F, et al. Anaesthetic impairment of immune function
is mediated via GABA(A) receptors. PLoS One. 2011;6(2):317152.
8. ordsworth AE, McDonald A, Lacy D, et al. Bronchial lavage in cystic fibrosis patients
during general anaesthesia for elective surgery. Tenth Annual North American Cystic
Fibrosis Conference. 1996;362:309.
• Cystic fibrosis
• Aspiration
• Hyperchloremic nongap metabolic acidosis
• Propofol infusion syndrome
CLINICAL PEARLS
• Large infusions of anesthetics such as propofol and isoflurane can result in metabolic
acidosis.
• Large administration of saline during intraoperative care can result in a nongap,
hyperchloremic, metabolic acidosis.
CHOLECYSTECTOMY
Sulin G. Yao, MD
Calvin Lyons, MD
BASICS
DESCRIPTION
General
• Surgical removal of the gallbladder, open or laparoscopic, for treatment of symptomatic
cholelithiasis (stones in the biliary tract resulting in mechanical obstruction), cholecystitis
(inflammation of gallbladder secondary to obstruction of cystic duct), or gallbladder cancer.
• Open cholecystectomy
– Resection from the liver and isolation of the cystic duct and artery are performed.
– Chosen for patients with significant inflammation, intraabdominal adhesions,
coagulopathies, known gallbladder cancer, or the inability to tolerate laparoscopic
procedures.
– Laparoscopic approach may be converted to an open approach if technically difficult.
• Laparoscopic cholecystectomy
– Four trochars are inserted to pass instruments; one in the umbilicus and three in the right
upper quadrant (RUQ).
– A pneumoperitoneum is created to aid with visualization; insufflation is done with carbon
dioxide (CO2) at pressures of 10–15 mm Hg.
– Following resection from the liver and isolation of the cystic duct and artery, the
gallbladder is detached via cauterization, clipping, or stapling.
– The gallbladder is placed in a bag and removed through the trocar site in the abdominal
wall.
• Cholangiograms (injection of contrast dye via a catheter in the cystic duct) can be
performed intraoperatively to detect gallstones in the cystic duct (choledocholithiasis). An
absence of spread/filling on radiography indicates that a stone is present. Some surgeons
use ultrasound in place of cholangiograms.
• Common bile duct exploration is performed via a small incision (choledochotomy). A
fiberoptic scope (choledoscope) is passed through the incision to aid in visualization.
Position
Supine; reverse Trendelenburg with right side up to displace bowel (laparoscopic and open
procedures)
Incision
• Laparoscopy: 5–7 mm incisions for the insertion of trocars. Supraumbilical, epigastric,
midclavicular, and anterior axillary ports are most frequently placed.
• Open: Right subcostal approach or upper midline (less common) 5–7 inches.
Approximate Time
20–60 minutes; intraoperative cholangiogram may add 10–20 minutes.
EBL Expected
• Open cholecystectomy: <250 mL
• Laparoscopic: Minimal EBL
Hospital Stay
• Some ambulatory centers discharge the same day after careful observation.
• Complicated cases may require 1 day hospitalization or longer.
• Laparoscopic equipment
• Possible fluoroscopy for cholangiogram
EPIDEMIOLOGY
Prevalence
• In the US, ~500,000 cholecystectomies are performed each year.
• 10% of the US adult population has cholelithiasis; 20% over the age of 40 years, and 30%
over the age of 70 years. (1)[A].
• Urgent laparoscopic conversion rate: <15%
• Elective laparoscopic conversion rate: <5%
Prevalence
• Mostly adults, increases with age
• Female to male ratio 4:1 during reproductive years; ratio narrows as age increases (1)[A].
• Risk factors: Obesity, diabetes mellitus, estrogen, pregnancy, hemolytic diseases, and
cirrhosis.
• “Fat, Female, Fertile, Forty” is a pneumonic used to describe patients prone to cholelithiasis.
Morbidity
• Hemorrhage, bile leak, perforation of gallbladder, common bile duct injury, retained bile
duct stones.
• Open cholecystectomy morbidity rate is 3.3 times more than that for laparoscopic
cholecystectomy (2)[A]. This may be a function of the selection criteria of patients needing
an open procedure.
Mortality
• Standardized mortality ratio (SMR) within 90 days for open cholecystectomy is 3.89.
• SMR within 90 days for laparoscopic cholecystectomy is 0.73 (2)[A].
• Assess for the possibility of a “full stomach.”
• Determine volume status and rule out electrolyte abnormalities. Increased abdominal
pressure from insufflation and reverse Trendelenburg can cause hemodynamic compromise.
• Evaluate respiratory function: Open cholecystectomy will have post-op splinting and
impaired respiratory function due to incision; consider epidural for post-op pain
management.
• Cirrhotics require careful assessment and optimization of their disease prior to surgical
intervention.
SYMPTOMS
• Epigastric/RUQ pain, nausea, vomiting
• Toxicity: Fever and diaphoresis
History
• Duration of symptoms
• Oral intake, quantity and quality of urine
• Last menstrual cycle in women of child-bearing age
Signs/Physical Exam
• Tachycardia, hypotension, and jaundice
• Guarding or rebound with acute cholecystitis; otherwise, normal abdominal exam with mild
tenderness.
• Fluid status: Capillary refill, mucus membranes, urine output, lethargy, and orthostatic BPs.
MEDICATIONS
Gastric medication
Labs/Studies
• White count to rule out infection
• Cirrhotic patients: Consider coagulation profile, albumin, and hemoglobin.
• Abdominal ultrasound is the test of choice for diagnosis of cholelithiasis: 90–95% sensitive
(1)[A].
• Diabetes mellitus, ileal disease, hemolytic disorders, choledocholithiasis, cholangitis, or
active pancreatitis.
• Cirrhotics have an increased incidence of biliary tract disease.
• Pregnancy is usually delayed until delivery of fetus unless acute cholecystitis presents.
TREATMENT
Premedications
• Patients at risk for gastric aspiration: Give H2 blockers, antacids, promotility, or proton
pump inhibitors.
• Nasogastric tube may be considered.
• Fluid resuscitation as appropriate prior to induction.
• Transfusion of fresh frozen plasma or other blood products as appropriate in cirrhotics.
• If pain medication needed, meperidine may cause less Sphincter of Oddi spasm than other
opiates.
• Surgeons consent for the potential to convert to an open procedure.
• Open procedures may benefit from an epidural for postoperative pain management.
• Indicated for acute cholecystitis and/or cholangitis; should cover gram-negative aerobes
(Escherichia coli, Klebsiella) as well as anaerobes (Bacteroides species)
• Third-generation cephalosporins (ceftriaxone) with good anaerobic coverage or a second-
generation cephalosporin (cefuroxime or cefotetan) combined with metronidazole is a
typical regimen.
• Cephalosporin allergy: Aminoglycoside and metronidazole.
INTRAOPERATIVE CARE
• Laparoscopic technique: General endotracheal anesthesia with a cuffed tube allows for
positive pressure ventilation, muscle relaxation, protection against aspiration, and
minimizes hypercarbia from absorbed CO2. These same requirements preclude the use of
laryngeal mask airway (LMA); GETA can also generate greater positive pressure (reduced
compliance requires higher peak inspiratory pressures) that LMA use cannot. As a sole
anesthetic technique, an epidural/spinal is not ideal because it requires a high block/level.
If performed, consider supplementing with nitrous oxide and keeping insufflation pressures
<10 mm Hg.
• Open technique: Epidural anesthesia may be utilized for open procedures in conjunction
with GETA.
Monitors
• Invasive hemodynamic monitoring may be needed for ASAIII–IV patients.
• Foley catheter is a surgical preference.
Rapid sequence induction if not NPO; also consider other risks for aspiration (nausea,
vomiting, narcotic use, gastroesophageal reflux).
Maintenance
• Orogastric/nasogastric tube placement allows for suctioning of gastric and biliary juices and
decompressing the stomach to facilitate laparoscopic visualization.
• Balanced anesthetic with volatile or total intravenous anesthetic.
• Muscle relaxation facilitates resection for laparoscopic and open procedures.
• Vagal episodes can occur when a pneumoperitoneum is instituted; it typically resolves
immediately with desufflation.
• Opioids may cause Sphincter of Oddi spasm; theoretically, meperidine has a reduced
incidence.
• Reverse Trendelenburg affects the cardiopulmonary system
– Cardiac: Preload to the right atrium is reduced due to gravity; this effect can be
exacerbated in patients who are volume depleted.
– Pulmonary: Parameters are usually improved due to increased compliance and functional
residual capacity.
• Laparoscopic-induced pneumoperitoneum in the reverse Trendelenburg position affects the
cardiopulmonary systems:
– Cardiac: Preload to the right atrium is further decreased; pneumoperitoneum pressures are
often equal to or greater than right atrial filling pressures.
– Pulmonary: Reverse Trendelenburg position initially improves pulmonary mechanics, but
pneumoperitoneum reduces pulmonary compliance and functional residual capacity; may
need to adjust ventilator settings. Use of CO2 for insufflation can increase PaCO2 unless
the tidal volume or respiratory rate is increased.
• Give prophylactic antiemetics prior to extubation.
• Bile is an emetic and caustic; suction the gastric tube prior to extubation.
• Patient should be awake and capable of protecting their airway.
FOLLOW-UP
BED ACUITY
Pulmonary dysfunction may be greater with patients undergoing open procedures.
ANALGESIA
• Reduced pain with laparoscopic procedure.
• Shoulder pain may be more effectively treated with ketorolac.
• Epidural catheters may be considered in open procedures; however, the open technique is
often performed in cirrhotics, thus, need to confirm coagulation profile prior to placement.
COMPLICATIONS
• Pancreatitis, bowel injury, bile duct injury, or bile leak, pneumothorax, atelectasis.
• Shoulder pain with laparoscopic procedures, due to C3,4,5 irritation
• Hemorrhage
• Postcholecystectomy syndrome: Continued pain after cholecystectomy.
PROGNOSIS
• 15.2% postcholecystectomy patients continue with postoperative abdominal pain.
• 5.6% with continued vomiting.
• 40.2% with gas/flatulence (3)[A].
REFERENCES
1. chirmer BD, Winters KL, Edlich RF. Cholelithiasis and cholecystitis. J Long Term Eff Med
Implants. 2005;15(3):329–338.
2. Zacks SL, Sandler RS, Rutledge R, et al. A population-based cohort study comparing
laparoscopic cholecystectomy and open cholecystectomy. Am J Gastroenterol.
2002;97(2):334–340.
3. Weinert CR, Arnett D, Jacobs D Jr, et al. Relationship between persistence of abdominal
symptoms and successful outcome after cholecystectomy. Arch Intern Med.
2000;160(7):989–995.
4. Di Sebastiano N, Bonetti L, Boninsegni P, et al. Respiratory mechanics and gas exchange in
anesthesia for laparoscopic cholecystectomy. Minerva Anesthesiol. 1993;59(10):487–492.
5. Girardis M, DaBroi U, Antonutto G, et al. The effect of laparoscopic cholecystectomy on
cardiovascular function and pulmonary gas exchange. Anesthes Analges. 1996;83(1):134–
140.
6. Suh MK, Seong KW, Jung SH, et al. The effect of pneumoperitoneum and Trendelenburg
position on respiratory mechanics during pelviscopic surgery. Korean J Anesthesiol.
2010;59(5):329–334.
ADDITIONAL READING
• Rist M, Hemmerling TM, Rauh R, et al. Influence of pneumoperitoneum and patient
positioning on preload and splanchnic blood volume in laparoscopic surgery of the lower
abdomen. J Clin Anesth. 2001;13(4):244–249.
• Laparoscopy
• Cirrhosis
CLINICAL PEARLS
• Laparoscopic cholecystectomy is the preferred technique for gallbladder removal. Benefits
include small incision, and reduced instances of postoperative pain, incisional hernias,
wound infections, respiratory compromise, and quicker discharge to home due to quicker
return of ambulation.
• Consider possible laparoscopic-related effects on IVF status, gastric regurgitation, increased
airway resistance, possible venous embolism, and expect an increase in ETCO2.
• Significant ETCO2 increase may be due to subcutaneous emphysema; it is rapidly absorbed
but problematic for pulmonary-compromised patients who are already extubated.
CHRONIC ANGINA
BASICS
DESCRIPTION
• Stable angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder,
back, or arms, typically elicited by exertion or emotional stress and relieved by rest or
nitroglycerin.
• Chronic angina
– Does not increase in frequency or severity, and is predictable in nature.
– May be associated with ST segment depression on ECG.
– May occur in patients with seemingly normal coronary arteries subjected to acute or
chronic increases in myocardial work.
• Coronary artery spasm can provoke pain in the absence of increased myocardial demands
such as variant (Prinzmetal’s) angina and some cases of stable or unstable angina.
Incidence
• New and recurrent coronary attack in the US: 1,255,000/year
• Approximately 34% of people, who experience a coronary attack in a given year, die from it.
Prevalence
• 17.6 million people in the US have coronary heart disease (CHD; of which 10.2 million
persons have angina pectoris, and 8.5 million have experienced a myocardial infarction
(MI).
• The estimated age-adjusted prevalence of angina in women age 20 years and older was 4.5%
for non-Hispanic white women, 5.4% for non-Hispanic black women, and 4.8% for Mexican-
American women. Rates for men in these three groups were 4.7%, 4.0%, and 2.9%,
respectively.
Morbidity
• New cases of stable angina: ∼500,000 new cases/year (Framingham Heart Study, National
Heart, Lung, and Blood Institute).
• About 10% of patients/year with stable angina will develop worsening symptoms that
require revascularization.
Mortality
• In the US in 2006 there were 425,425 deaths from coronary artery disease (CAD) (about 1
of every 6 deaths) and overall death rate from cardiovascular disease was 262.5 per
100,000 persons.
• The death rate is as follows:
– Greater in men (3 times higher at ages 25–34 years and, falling to 1.6 times at ages 75–84
years).
– Greater in blacks compared to whites, an excess that disappears by age 75. Among the
Hispanic population, coronary mortality is not as high as it is among blacks and whites.
• A perioperative MI has been associated with a 30–50% perioperative mortality and reduced
long-term survival.
• The most frequent causes of angina are as follows: coronary atherosclerosis, coronary artery
vasospasm, fibrosis, embolism, dissection, and arteritis.
• Nonmodifiable risk factors: Age, family history, and male gender.
• Modifiable risk factors: Cigarette smoking, hypertension, dyslipidemia, diabetes, chronic
kidney disease, obesity, and physical inactivity.
• Myocardial ischemia is caused by an imbalance between myocardial oxygen supply and
myocardial oxygen consumption.
• Myocardial oxygen supply is determined by arterial oxygen saturation and coronary flow
that is dependent on the luminal cross-sectional area of the coronary artery and coronary
arteriolar tone. Atherosclerotic plaques may dramatically decrease both the cross-sectional
area and coronary artery tone. When combined with increased oxygen demand from
tachycardia, increased myocardial contractility and wall stress, the oxygen supply may
become inadequate.
• Ischemia reduces the formation of adenosine triphosphate (ATP), an oxygen-dependent
process. This results in the development of lactic acidosis, loss of the normal Na+/K+
ATPase pump, impaired myocardial membrane integrity, and release of chemical substances
that stimulate chemosensitive and mechanoreceptive receptors within cardiac muscle fibers
and around the coronary vessel.
• The primary mediator of angina is adenosine, via stimulation of the A1 adenosine receptor.
• Preoperative assessment should assess current myocardial function and if there is
myocardium at risk for ischemia; a relevant clinical history may warrant further testing (1).
• Ensure an adequate myocardial oxygen supply: Assess hemoglobin, diastolic perfusion
pressure, oxygen saturation, and adequate diastolic time (low heart rate; HR).
• Avoid increases in myocardial oxygen demand: Assess HR, myocardial contractility,
afterload, and preload.
• Characterized as a discomfort rather than pain, and may be difficult to describe.
• Location is most commonly felt beneath the sternum, but can vary. Radiation may occur to
the left shoulder and down the inside of the left arm, even to the fingers; straight through to
the back; into the throat, jaws, and teeth; and, occasionally, down the inside of the right
arm. It may also be felt in the upper abdomen.
• Onset and offset is typically gradual; the intensity of the discomfort increases and decreases
over several minutes.
• Provoking factors: Physical activity, cold, emotional stress, sexual intercourse, meals, or
lying down (which results in an increase in venous return and increase in wall stress).
• Duration: Generally lasts for 2–5 minutes unless the patient is experiencing an acute
coronary syndrome, especially MI.
• Relief: Symptoms usually subside with rest.
• Associated symptoms include shortness of breath, belching, nausea, indigestion, diaphoresis,
dizziness, lightheadedness, clamminess, and fatigue.
• Information about the character and location of discomfort, radiation, associated symptoms,
and precipitating, exacerbating, or alleviating factors.
• A complete inventory of comorbid conditions, including cardiac risk factors and family
history.
• Tachycardia due to reflex sympathetic nervous system activation and in response to
discomfort.
• Elevated BP
• Heart sounds: The 2nd heart sound may become paradoxical because left ventricular (LV)
ejection is more prolonged during an ischemic attack; a 4th heart sound is common, and a
3rd heart sound may develop.
• Murmurs: A mid- or late-systolic apical murmur (shrill or blowing but not especially loud)
may occur if ischemia causes localized papillary muscle dysfunction, producing mitral
regurgitation.
• Precordial pulsation: Palpation of the chest wall may reveal abnormal pulsations that
correlate with transient dysfunction.
TREATMENT HISTORY
• Coronary angiography
• Revascularization
• Percutaneous coronary intervention (PCI)
• Coronary artery bypass grafting (CABG)
• Implanted pacemakers and defibrillation devices
MEDICATIONS
• Antianginal therapy
– Nitrates: Anti-ischemic efficacy pertains to their ability to decrease myocardial oxygen
demand as a result of systemic vasodilatation rather than as a coronary vasodilator.
– Beta-blockers: Relieve anginal symptoms by reducing both HR and contractility.
– Calcium channel blockers: Improve anginal symptomatology by coronary and peripheral
vasodilatation and by reducing contractility.
• Additional treatment
– ACE inhibitors: Recommended for patients with stable angina pectoris and coexisting
hypertension, diabetes, heart failure, asymptomatic LV dysfunction, or post-MI.
– Angiotensin receptor blockers (ARBs): Recommended for patients who have hypertension,
heart failure; indications for, but an inability to tolerate ACE inhibitors; or have had an MI
with LV ejection fraction ≤40%.
– Statins
• Antiplatelet drugs
– Aspirin: The optimal antithrombotic dosage of aspirin appears to be 75–162 mg/day.
– Clopidogrel: An alternative for patients who are allergic to aspirin.
• Laboratory tests: CBC, hemoglobin, Cr, fasting glucose, markers of myocardial damage if
evaluation suggests clinical instability.
• Resting 12-lead ECG (normal in ∼50% of patients with chronic stable angina):
– In patients with at least 1 clinical risk factor, who are undergoing vascular surgical
procedures.
– In patients with known CHD, peripheral arterial disease, or cerebrovascular disease who
are undergoing intermediate-risk surgical procedures.
• Exercise and stress tests are performed when there is suspicion that the myocardium is at
risk for ischemia.
• Dobutamine stress ECG or stress cardiac imaging (intravenous dipyridamole/adenosine
myocardial perfusion imaging with both thallium-201 and technetium-99m) in patients who
cannot exercise.
• Arrhythmias
• ST segment changes on ECG
• Symptoms of worsened, or decompensated heart failure
• Symptoms of increased activation of the adrenergic system: Elevated BP and increased HR
• Supraventricular or ventricular arrhythmias with hemodynamic instability
CLASSIFICATIONS
• Canadian Cardiovascular Society Angina Classification
– Class 0: Asymptomatic
– Class 1: Angina with strenuous exercise
– Class 2: Angina with moderate exertion
– Class 3: Angina with mild exertion
Walking 1–2 level blocks at normal pace
Climbing 1 flight of stairs at normal pace
– Class 4: Angina at any level of physical exertion
TREATMENT
Premedications
Anxiolytics may be indicated to decrease anxiety and the associated increase in cardiac
oxygen demand (tachycardia, hypertension).
• All inhaled volatile anesthetic agents have some cardiovascular effects, including depression
of myocardial contractility and afterload reduction.
• Neuraxial anesthetic techniques can cause sympathetic blockade, resulting in decreases in
both preload and afterload.
Monitors
• ECG analysis of the ST segment in multiple leads (i.e., II, V4, and/or V5)
• Arterial line may be considered
• Transesophageal echocardiography (TEE) may be considered
During induction, laryngoscopy, and intubation, maintain hemodynamic stability: Avoid
excessive tachycardia, hypertension, hypotension, and drug-induced depression of cardiac
function.
Maintenance
• Maintenance of anesthesia techniques should target avoidance of cardiac ischemia
perioperatively (caused by increased cardiac oxygen demand or decreased oxygen supply).
• Intraoperative ischemia management
– Increased oxygen demand
Increased HR: Beta-blockers and analgesics
Increased BP: Deepen anesthetic, analgesics, and antihypertensives
Increased pulmonary capillary wedge pressure (PCWP): Nitroglycerin and diuretics
– Decreased oxygen supply
Decreased HR: Atropine and pacing
Increased HR: Beta-blockers and analgesics
Decreased BP: Decrease anesthetic depth and vasoconstrictors
Decreased PCWP: Volume and inotropy
Blood transfusion if HCT<30%
– Avoidance of hypothermia
Maintenance of hemodynamic stability and avoidance of factors increasing cardiac oxygen
demand (shivering, vasoconstriction, pain, agitation).
POSTOPERATIVE CARE
BED ACUITY
• Vigilance for chest pain, arrhythmias, and hemodynamic instability
• Normothermia
• Perioperative ischemia and/or MI.
• Patients with symptomatic MI after surgery have a marked increase in the risk of death (40–
70%).
– Postoperative troponin measurement is recommended in patients with ECG changes or
chest pain typical of acute coronary syndrome.
• Perioperative arrhythmias and conduction disorders
REFERENCES
1. Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA2007 guidelines on perioperative
cardiovascular evaluation and care for noncardiac surgery: A report of the American
College of Cardiology/American Heart Association Task Force on Practice. Circulation.
2007;116:e418–e499.
CODES
ICD9
• 411.1 Intermediate coronary syndrome
• 413.1 Prinzmetal angina
• 413.9 Other and unspecified angina pectoris
ICD10
• I20.0 Unstable angina
• I20.1 Angina pectoris with documented spasm
• I20.9 Angina pectoris, unspecified
CLINICAL PEARLS
• Cardiovascular complications represent the most common and troublesome adverse
consequence of noncardiac surgery.
• It is important that the care team responsible for the long-term care of the patient be
provided with complete information about any cardiovascular abnormalities or risk factors
for CAD identified during the perioperative period.
CHRONIC BRONCHITIS
BASICS
• Chronic bronchitis is one of the two types of chronic obstructive pulmonary disease (COPD),
the other being emphysema.
• Defined as a productive cough > 3 months for two consecutive years.
– Additionally, it is characterized by irreversible airway obstruction, chronic airway
irritation, hypersecretion of mucus, and bronchial inflammation.
– Diagnosis and treatment are guided by the Global Initiative for Chronic Obstructive Lung
Disease (GOLD) (1).
– Varying degrees of emphysematous disease are commonly present.
• Postoperatively, patients with chronic bronchitis have an increased risk of bronchospasm,
laryngospasm, atelectasis, wheezing, difficulty clearing mucous, and prolonged intubation.
Additionally, preoperative pulmonary function tests (PFTs) do not reliably predict
postoperative outcome.
• In the ambulatory surgery setting, home discharge may be challenging and patients should
be carefully selected and screened.
• In the US: 10–12 million
• Women are twice as likely as men to have chronic bronchitis (2).
• Highest prevalence in those >65 years of age
Morbidity
• Treatment costs: $11.7 billion annually
• Hospitalizations costs: $6 billion annually
Mortality
• 4th leading cause of death in the US (2).
• There is an increased risk of death within 5 years, following an episode of respiratory
failure.
• Overall mortality is associated with pack-year smoking history (average number of packs of
cigarettes per day multiplied by total number of years smoking).
• Smoking
• Exacerbations can result from respiratory tract infections.
• Cough and chronic mucus production result from immune responses to inhaled toxic
particles and gases in cigarette smoke. Inflammation in the epithelium of the central
airways and mucous-producing glands result in increased mucous production, reduced
mucociliary clearance, and increased permeability of the airspace epithelial barrier (3).
– Inflammatory cells release serine proteases that are potent secretagogues for mucous.
– Oxidant release from cigarette smoke induces the MUC5AC gene, causing overproduction
of mucin.
• During the early stages of COPD, it is unclear what the effects of mucus hypersecretion are.
However, in the later stages of the disease, changes become apparent:
– Decreases in forced expiratory flow rates due to obstruction.
– Increases in residual volume (RV). Air trapping results in progressive hyperinflation with a
resultant increase in total lung capacity (TLC) and flattening of diaphragms.
– Increases in the residual volume to total lung capacity ratio (RV:TLC).
• Airway reactivity may be the result of smoking-induced inflammation or the airway
narrowing that occurs with chronic disease (4).
• Nonuniform distribution of ventilation causes ventilation/perfusion mismatch and an
increase in dead space, leading to carbon dioxide (CO2) retention. Some areas of the lung
are underventilated in relation to perfusion because of airway obstruction. Air is forced
from these areas to other parts of the lung, causing overventilation relative to perfusion.
• Compensatory mechanisms
– Compensatory responses of the lungs changes their mechanical behavior. It decreases the
tendency for alveoli to collapse and makes atelectasis less likely.
– Erythrocytosis, accompanied by an increase in blood viscosity, results from chronic
hypoxemia.
– Chronic bronchitis “blue bloaters” have hypercarbia with resultant respiratory acidosis,
which is metabolically compensated.
• Cor pulmonale. Chronic alveolar hypoxemia causes pulmonary hypertension that becomes
fixed over time due to changes in the pulmonary arterial vessels. High pressure in the
pulmonary circulation causes right ventricular hypertrophy. Chronic findings can include
right bundle branch block, right heart strain, and right heart failure.
• Assess severity of disease
• Optimize pulmonary function
• Continue maintenance medications
• Treat acute exacerbation
• Avoid perioperative bronchospasm
• Productive cough
• Shortness of breath (SOB)
• Age of onset
• Current smoking status
• Quality of current cough/mucus
– Frequency of exacerbations
– Bronchodilator use
– Steroid use
– ER visits
– Hospitalizations
– Intensive care unit (ICU) admissions
– Intubations
• Wheezing
• Tachypnea
• Prolonged expiration
• JVD
• “Blue bloaters”
• Low baseline room air O2 saturation with worsening on exertion.
TREATMENT HISTORY
Supplemental O2 is indicated when baseline O2 saturation is <88% or <90% when there are
signs of pulmonary hypertension or right heart failure. It is used to maintain PaO2 between
60 and 80 mm Hg and is the only current treatment that reduces mortality.
MEDICATIONS
• Corticosteroids
– Inhalational route has minimal systemic effects and scheduled dosing has been shown to
decrease exacerbations.
– Oral route causes more side effects with little improvement in benefit; may be prescribed
to treat an acute exacerbation or prophylactically in patients with severe disease prior to a
surgical procedure.
• Bronchodilators reduce exacerbations and improve symptoms.
– Anticholinergics (ipratropium bromide)
– Beta-adrenergic agonists (salmeterol, albuterol)
• Theophylline is a methylxanthine used to improve ventilation by relaxing bronchial smooth
muscle. It is a phosphodiesterase inhibitor and adenosine receptor antagonist. Because of
the narrow therapeutic window and adverse cardiac effects, it is used infrequently. High
levels can cause tachycardia, arrhythmias, hypotension, and CNS excitation.
• Antibiotics are useful in treating acute exacerbations triggered by infection; scheduled,
prophylactic antibiotics have not shown benefit.
• Bupropion or nicotine replacement
• Diuretics for cor pulmonale
• Baseline room air O2 saturation
• EKG may show right axis deviation as a result of right ventricular hypertrophy.
• Chest x-ray (CXR) should be performed if infection is suspected. May show hyperinflation,
bullae, blebs, and increased pulmonary vascular markings.
• ABGs (often PaCO2 >45 mm Hg and PaO2 <65 mm Hg)
• Sputum sample (neutrophils, bacteria)
• Pulmonary function (FEV1/FVC <0.7 and not reversible with bronchodilator)

• Cor pulmonale
• Emphysema
• Acute exacerbation as demonstrated by dyspnea, increased O2 requirement, increased
mucous production, fatigue or lethargy, or a PaCO2 increased from baseline (or an acute
respiratory acidosis where metabolic compensation has not yet occurred).
• Pneumonia or upper respiratory infection
• Pulmonary edema
CLASSIFICATIONS
Based on spirometric measurements. Diagnosis requires an FEV1/FVC ratio <0.7. Severity is
gauged by the postbronchodilator FEV1 (1):
• Mild: FEV1 ≥80% predicted
• Moderate: FEV1 50–80% predicted
• Severe: FEV1 30–50% predicted
• Very severe: <30% predicted
TREATMENT
Premedications
• Antibiotics if sputum quality or quantity suggests infection.
• Bronchodilator use for symptom improvement should be continued perioperatively via puffs
or nebulizer.
• Inhaled corticosteroids should be continued.
• Smoking cessation for any length of time is beneficial, but optimally should be initiated 8
weeks before surgery. Abrupt discontinuation may actually increase mucus production.
• Anxiolytics are appropriate if care is taken to avoid hypoventilation and CO2 retention.
These patients are more sensitive to the respiratory depressant effects of sedatives and
opioids.
• Consider regional techniques to avoid airway instrumentation, mechanical ventilation, and
systemic opioid administration.
• A combination of regional and general anesthesia may assist with early ambulation,
decrease in opioid use, and return of respiratory function.
Monitors
• Standard ASA monitors.
• Arterial line placement for frequent ABG draws may be considered. A large gradient may
exist between the arterial and end-tidal CO2 due to an increase in dead space. PaO2
measurements may aid with ventilator settings.
• A slow and controlled induction should be performed to allow for attainment of an adequate
depth of anesthesia and onset of muscle relaxation prior to airway instrumentation.
• Agents
– Propofol does not bronchodilate the airways but blunts the laryngeal response.
– Ketamine can provide bronchodilation; however, its side effect of increasing secretions is
often undesirable.
– Volatile agents may be introduced after IV induction to bronchodilate the airways.
Alternatively, mask induction may be chosen.
– Lidocaine 1–1.5 mg/kg IV or 4% sprayed topically prior to intubation may reduce
intraoperative or postoperative coughing.
• Avoid hyperventilation while bag masking if the patient is a CO2 retainer.
Maintenance
• The patient should be adequately anesthetized to avoid laryngospasm and bronchospasm.
• Nitrous oxide can increase pulmonary artery pressures and is often avoided.
• Ventilation
– Maximize oxygenation to avoid increases in pulmonary hypertension.
– Correct severe hypercapnia without hyperventilating (can result in respiratory alkalosis
due to chronic increase).
– PEEP may prevent airway closure and improve lung compliance.
– I:E ratio should allow sufficient time for expiration and avoid auto-PEEP.
• Mucus can be softened with adequate IV fluid maintenance and warm, humidified
inspiratory gases.
• Suction the endotracheal tube prior to extubation.
• Consider deep extubation when appropriate.
• The use of IV lidocaine prior to extubation may help to suppress airway reflexes.
FOLLOW-UP
BED ACUITY
• Vigilance for bronchospasm
• Supplemental O2 (nasal cannula, face mask) without suppressing hypercarbic drive
• Thoracic and upper abdominal surgeries are associated with atelectasis, hypoxemia, and
slow return to baseline respiratory function. FRC may not return to baseline following these
procedures until 2 weeks postoperatively.
• Pulmonary care
– Chest physiotherapy
– Incentive spirometry
– CPAP
• Acute respiratory failure
• Atelectasis
• Bronchospasm
• Pneumonia
REFERENCES
1. abe KF, Hurd S, Anzueto A, et al. Global strategy for the diagnosis, management, and
prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J
Respir Crit Care Med. 2007;176:532–555.
2. merican Lung Association Epidemiology and Statistics Unit Research and Program Services
Division. Trends in COPD (Chronic Bronchitis and Emphysema): Morbidity and Mortality.
February 2010.
3. MacNee W. Pathogenesis of chronic obstructive pulmonary disease. Proc Am Thorac Soc.
2005;2(4):258–266.
4. Warner DO, Warner MA, Offord KP, et al. Airway obstruction and perioperative
complications in smokers undergoing abdominal surgery. Anesthesiology. 1999;90(2):372–
379.
ADDITIONAL READING
• Blanchette CM, Roberts MH, Peterson H, et al. Economic burden of chronic bronchitis in the
United States: A retrospective case-control study. Int J Chron Obstruct Pulmon Dis.
2011;6:73–81.
• www.aafp.org Management of Chronic Bronchitis
• Cor pulmonale
• Cigarette smoking
CODES
• 491.9 Unspecified chronic bronchitis
• 496 Chronic airway obstruction, not elsewhere classified
ICD10
• J42 Unspecified chronic bronchitis
• J44.9 Chronic obstructive pulmonary disease, unspecified
CLINICAL PEARLS
• Assess the severity of disease in order to plan appropriate preoperative medications and
intraoperative technique, as well as postoperative extubation, level of acuity, and
pulmonary rehabilitation.
• Evaluate for respiratory tract infections by noting fever, mucus quality or quantity greater
than normal, and increase in SOB.
• Baseline O2 saturation and review of home O2 dependence aid in PACU management and
discharge plan.
CHRONOTROPY
Ramana V. Duvvuri, MD
BASICS
DESCRIPTION
• Chronotropy refers to the ability of the heart to change its rate of electrical depolarization,
with corresponding mechanical contraction.
• Positive chronotropy indicates an increase in heart rate
– Generally occurs in response to physiologic stress and is mediated by the autonomic
nervous system.
– Increases cardiac output directly.
– Normal positive chronotropic response decreases in elderly patients.
• Negative chronotropy indicates a decrease in heart rate and can be beneficial in clinical
situations such as myocardial ischemia, Tetralogy of Fallot, hypertrophic cardiomyopathy
and stenotic valves.
• Pacemaker cells exist in different regions of the heart: The sinoatrial (SA) node, the
atrioventricular (AV) node, and the His–Purkinje bundle. Each region has its own intrinsic
rate of action potential firing. Pacemaker cells in the SA node have the highest intrinsic rate
of all regions and thus drive the rest of the conduction system; they are considered to be the
“pacemaker” of the heart (1).
• Spontaneous depolarization. The SA nodal cells have no true resting potential, but instead
generate regular, spontaneous action potentials.
• Intracellular Ca2+ modulation leads to diastolic depolarization in the node. The
depolarization propagates through the rest of the conduction system and leads to systolic
contraction of myocytes (1).
• Rate of spontaneous depolarization. Under the control of sympathetic and parasympathetic
nerve activity as well as circulating catecholamines.
• Muscarinic acetylcholine receptors are densely located in the SA node. When agonized, they
hyperpolarize the SA node cell membranes and decrease the spontaneous phase 4 slope,
resulting in negative chronotropy. They also function to prolong refractoriness and AV
nodal action potential propagation.
– Agonism can result from parasympathetic nervous system activity, such as an increase in
vagal tone.
– Antagonism can result from sympathetic nervous system activity (1).
FIGURE 1. Sympathetic activity results in a hypopolarized (more positive) membrane resting potential and an increased
spontaneous phase 4 slope. Conversely, vagal activity results in a hyperpolarized (more negative) membrane resting
potential and a decreased spontaneous phase 4 slope.
• Beta-receptors are located in the SA node; when agonized, they lead to altered intracellular
Ca2+ release, via a cAMP pathway, resulting in positive chronotropy (1).
– Mostly beta-1 receptors but some role for beta-2 receptors have also been described (1).
– Agonism from intrinsic molecules include epinephrine, norepinephrine, and dopamine (2).
ANATOMY
• The SA node is located at the junction of the superior vena cava and the right atrial
appendage
– It is innervated by fibers from both the sympathetic and parasympathetic (vagal) nervous
systems (1).
• Positive chronotropy can be used to
– Increase cardiac output (stroke volume times heart rate). Used to treat severe bradycardia
(e.g., oculocardiac reflex or vasovagal reflex).
– Decrease regurgitant volume in aortic or mitral regurgitation. By decreasing the systolic
time, the regurgitant volume also decreases.
• Negative chronotropy is a therapeutic modality used in several disease states:
– Coronary artery disease/myocardial ischemia. Decreases myocardial oxygen demand (3)
as well as supply (increases diastolic time and duration that the left ventricle is perfused).
– Acute aortic dissection. Decreased heart rate reduces shear stress on the aorta (4)[A].
– Hypertrophic/obstructive cardiomyopathy. Dynamic outflow obstruction will decrease as
the heart has more time to fill and does not empty as much (3).
– Stenotic valve lesions (e.g., aortic stenosis and mitral stenosis). Allows for increased
ventricular filling (increased diastolic time during each cardiac cycle) along with
improved ejection of blood (increased systolic time during each cardiac cycle).
• Chronically elevated resting heart rate has multiple negative myocardial and vascular
consequences:
– Impaired left ventricular (LV) function
– Impaired LV relaxation
– LV hypertrophy
– Endothelial injury/atherosclerosis (3)
Neonatal left ventricles are stiffer than in adults and are less able to tolerate volume loads.
Because stroke volumes are relatively fixed, they become dependent on the heart rate to
maintain cardiac output (5)[A].
Elderly patients are more prone to chronotropic incompetence—the inability to adequately
increase heart rate in response to normal stimuli (<85% maximal predicted heart rate). This
may be secondary to remodeling that is associated with an augmentation of collagen content.
It has also been hypothesized that it can be a sign of occult coronary artery disease and may
correlate with increased mortality (6).
Negative chronotropy is accomplished using
• Beta-receptor antagonists: Metoprolol, propranolol, esmolol, and atenolol. They function to
decrease spontaneous depolarization of SA node cells and thus slow the heart rate (7).
• Ca2+ channel antagonists (class IV antiarrhythmics): Diltiazem and verapamil (8). They
function to block L-type Ca2+ channels found in the SA and AV nodes, thus slowing
automaticity as well as AV conduction (9).
Positive chronotropy can result from
• Sympathomimetics
– Endogenous molecules (available for exogenous administration)
Norepinephrine stimulates both alpha-1 and beta-1 receptors. Unopposed
vasoconstriction from alpha-1 stimulation may cause a reflex bradycardia that is capable
of off-setting chronotropic responses from beta-1 stimulation (2).
Epinephrine stimulates beta-1, beta-2, and alpha-1 receptors and is a powerful
chronotrope, especially at low doses (0.01–0.05 μg/kg/min) (2).
Dopamine stimulates D1, beta-1, and alpha-1 receptors; it has a predominant
chronotropic beta-1 response at mid-range doses (2–10 μg/kg/min) (2).
– Synthetic molecules
Isoproterenol is a nonselective beta-1 and beta-2 agonist (2).
Dobutamine is a selective beta-1 agonist (2).
Ephedrine acts indirectly to increase the release of stored norepinephrine from synaptic
junctions as well as directly binds to beta-1 receptors. Ephedrine is less effective when
stores of norepinephrine have been depleted from the synaptic junction as in congestive
heart failure (2).
• Muscarinic acetylcholine antagonists also increase chronotropy by blocking vagal
transmission to the SA and AV node. They include atropine and glycopyrrolate.
EQUATIONS
Cardiac Output (CO) = Stroke Volume (SV) × Heart Rate (HR)
REFERENCES
1. Lakatta EG. Beyond Bowditch. The convergence of cardiac chronotropy and inotropy. Cell
Calcium. 2004;35:629–642.
2. Kee VR. Hemodynamic pharmacology of intravenous vasopressors. Crit Care Nurse.
2003;23:79–82.
3. Liu H, Fox CJ, Zhang S, et al. Cardiovascular pharmacology: An update. Anesthesiol Clin.
2010;28:723–738.
4. Menon V, Sengupta J, Unzek S. Optimal management of acute aortic dissection. Curr Treat
Options Cardiovasc Med. 2009;11:146–155.
5. Romero T, Covell J, Friedman WF. A comparison of pressure-volume relations of the fetal,
newborn, and adult heart. Am J Physiol. 1972;222(5):1285–1290.
6. Lauer MS, et al. Impaired heart rate response to graded exercise: Prognostic implications of
chronotropic incompetence in the Framingham Heart Study. Circulation. 1996;93:1520–
1526.
7. Gorre F, Vandekerckhove H. Beta-blockers: Focus on mechanism of action. Which beta-
blocker, and why? Acta Cardiologica. 2010;65(5):565–570.
8. Reil JC, et al. Heart rate reduction in cardiovascular disease and therapy. Clin Res Cardiol.
2011;100:11–19.
9. Tamargo J, Caballero R, Delpón E. Pharmacological approaches in the treatment of atrial
fibrillation. Curr Med Chem. 2004;11:13–28.
ADDITIONAL READING
• Sun LS, Schwarzenberger JC. Cardiac physiology. In: Miller RD, Ericksson LI, Fleisher LA et
al., Eds. Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill Livingstone, 2009.
• cAMP
• Pacemaker cells in heart
• Thoracic aneurysm repair
• Hypertrophic cardiomyopathy
• Mitral regurgitation
• Mitral stenosis
• Tachycardia
CLINICAL PEARLS
• Chronotropy is under the control of the autonomic nervous system; both sympathetic and
parasympathetic nerve endings are located at the pacemaker cells of the heart. Additionally,
circulating catecholamines can agonize beta- receptors. Positive chronotropy mediated by
the body does not typically result in an isolated phenomenon; it is usually in response to an
overall sympathetic state that serves to increase inotropy and systemic vascular resistance.
• Understanding of this physiology allows the clinician to modulate the heart rate in the
perioperative period and with certain disease states.
CILIARY FUNCTION
BASICS
DESCRIPTION
• Ciliary function and the integrity of the mucus layer are the two most important
determinants of mucociliary clearance (MC).
– Toxins, dust, microorganisms, and other debris entrapped in the mucus are removed from
the respiratory system by the cephalad stroke of cilia.
– In addition to binding various substances and hindering their way further down into the
respiratory tract, tracheobronchial mucus also has directly antibacterial as well as
immunological functions.
• For clinical purposes, ciliary function and mucus integrity need to be treated as one unit
that determines MC.
• Cilia
– Cilia in the respiratory tract “sweep” mucus cephalad until it can be expectorated.
– On the microscopic level, ATPase activity, resulting in adenosine triphosphate (ATP)
hydrolysis, provokes conformational changes in the interconnecting dynein arms of ciliary
microtubules. ATPase functions as a motor that results in sliding between adjacent
microtubules A and B (see Anatomy).
– The bending or “stroke” of the cilium is explained by the initial activation of dynein in
only half the microtubules, with the activation of the other half accounting for the
backwards movement of the cilium (1). This is referred to as the effective stroke or
principal bend and the recovery stroke or reverse bend, respectively.
– Ciliary beat frequency is 11–15 Hz.
• Mucus
– Liquid secretion from submucosal glands is largely under neuronal control, where vagal
stimulation causes an increase in glandular secretion (via local ACH release).
– Substance P and vasoactive intestinal peptide (VIP) are second-line regulatory mechanisms
that provoke the upregulation of mucus secretion.
– On the cellular level, liquid secretion is largely driven by active Cl− and HCO3− secretion,
creating a lumen-negative potential difference to pull cations through paracellular tight
junctions. This results in an osmotic gradient that drives water movement across the
epithelial barrier (2).
– Mucus contains ∼95% water.
– Tracheal mucus clearance is remarkably rapid with a speed of 4–20 mm per minute.
Velocities in the peripheral airways are lower.
• Both ciliary beat frequency and MC are significantly reduced (nearly halved) in elderly
patients!
• Ultrastructurally, microtubular abnormalities increase with age.
ANATOMY
• Cilia
– Cilia are found in the upper (nasal cavities, sinuses, Eustachian tubes, middle ear) and
lower (trachea to terminal bronchioles) airway, decreasing in height from 5 to 7 μm
(trachea) to 2 to 3 μm (bronchioles).
– There are ∼100–200 cilia on each ciliated cell, with ∼3 ×1012 cilia in total.
– Underneath the outer cell membrane of each cilium, the ciliary axoneme is composed of
over 250 proteins forming a “9 + 2” pattern with 9 peripheral microtubular pairs (A and
B) surrounding a central pair (1).
– The peripheral A microtubules have an attached inner and outer dynein arm; all pairs are
connected via nexin links.
– Central and peripheral microtubules are connected via radial spokes to finally form the
complex microtubular unit that equals 1 cilium.
• Mucus
– All ciliated respiratory epithelia are covered by a blanket of viscoelastic mucus that is
divided into 2 layers:
A deeper, more liquid sol-layer that allows unhindered movement of cilia.
A superficial mucous layer to entrap substances.
– Submucosal glands consist of
Secretory tubules that contain serous and mucous cells. Serous cells have apical vesicles
containing lysozyme, lactoferrin, IgA, peroxidases, and albumin (2). Mucous cells
produce gel-forming mucins or polysaccharides.
A collecting duct
A ciliated duct that passes through the smooth muscle and lamina propria of the mucosa
and finally opens to the airway surface.
• Reduced MC can result from certain conditions or diseases, artificial or mechanical
ventilation, and drugs.
– Conditions and diseases
Immotile cilia (Kartagener’s) syndrome; the absence of dynein arms or radial spokes can
result in impairment, or complete loss, of ciliary function.
Asthma results in inflammation and hypersecretion.
COPD and bronchiectasis can result in epithelial damage.
Cystic fibrosis; dehydrated and thick mucus is produced as a result of abnormalities in Cl
− ion transport.
Wegener’s granulomatosis
Acute respiratory tract infection as a result of cytotoxins
Acute illness such as in intensive care unit (ICU) patients.
Extremes of temperature
Sleep
Immobility
Artificial or mechanical ventilation related
High fresh gas flow can dry mucus.
High airway pressure reduces ciliary beat frequency (3)[C].
Lack of airway humidification can dry mucus.
Bronchial suctioning can result in epithelial damage.
Tracheal intubation (decreased MC when compared with laryngeal mask airway) (4)[B]
Drugs
Volatile anesthetic agents (halothane, isoflurane, sevoflurane, desflurane) (5)[B] can
potentially inhibit Cl− channels. The MC inhibitory effects of volatile agents last for
∼60–90 minutes after cessation of their administration.
Morphine; evidence is conflicting.
Remifentanil, when compared to morphine, may lower MC.
Pentobarbital has an inhibitory ciliary effect.
Temazepam, diazepam
Ketamine at clinical doses
Atropine; Evidence is conflicting.
Furosemide
Tobacco
Alcohol
Increased MC can also result from certain conditions, ventilatory maneuvers, or drugs.
Conditions
Exercise
Change of posture can have a mucus draining effect
Ventilation related
Positive end-expiratory airway pressure; studies and evidence are mainly from cystic
fibrosis patients.
Nasal continuous positive airway pressure; likely has only a short-term effect.
Air humidification (e.g., by means of HME devices)
Drugs
Ketamine at supraclinical doses has been seen during in vitro experiments.
Anticholinergic drugs; Evidence is conflicting
β2-adrenergic agents; evidence is conflicting. Studies have shown that they may
stimulate ciliary beat frequency, but also mucus production. The effect on MC especially
in diseased lungs is unclear.
Methylxanthines
Drugs with likely no significant effect on MC
Propofol
Midazolam
Dexmedetomidine
Thiopental
Fentanyl
MC is of utmost importance for unhindered gas exchange as a result of the
Maintenance of normal pulmonary physiology
Prevention of infection
Prevention of airway obstruction and atelectasis
Preservation of surfactant function
The rate of perioperative pulmonary complications can be reduced with simple
perioperative measures such as airway humidification or the avoidance of potentially
detrimental ventilation patterns (see above).
Laryngeal mask airways may result in reduced MC impairment compared to tracheal
intubation (4)[B].
Smoking has a negative impact on MC and on pulmonary complications in ICU patients.
Smoking cessation does not appear to have immediate effects on MC function. In fact,
compared to nonsmokers, mucus production is ∼50% greater in patients who ceased
smoking <8 weeks prior to surgery, 25% higher in those who quit >8 weeks prior to
surgery and not significantly different to nonsmokers when stopped smoking >6 months
prior to surgery.
GRAPHS/FIGURES
See link under “additional reading.”
REFERENCES
1. Stannard W, O’Callaghan C. Ciliary function and the role of cilia in clearance. J Aerosol
Med. 2006;19:110–115.
2. Ballard ST, Spadafora D. Fluid secretion by submucosal glands of the tracheobronchial
airways. Respir Physiol Neurobiol. 2007;159:271–277.
3. Piccin VS, Calciolari C, Yoshizaki K, et al. Effects of different mechanical ventilation
strategies on the mucociliary system. Intensive Care Med. 2011;37:132–140.
4. Keller C, Brimacombe J. Bronchial mucus transport velocity in paralyzed anesthetized
patients: A comparison of the laryngeal mask airway and cuffed tracheal tube. Anesth
Analg. 1998;86:1280–1282.
5. Ledowski T, Paech MJ, Patel B, et al. Bronchial mucus transport velocity in patients
receiving propofol and remifentanil vs. sevoflurane and remifentanil anesthesia. Anesth
Analg. 2006;102: 1427–1430.
ADDITIONAL READING
Electron-microscopic pictures and explanation of cilia structure and movement by Gwen
V. Childs, PhD, University of Arkansas for Medical Sciences.
How do cilia move? http://www.cytochemistry.net/Cell-biology/cilia.htm
Smoking
CLINICAL PEARLS
Preservation of MC is important.
An easy way to preserve/improve MC is by airway humidification, low-flow anesthesia,
and avoidance of high-pressure/high-volume ventilation.
Although preoperative cessation of smoking is generally considered beneficial, its impact
on MC may not be evident for several weeks. It may actually decrease MC initially; the
clinical relevance of this is unclear.
In patients prone to airway complications (e.g., cystic fibrosis patients) careful planning
of the anesthetic regime and avoidance of substances that hinder MC further may be
beneficial.
There is no “magic bullet” drug treatment to improve MC in anesthetized patients or
patients with preexisting airway disease.
CIRCLE OF WILLIS
BASICS
DESCRIPTION
The circle of Willis (coW) connects the cerebral blood flow (CBF) from the internal carotid
arteries (ICAs) (80% of CBF) with the vertebrobasilar system (VBS) (20% of CBF) in a ring of
vessels beneath the hypothalamus.
The circular arrangement of the cerebral arteries creates a collateral system of blood flow that
protects the brain from ischemia when one part of the circle becomes blocked or narrowed.
ANATOMY
• The coW consists of the following arteries (see Figure 1):
– Anterior communicating artery
– Paired anterior cerebral arteries
– Paired ICAs
– Paired posterior communicating arteries (PCOM)
– Paired posterior cerebral arteries (PCA)
FIGURE 1. Circle of Willis Anatomy (1)
• The basilar artery along with the two vertebral arteries are referred to as the vertebrobasilar
system. It supplies blood to the coW.
• The cerebral circulation can be divided into anterior and posterior vessels:
– The anterior circulation is supplied by the ICAs (arising from the common carotid
arteries). The first branch is the ophthalmic artery, followed by the PCOM, and then the
anterior choroidal artery. The ICAs terminate into the anterior and middle cerebral
arteries.
– The posterior circulation is supplied by the VBS. The vertebral arteries (arising from the
subclavian arteries) supply circulation to the spinal cord and give off branches to the
cerebrum, midbrain, pons, medulla, and cerebellum. Branches of the vertebral arteries
include the anterior spinal artery, paired posterior spinal arteries, and the posterior
inferior cerebellar artery. The vertebral arteries then unite to form the basilar artery. The
basilar artery terminates by dividing into paired PCA that supply the medial temporal
lobe, occipital lobe, and parts of the thalamus.
• The anatomy of the coW is highly variable in adults. These variations are largely the result
of fetal development in utero. As early as seven weeks postconception, a preliminary form of
the coW is present with approximately equal diameters of all vessels. As the fetus grows so
do the components of the coW, eventually assuming the adult morphology (2). The main
differences between the fetal and adult coW anatomy are the diameters of the PCOM and
the circular part of the PCA. The coW is complete in only 42.1–47% of individuals (3).
• It is possible that in some individuals a fetal-type PCA (one supplied primarily by the ICA
rather than the vertebral artery) will persist. ICA volume flow is significantly increased and
basilar artery flow significantly decreased. In those with absent A1 segments of the anterior
cerebral artery, flow between the ICAs is largely asymmetrical (6).
• Approximately 95% of all aneurysms can be found near the coW.
• Cerebral aneurysms are classified by size, shape, and location. Size is considered to be one
of the most important determinants of future rupture. The ISUIA trial (a large international
prospective study) evaluated 5-year cumulative cerebral aneurysm rupture risk based on
location and size (4).
– Size (anterior/posterior%):
<7 mm (0/2.5%)
7–12 mm (2.6/14.5%)
13–24 mm (14.5/18.4%)
– Shape:
Saccular (most common): The aneurysm has an outpouching.
Berry: A saccular aneurysm with a stem or neck.
Fusiform: Without an outpouching or stem.
• Location:
– 85% are located in the anterior circulation
Anterior communicating artery (most common site of rupture in anterior circulation)
Anterior cerebral arteries
Bifurcation of the ICAs
Middle cerebral arteries
PCOM
– 15% are located in the posterior circulation
PCA
Basilar artery bifurcation
• Ischemia, thrombosis, or hemorrhage of a cerebral artery is known as a cerebrovascular
accident (CVA). It is defined as a new focal or global neurological (motor or sensory) deficit
lasting >48 hours.
– A transient ischemic attack (TIA) is characterized by a sudden vascular-related focal
neurologic deficit that resolves within 24 hours.
– Occlusion of a specific major intracranial artery will result in predictable clinical
neurologic deficits.
– Isolated infarction of the anterior cerebral artery is uncommon.
– Carotid stenosis can lead to TIAs and CVAs if collateral CBF is not adequate.
• Subclavian steal syndrome is a phenomenon of transient cerebral ischemic attacks following
ipsilateral arm exercise in the presence of severe stenosis (>80%) or occlusion of the
subclavian artery proximal to the origin of the vertebral artery. It is a flow-related
phenomenon.
– At rest, the arm becomes dependent on the collateral vessels from the head, shoulder, and
neck.
– During exercise, blood flows retrograde from the ipsilateral vertebral artery to the distal
subclavian artery to supply the arm. In doing so, blood is diverted from the circle of Willis
and can result in transient cerebral ischemia.
• Arteriovenous malformation (AVM) is an abnormal connection between arteries and veins;
whereby high-pressure arteries connect directly to low-pressure veins without passing
through a capillary network. They are most often congenital lesions that can be found
anywhere in the body. They are usually asymptomatic. In rare circumstances, cerebral
lesions may bleed or expand, leading to CNS symptoms. The most common symptoms of
cerebral AVMs are seizures, headache, and pain.
• Moyamoya syndrome is a disease in which the lumen of certain cerebral arteries (mainly the
ICAs up to the middle and anterior cerebral arteries) overgrow inwardly to the point of
constriction or blockage. This leads to angiogenesis of collateral blood vessels to
compensate for lack of blood flow in the region. The collateral network of small blood
vessels has the appearance of a “puff of smoke” or “moyamoya,” in Japanese. Problems may
arise when these small fragile networks hemorrhage, aneurysm, or clot off.
• Cerebral vasculature imaging (i.e., angiography, MagneticResonance Angiogram (MRA) and
Computed Tomography Angiography (CTA)) may be utilized preoperatively or
intraoperatively to demonstrate vascular occlusions or emboli at vessel bifurcations after an
acute CVA, as well as to diagnose and treat aneurysms.
• It may be vitally important to evaluate the cerebral circulation prior to certain surgeries via
angiography. For example, in endovascular stent-graft repair for thoracic aortic disease, it is
commonly necessary to extend the stent-graft beyond the left subclavian artery (LSA). If the
contralateral vertebral artery is hypoplastic and the coW is incomplete or when the left
vertebral artery significantly participates in the supply of the superior portion of the
anterior spinal artery, then coverage of the LSA may disrupt collateral pathways to the
posterior cerebral circulation and spinal cord; this results in serious neurological
complications. In order to avoid such debilitating complications, careful imaging of the
right vertebral artery up to the basilar artery may be mandatory preoperatively (7).
– In certain situations, neurologic complications can be minimized when a prophylactic
carotid subclavian bypass is performed, as well as avoidance of intraoperative
hypotension (8).
• During carotid endarterectomy (CEA) surgery, an incomplete coW formation predisposes
approximately one-sixth of individuals to cerebral ischemia during carotid clamping or
transient closure of the carotid artery. In those with coexisting contralateral ICA occlusion,
the risk of cerebral ischemia rises more than threefold (9).
– Some institutions utilize preoperative angiography of the cerebral vasculature to assess
collateral flow and determine the possible need for intra-luminal shunting during the
procedure.
• Middle cerebral artery blood flow velocities can be measured in real-time by transcranial
Doppler (TCD) to detect and quantify embolic signals intraoperatively or at the bedside. It
can be beneficial in situations such as patients status post-CEA and/or patients undergoing
thrombolytic therapy.
– TCD predictors of stroke after CEA include emboli during wound closure, >90% decrease
in middle cerebral artery peak systolic velocity at cross-clamping, and >100% increase of
the pulsatility index of the Doppler signal at clamp release (10).
REFERENCES
1. Illustration by Brooke Albright, MD.
2. ucchiara B, Detre J. Migraine and circle of Willis anomalies. Medical Hypotheses.
2008;70:860–865.
3. Ardakani SK, Dadmehr M, Nejat F, et al. The cerebral arterial circle (circulus arteriosus
cerebri): An anatomical study in fetus and infant samples. Pediatr Neurosurg.
2008;44:388–392.
4. eibers DO, Whisnant JP, Huston J 3rd. Unruptured intracranial aneurysms: Natural history,
clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003;362:103–
110.
5. Lall RR, Eddleman CS, Bendok BR, et al. Unruptured intracranial aneurysms and the
assessment of rupture risk based on anatomical and morphological factors: Sifting through
the sands of data. J Neurosurg FOCUS. 2009;26(5):E2.
6. endrikse J, van Raamt AF, van der Graaf Y, et al. Distribution of cerebral blood flow in the
circle of Willis. Radiology. 2005;235:184–189.
7. Manninen H, Tulla H, Vanninen R, et al. Endangered cerebral blood supply after closure of
left subclavian artery: Postmortem and clinical imaging studies. Ann Thorac Surg.
2008;85:12–16.
8. Feezor RJ, Martin TD, Hess PJ, et al. Risk factors for perioperative stroke during thoracic
endovascular aortic repairs (TEVAR). J Endovasc Ther. 2007;14(4):568–573.
9. Manninen H, Mkinen K, Vanninen R, et al. How often does an incomplete circle of Willis
predispose to cerebral ischemia during closure of carotid artery? Postmortem and clinical
imaging studies. Acta Neurochir. 2009;151:1099–1105.
10. Ackerstaff RG, Moons KG, va de Vlasakker CJ, et al. Association of intraoperative
transcranial Doppler monitoring variables with stroke from carotid endarterectomy. Stroke.
2000;31(8):1817.
• Carotid endarterectomy surgery
• Cerebral aneurysms
• Arteriovenous malformations
• Transient ischemic attacks
• Subclavian steal syndrome
CLINICAL PEARLS
• The coW is complete in only 42.1–47% of the population. An incomplete coW significantly
predisposes individuals to cerebral ischemia during certain procedures such as CEA and
TEVAR.
• Some institutions are beginning to utilize preoperative cerebral vasculature angiograms to
guide surgical intervention and predict the need for additional cerebral protection and/or
monitoring.
• Although the majority of aneurysms develop in the anterior circulation, current literature
suggests higher risks of rupture are associated with posterior circulation aneurysms with
size >7 mm (5)[A].
CIRCULATORY ARREST
January Y. Tsai, MD
BASICS
DESCRIPTION
• Cessation of the systemic circulation is either
– Unintentional: Due to cardiac arrhythmia or arrest, ischemia, electrolyte abnormality, or
extreme hypothermia.
– Therapeutic (planned or emergent): Hypothermic circulatory arrest temporarily suspends
blood flow under very cold body temperatures to allow for a motionless and bloodless
surgical field for intracardiac and aortic procedures. This requires increased coordination
among the anesthesiologist, surgeon, and perfusionist.
• At cold temperatures, cellular activity levels slow significantly and allow blood circulation
to be suspended for up to 40 minutes without neurological harm to the patient.
• Additionally, adjunctive selective cerebral perfusion (antegrade or retrograde) is commonly
used now, whereas previous deep hypothermic circulatory arrest (DHCA) relied on
hypothermia alone for neuroprotection.
• Unintentional: High/normal cerebral metabolic rate of oxygenation (CMRO2) during periods
of limited or no cerebral perfusion may rapidly lead to irreversible hypoxic brain injury.
• Therapeutic: CMRO2 decreases 7%/°C. At 23°C, the CMRO2 theoretically approaches zero.
Types of cerebral perfusion include retrograde and antegrade.
• Retrograde cerebral perfusion (RCP)
– Cannulation is via the superior vena cava (SVC).
– Perfusion with cold blood
– Perfusion theoretically occurs via the SVC to the internal jugular (IJ) vein to the sigmoid
sinuses to the venules to the capillaries to the arterioles to the circle of Willis (coW) to the
internal carotid artery (ICA) to the right and left common carotid arteries (RCC/LCC) and
then to the aortic arch.
– Conventional maximum flow rate of 500 mL/min in the circuit is utilized to maintain the
SVC catheter pressure <25 mm Hg.
– Advantages
More homogenous brain cooling
Washout of air bubbles, embolic debris, and metabolic waste products
Prevention of cerebral blood cell microaggregates
Delivery of O2 and metabolic substrates
– Potential disadvantages
Excessive RCP pressure has been related to the potential for increased cerebral edema
leading to neurologic injury (1).
Increased intracranial pressure and cerebral edema may occur due to direct perfusion of
hypothermically vasoconstricted microvasculature and tissues. Impeded venous return
may also exacerbate intracranial pressure and edema.
Low levels of substrate
Duration before cerebral consequences: 45 minutes
• Anterograde cerebral perfusion
– The right axillary artery is either directly cannulated or a graft is inserted.
– Perfusion with cold blood
– Once antegrade perfusion is initiated, the brachiocephalic artery is clamped, and blood
flow proceeds from the right axillary artery to the right subclavian artery to the
brachiocephalic artery (very short segment) to the RCC and then to the brain.
– Mean perfusion pressure usually 40–70 mm Hg.
– Cerebral oximetry may be used to evaluate changes in regional brain perfusion. If left-
sided cerebral perfusion decreases, direct visual cannulation of the left carotid artery and
perfusion with cold blood may be performed to enhance flow.
– Advantages
Uninterrupted supply of nutrients to the brain
Prolonged duration of safe circulatory arrest compared to RCP
– Potential disadvantages
Air or plaque emboli due to manipulation of frequently atheromatous great vessels and
direct antegrade flow to the cerebral circulation.
Unilateral flow requires an intact coW, which is present in only ∼30% of the population.
The most common absences include a lack of the P1 segment of the posterior cerebral
artery (PCA), posterior communicating artery (PComm), or A1 segment of the anterior
cerebral artery (ACA). Prior ischemic stroke in any of these territories may also result in
an incomplete circle (2).
Axillary cannula or graft insertion can increase the complexity of surgery.
A greater number of cannulae are present on the surgical field.
Duration before cerebral consequences: 60 minutes.
• Controversial topics
– Optimal lowest temperature is unknown. While hypothermia decreases the CMRO2
(provides neuroprotection), it can adversely affect coagulation and microvascular
perfusion; profound hypothermia (∼14°C) may have more profound adverse effects. In
addition, lower temperature is associated with longer cardiopulmonary bypass (CPB)
times due to longer rewarming times (longer CPB time is associated with poorer
outcomes). With the advent of antegrade cerebral perfusion, the duration of circulatory
arrest may be prolonged, and decreased levels of hypothermia may be utilized (up to
25°C) (3).
– Optimal flow rate and pressure are unknown. Both flow and perfusion pressure should
meet tissue metabolic requirements without causing tissue injury. Although conventional
values have been established, whether they should be adjusted for temperature-related
differences in vascular tone is not known.
– Barbiturates or propofol may be used for neuroprotection in conjunction with EEG
monitoring. Isoelectric EEG implies decreased CMRO2 and improved cerebral protection.
However, studies have shown that patients receiving thiopental required more inotropic
support, but significant neuroprotection was not provided (4).
– Steroids (large-dose methylprednisolone 30 mg/kg) are also commonly used for
neuroprotection, but experimental results are mixed. For example, one animal study found
that systemic pretreatment fails to attenuate neuronal cell injury after prolonged DHCA
and that the steroid group showed increased neuronal apoptosis in the dentate gyrus (5).
However, another study found improved global and regional cerebral blood flow (CBF)
and CMRO2 with steroid use (6).
ANATOMY
Therapeutic circulatory arrest is used for large or difficult to access cerebral aneurysms and
aortic repair in order to create a motionless, bloodless field. Continuous circulation during
open exposure of the aortic arch or cerebral circulation would create a difficult surgical field
or massive hemorrhage.
Brachiocephalic artery repair. Loss of the left radial arterial line waveform can occur during
left-sided repair.
• Inadequate cardioprotection
– Cardiac ischemia may occur due to inadequate cardioplegia administration or inability to
terminate electrical activity during circulatory arrest.
– Inability to wean from CPB may be secondary to myocardial stunning.
– Ventricular fibrillation may occur during rewarming. Arrhythmias may also occur
postoperatively.
• Hypothermia
– Hemoconcentration with hypothermia and increased blood viscosity may decrease
microvascular perfusion.
– Consider isovolemic hemodilution
• Coagulopathy
– Temperatures required for protection are outside the normal range of coagulation
enzymes.
– Increased bleeding after termination of CPB and protamine administration
– Consider antifibrinolytics, DDAVP, autologous blood transfusion, early plasma, and factor
administration based on clinical evaluation or coagulation panels.
• Postoperative shivering
– Increased metabolic rate
– Increased O2 consumption
• Cerebral injury is a major cause of morbidity and mortality following aortic arch surgery.
– Stroke due to insufficient neuroprotection may occur early (temporary neurological
dysfunction) or late (permanent neurological dysfunction) due to cerebral hypoperfusion
or atheromatous emboli. It may be due to ischemia reperfusion injury or rewarming
injury.
– Spinal cord ischemia due to prolonged arrest of vertebral artery flow. Neuromonitoring
techniques may be used to detect changes.
• Inadequate lower body organ protection
– Renal insufficiency
– Hepatic ischemia
• Decreased metabolic rate
– Metabolism of most drugs is decreased while hypothermic.
– Muscle relaxation may outlast sedation postoperatively, especially if redosed.
• General end-organ effects
– Endothelial dysfunction
– Apoptosis
– Necrosis
• Stress response and hyperglycemia
– May be refractory to insulin during circulatory arrest and then increasingly sensitive with
rewarming.
– Aggressive, tight treatment is usually not warranted.
REFERENCES
1. Estrera A, Garami Z, Miller C, et al. Determination of cerebral blood flow dynamics during
retrograde cerebral perfusion using power M-mode transcranial Doppler. Ann Thorac Surg.
2003;76:704–710.
2. reasy J. Dating Neurologic Injury. Springer 2011:12.
3. Salazar J, Coleman R, Griffith S, et al. Brain preservation with selective cerebral perfusion
for operations requiring circulatory arrest: Protection at 25°C is similar to 18°C with
shorter operating times. Eur J Cardiothoracic Surg. 2009;36(3):524–531.
4. Zaidan J, Klochany A, Martin W, et al. Effect of thiopental on neurologic outcome
following coronary artery bypass grafting. Anesthesiology. 1991;74:406–411.
5. Schubert S, Stoltenburg-Didinger G, Wehsack A, et al. Methylprednosolone fails to
attenuate neuronal injury after deep hypothermic circulatory arrest in a neonatal piglet
model. A&A. 2005; 101(5):1311–1318.
6. Langley S, Chai P, Jaggers J, et al. Preoperative high dose methylprednisolone attenuates
the cerebral response to deep hypothermia circulatory arrest. Eur J Cardiothoracic Surg.
2000;17:279–286.
ADDITIONAL READING
• Apostolakis E, Koletsis EN, Dedeilias P, et al. Antegrade versus retrograde cerebral perfusion
in relation to postoperative complications following aortic arch surgery for acute aortic
dissection type A. J Card Surg. 2008;23(5):480–487.
• Neuroprotection
• Thoracic aneurysm repair
• Hypothermia
CODES
ICD9
ICD10
I46.9 Cardiac arrest, cause unspecified
CLINICAL PEARLS
• Use NIRS and/or EEG to monitor cerebral activity.
• May need both radial and femoral arterial lines for monitoring.
• Ventricular fibrillation is likely during cooling and rewarming. Consider lidocaine,
magnesium, esmolol, and amiodarone to decrease the incidence; be prepared to defibrillate.
Pacing may be required.
• Steroids are possibly beneficial for cerebral edema.
• Coagulopathy may require early and aggressive monitoring and blood product transfusion.
Order products early if necessary and have sufficient venous access.
• Redistribution of temperature postoperatively may cause significant hypothermia, which
may require aggressive rewarming.
CIRRHOSIS
Phoebe Lee, MD
BASICS
DESCRIPTION
• Cirrhosis is the common histological outcome of chronic liver disease resulting in cell
necrosis and altered liver structure and function. It is characterized by
– Fibrosis
– Regenerative nodules of hepatic cells
– Impaired metabolic and synthetic function
– Increased hepatic resistance to blood flow
• Portal hypertension is the hallmark of decompensated cirrhosis, recognizable by ascites
formation, venous collateral development, and episodes of hepatic encephalopathy.
EPIDEMIOLOGY
Prevalence
Difficult to quantify and regionally dependent on the presence of different risk factors
Prevalence
True prevalence of cirrhosis is unknown, as many compensated cases are undiagnosed.
Morbidity
• In 2002: Cirrhosis caused 421,000 hospitalizations in the US.
• In 2005: 112,000 discharges with chronic liver disease or cirrhosis as the first-listed
diagnosis in the US.
• Cirrhotic patients are at risk of developing hepatocellular carcinoma (10–25% of cases).
Mortality
• Deaths per 100,000 population: 9.7
• 12th leading cause of death in the US in 2007 (1.2% of all deaths)
Hepatitis C 26%; alcohol related 21%; hepatitis C plus alcohol 15%; hepatitis B 15%;
cryptogenic causes 18% (70% are nonalcoholic fatty liver disease [NAFLD], an increasingly
recognized cause of cirrhosis); miscellaneous 5% (autoimmune hepatitis, cholestatic liver
diseases, cholangitis, hemochromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency, drug-
induced, right-sided heart failure, Budd–Chiari)
• Impaired metabolic and synthetic function
– Albumin. Important for maintaining oncotic pressure in capillaries; affects drug
distribution and elimination by its binding.
– Coagulation factors. Vitamin K-derived factors (II, VII, IX, X), protein C, protein S, and
antithrombin.
– Cytochrome P450 enzymes. Decreased drug metabolism.
• Portal hypertension results from impaired hepatic vascular resistance together with
increased mesenteric blood flow. This may lead to
– Ascites. Describes the accumulation of fluid in the peritoneal cavity. Pathogenesis is
controversial and probably different at various phases of the disease. Portal hypertension,
splanchnic vasodilation, hypoalbuminemia, and increased levels of sodium retentive
hormones contribute to capillary leakage.
– Venous collateral development. Results in esophageal varices and acute bleeding as well
as hypersplenism with associated leukopenia and/or thrombocytopenia.
– Hepatic encephalopathy. Results from elevated circulating neurotoxic gut toxins (due to
portocaval shunting and decreased hepatic metabolism). Patients present with depressed
levels of consciousness, personality changes, and intellectual impairment.
• Maintain perfusion and oxygenation of the liver to minimize postoperative deterioration of
liver function.
• Altered pharmacology can result in sensitivity to sedatives, hepatic encephalopathy, and
impaired pulmonary or cardiovascular function. Additionally, altered pharmacokinetics
includes an increased volume of distribution (Vd), impaired cytochrome P450, and
hypoalbuminemia.
• Perioperative mortality is severely increased in cirrhotic patients.
SYMPTOMS
Fatigue, nausea, decreased appetite, itching, right upper quadrant pain, abdominal distension,
jaundice, dark urine, light stools, and easy bruising.
History
Prior blood transfusions, tattoos, illicit drug use, alcohol intake, sexual history, exposure to
needle sticks, history of jaundice, and family history of liver disease.
Signs/Physical Exam
Icterus, palmar erythema, spider telangiectasia, gynecomastia, caput medusae,
hepatosplenomegaly, abdominal distension and umbilical hernia from ascites, lower
extremity edema, temporal wasting, loss of muscle mass, abnormal mental status, and
asterixis.
TREATMENT HISTORY
• Medical management depends on the etiology of initial liver disease. Antiviral treatment for
hepatitis B and C, abstinence from alcohol, steroids and azathioprine for autoimmune
hepatitis.
• Transjugular intrahepatic portosystemic shunts (TIPS) and large volume paracentesis are
considered in medically refractory ascites.
• Endoscopic variceal ligation and octreotide infusion for acute bleeding.
MEDICATIONS
• Ascites: Sodium restriction (first line), diuretics (second line).
• Spontaneous bacterial peritonitis: Cephalosporins usually indicated.
• Hepatic encephalopathy: Lactulose and poorly absorbable antibiotics like rifaximin,
neomycin, and metronidazole.
• Hepatorenal syndrome: Splanchnic vasoconstrictors (midodrine, octreotide) and volume
expansion with albumin.
Labs/Studies
• Complete Blood Count (CBC), Complete Metabolic Panel (CMP), Prothrombin Time (PT),
International Normalized Ratio (INR), Right Upper Quadrant (RUQ), Ejection Fraction (EF),
Model for End Stage Liver Disease (MELD)
• RUQ abdominal ultrasound with Doppler to evaluate parenchyma and portal venous blood
flow
• Abdominal CT or MRI to evaluate parenchyma (hepatocarcinoma) and vasculature
• Cardiovascular (1)[A]
– Hyperdynamic circulation: Decreased systemic vascular resistances, arterial BP, and
increased heart rate lead to a high cardiac output (HCO) status. Increased CO is unequally
distributed with a preferential flow toward the visceral compartment. Peripheral arteries
may be dilated or constricted in advanced disease.
– Autonomic dysregulation with blunted sympathetic and parasympathetic responses.
– Cirrhotic cardiomyopathy: Impaired cardiac contractility, systolic and diastolic
dysfunction, and ECG abnormalities (e.g., prolonged QT) may lead to ventricular
arrhythmias and sudden cardiac death. Typically improves after liver transplantation.
– Diagnostic tools include a 12 lead ECG (QTc, QT dispersion); resting or stress ECG (EF,
volumes, fractional shortening, wall motion, E/A ratio); exercise ECG (exercise capacity,
oxygen consumption, pressure × heart rate product).
• Hepatorenal syndrome (2)[A]
– Acute or subacute renal failure in advanced cirrhosis is caused by vasoconstriction of renal
arteries and is characterized by oliguria/anuria and a creatinine >1.5 mg/dL. Kidneys
show only minimal histological changes.
– Type 1: Rapid course in <2 weeks mandates dialysis and liver transplantation.
– Type 2: Slowly progressing course, usually responds to volume expansion.
• Hepatopulmonary syndrome
– Seen in advanced cirrhosis
– Hypoxemia results from pulmonary vasodilation that causes ventilation/perfusion
mismatching and intrapulmonary shunting.
– Clinical findings include platypnea and orthodeoxia.
– Diagnosis is via contrast ECG with the presence of bubbles in the left atrium four or more
beats after the appearance in the right atrium.
– Portopulmonary hypertension is the coexistence of portal and pulmonary hypertension.
Mean survival is 15 months in the absence of a liver transplant.
• Hemostasis (3)[A]
– Hemostatic balance is unstable and can tip either way with bleeding or thrombosis.
– Hypocoagulability and bleeding tendencies are due to the decreased liver synthesis of
coagulation factors and thrombocytopenia.
– Hypercoagulability can also be present as suggested by frequent portal vein thrombosis.
– Cirrhosis “rebalanced hemostasis” can result from decreased synthesis of anticoagulants
like antithrombin III, Protein C and S; may result in normal thrombin generation in vivo.
– Traditional coagulation tests such as PT, PTT, and platelet count do not accurately reflect
the state of hemostasis.
– Prophylactic correction of abnormal laboratory tests to prevent intraoperative bleeding
does not have scientific evidence.
Circumstances to delay/Conditions
• Acute hepatitis (transaminases >10 times normal values) (4)[A]
• Child–Pugh type C
• MELD score >14
CLASSIFICATIONS
• Child–Turcotte–Pugh (CTP) and MELD classification systems were initially used for
predicting mortality after portocaval shunt/TIPS placement. They are now used to predict
surgical risk in patients with liver disease (4)[A].
– Child’s A (5–6 points): Postoperative mortality 10%; Child’s B (7–9 points): Postoperative
mortality 31%; Child’s C (10–15 points): Postoperative mortality 76%.
• MELD score: Complex logarithmic formula incorporating, bilirubin, INR, and serum
creatinine (scale 6–40).
– Score <8: Postoperative mortality 5.7%; Score >20: Postoperative mortality >50%
TREATMENT
Premedications
Judicious use of sedatives; may have prolonged central nervous system depression, and
trigger/worsen hepatic encephalopathy.
• Abnormal mental status may preclude giving a valid medical consent.
• Potential for blood or plasma transfusion.
INTRAOPERATIVE CARE
• Depends on the procedure
• Regional anesthesia: Usual cautions and contraindications apply. Epidural hematomas are of
greatest concern from the coagulopathy associated with liver surgery, especially in cirrhotic
patients.
Monitors
• Dependent on surgery. High-risk or prolonged procedure should have a low threshold for
invasive monitors (arterial lines, central lines, “less invasive” cardiac output monitors).
• Thromboelastogram may help clinicians to distinguish between medical versus surgical
bleeding and guide the transfusion of blood products.
• Induction may be associated with profound hypotension. Patients are often intravascularly
volume depleted, but with total body volume overload.
• Atracurium or cisatracurium are preferred muscle relaxants (metabolism is independent of
the liver or kidney). Other muscle relaxants may be acceptable but can have prolonged
duration.
• Rapid sequence induction should be considered in patients with ascites or gastrointestinal
bleeding.
• Patients with ascites causing respiratory impairment (tachypnea, use of accessory muscles,
hypoxia on pulse oximetry, or arterial blood gas) may require peritoneal drainage and
albumin replacement prior to anesthesia induction.
Maintenance
• Isoflurane, sevoflurane, and desflurane have limited liver metabolism and minimal
impairment of hepatic arterial blood flow.
• Halothane should be avoided; associated with mild hepatic dysfunction and severe immune-
mediated hepatitis.
• All opiates, except remifentanil, are metabolized by the liver, and should be used
judiciously.
• Standard extubation criteria
• Slower emergence and return of neuromuscular function may result from a reduced ability
to clear medications.
• Patients at risk for aspiration should be wide awake prior to extubation; patients who have
an altered level of consciousness may warrant postoperative intubation.
FOLLOW-UP
BED ACUITY
Admission to an intensive care unit (ICU) may be indicated to monitor and support
circulatory and respiratory function after intermediate/high risk procedure.
Hepatology and hematology consultation may be considered for management of
coagulopathy.
COMPLICATIONS
• Postoperative liver failure
• Hemostatic derangements
• Postoperative delirium
• Pulmonary edema
• Pleural effusion
REFERENCES
1. Moller S, Henriksen JH. Cardiovascular complications of cirrhosis. Gut. 2008;57:268–278.
2. Gines P, Schrier RW. Renal failure in cirrhosis. N Engl J Med. 2009;361:1279–1290.
3. Lisman T, Caldwell SH, Porte RJ, et al. Hemostasis and thrombosis in patients with liver
disease: The ups and downs. J Hepatology. 2010;53(2):362–371.
4. Malik SM, Ahmad J. Preoperative risk assessment for patients with liver disease. Med Clin
North Am. 2009;93:917–929.
• Liver transplant
• Thromboelastogram
CODES
ICD9
• 571.2 Alcoholic cirrhosis of liver
• 571.5 Cirrhosis of liver without mention of alcohol
ICD10
• K70.30 Alcoholic cirrhosis of liver without ascites
• K74.60 Unspecified cirrhosis of liver
CLINICAL PEARLS
• Assess perioperative risk with CPT/MELD scores.
• Optimize liver perfusion and oxygenation; may require invasive monitoring.
• Altered pharmacokinetics of drugs requires cautious titration to effect; consider adjusting
bolus doses and frequency as appropriate.
• Consider admitting cirrhotic patients to an ICU after intermediate/high risk surgery.
CLEFT PALATE AND LIP REPAIR
Ranu Jain, MD
BASICS
DESCRIPTION
General
• Cleft palate, along with cleft lip, is among the most common congenital malformations. It is
defined as a defect in palatal growth in the first trimester and can be associated with
various other syndromes.
• Cleft palate is classified and described as follows:
– Primary: Anterior to the incisive foramen. Includes lip and alveolus
– Secondary: Posterior to the incisive foramen. Includes hard palate, soft palate, and the
uvula. Submucous clefts can occur.
– Midline (most common), unilateral, or bilateral
– Complete or incomplete. Depends on whether or not the cleft involves the entire anatomic
structure.
– Occurring with cleft lip (75%)
– Cleft lip occurring without cleft palate; when this occurs, it is unilateral 80% of the time
and bilateral 20% of the time.
• Closure of the soft palate is recommended at 3–6 months of age, and the hard palate around
12–15 months of age. This allows for growth of the soft palate, which is important for
speech development and periosteal maturation. As a result the palate is repaired before
speech evolvement.
– Pharyngoplasty or pharyngeal flaps may be required for the treatment of velopharyngeal
incompetence (incomplete contact between the soft palate and posterior pharynx required
for normal speech and swallowing) secondary to anatomic or neurologic dysfunction. This
is done during the toddler years or later.
– Palatal revision and alveolar bone grafts occur at about 10 years of age.
– Rhinoplasty and maxillary osteotomy to complete repair may take place at 17–20 years of
age.
• Etiology is believed to be multifactorial
– Genetic
– Drugs
– Viruses
– Toxins
– Associated with other syndromes
– Associated with birth defects: Umbilical hernia, clubfoot, limb, and ear abnormalities.
Position
• Supine, with a shoulder roll. Alternatively the Rose position may be utilized (supine with
head over the operating table edge)
• Table rotated 90–180°
Incision
Edges of the cleft palate
Approximate Time
2–4 hours
EBL Expected
Approximately 50 mL
Hospital Stay
Overnight stay
• Dingman mouth gag
• Oropharyngeal pack
EPIDEMIOLOGY
Prevalence
• Cleft lip and palate, together, comprise approximately 1:700 births worldwide.
• Cleft palate alone is approximately 1:2500 births.
Prevalence
• More common in males than females
• Siblings and offspring of patients with cleft lip or palate are at greater risk.
Morbidity
• Recurrent ear infection with effusion is reported in 90% of children with cleft palate. It is
due to abnormal compliance and insufficient ventilation of the Eustachian tubes.
• If the cleft palate is associated with cleft lip, the defect may expose the nasal cavity to the
oral cavity, resulting in swallowing difficulties and failure to thrive, repeated aspiration,
and pulmonary infection.
• Other secondary defects like abnormal dental development, growth of ala nasi, and
velopharyngeal function can also occur.
• Associated with more than 300 syndromes
Mortality
Associated with the surgery: <0.5%
• There is a potential for a difficult airway, especially in patients with syndromes.
• Narcotics should be administered judiciously to avoid respiratory depression and allow for
an awake extubation at the end of the case. Use of regional anesthesia as an adjunct to pain
management can be considered.
SYMPTOMS
• Failure to thrive
• Feeding problems
• Fever may suggest acute infection (ear, pulmonary)
History
• Cleft palate is usually diagnosed in utero, or at birth
• Flow of milk through nasal passages during feeding
• Recurrent ear infections
• History of aspiration pneumonia
Signs/Physical Exam
• Unilateral or bilateral
• Ranges from a small notch in the lip or can extend from the lip through the upper gum and
palate into the bottom of the nose.
• Misaligned teeth
• Change in nose shape; amount of distortion varies
MEDICATIONS
• Antibiotics for ear infection
• Treatment
– Before surgery, the goal is to minimize the chance of aspiration and pulmonary
compromise. Infants are fed in the upright position with either a preemie or infant nipple.
The Haberman nipple is more successful in these patients since they do not have to
generate suction to get fluid from the nipple.
– In patients with repeated episodes of aspiration, feeding may be performed via a
nasogastric tube.
– Bilateral myringotomies with ear tube placement may be placed for recurrent ear
infections.
Labs/Studies
• Diagnosis of cleft palate occurs during examination after birth, whereas the diagnosis of cleft
lip takes place in utero by ultrasound at 18–20 weeks postconception.
• Swallow studies to rule out aspiration
• Cardiac workup in syndromic patients
• Associated anomalies occur 30 times more frequently in patients with isolated cleft palate
than in the noncleft population
– Umbilical hernia
– Clubfoot
– Limb abnormalities
– Middle ear abnormalities
• Syndromes with associated cleft palate and lip
– Pierre Robin syndrome
– Fetal alcohol syndrome
– Goldenhar syndrome
– Treacher Collins syndrome
– Nager syndrome
– Down syndrome
TREATMENT
Premedications
Since the surgery is done around 6 months of age, the child may begin to have stranger
anxiety. Consider premedicating with oral midazolam.
• If associated with other syndromes, parents should be informed about the possibility of
difficult intubation and need for postoperative intubation.
• Blocks for postoperative pain control.
Antibiotic prophylaxis may be needed if cardiac abnormalities are present
INTRAOPERATIVE CARE
Monitors
• Skin/axillary/rectal temperature probes may be used instead of oral/nasal probe.
• Additional invasive monitoring may be needed, depending on comorbidities.
• Induction can be performed with an inhalational or IV technique (if an IV is in place).
• Airway obstruction can result in infants with a hypoplastic mandible and wide cleft palate;
the tongue can prolapse into the nasopharynx. If there is difficulty with mask ventilation, an
oral airway may be used.
• A difficult airway should be considered in patients with syndromes (Pierre Robin, Treacher
Collins).
– Be prepared to perform an awake fiberoptic intubation.
– If an inhalational induction was performed and the patient is adequately spontaneously
ventilating, supplemental IV sedation may be administered while a fiberoptic
bronchoscopy is performed.
– Elective tracheostomy may be considered in patients with severe airway abnormalities.
• An oral RAE is commonly utilized and taped to the middle chin line. Additional measures,
such as benzoin and op-sites, may be used to secure the tube.
Maintenance
• The eyes should be securely taped and lubricated, as appropriate, to prevent trauma.
• A balanced technique with volatile inhalation agents, opioids, and possibly nondepolarizing
muscle relaxation.
• A mouth gag is placed, along with a throat pack to provide good surgical visualization. This
apparatus has a groove for the endotracheal tube and should sit in the groove without being
occluded. Pay special attention to breath sounds and chest compliance during placement of
the gag, as malposition can lead to partial or complete obstruction of the tube. The gag may
also cause decreased perfusion of the tongue; it should be released intermittently to allow
reperfusion.
• Be aware of position changes. Flexion and extension of the neck may cause endobronchial
intubation or inadvertent extubation.
• Normothermia. A warming blanket should be used to prevent hypothermia. Hypothermia
can delay emergence as well as cause metabolic acidosis (nonshivering thermogenesis of
brown fat) with resultant respiratory and cardiac depression.
• Blood loss. Although blood loss is rarely >10%, it should be monitored and transfusion
should be considered when significant.
• Local anesthetic infiltration done by the surgeon can provide postoperative pain control.
• Nasopalatine and palatine nerve blocks (performed either by the surgeon or the
anesthesiologist) can provide pain control of the hard and the soft palatal tissue, whereas an
infraorbital nerve block can provide pain control for cleft lip surgery.
• If muscle relaxation was administered, adequate reversal with sustained tetany and train of
four should be ensured prior to extubation.
• Prior to extubation, the oropharynx should be gently suctioned with a soft catheter and the
throat pack must be removed. The surgeon can perform the suctioning with the mouth gag
in place under direct visualization.
• Arm restraints or “welcome” sleeves are routinely used to keep the patient’s hands away
from the face.
FOLLOW-UP
• Medications: NSAIDS may increase bleeding and are typically avoided. Consider the use of
low-dose narcotics, titrated to effect.
• Labs: If the surgery was uneventful, none are indicated. Consider hemoglobin if there was
increased bleeding.
• Consults: If available, consider a pain consult.
BED ACUITY
• Hospital stay is warranted in a telemetry unit until the patient’s pain is controlled by oral
pain medication and the child is able to tolerate oral feeds.
• An intensive care unit (ICU) bed may be required for patients with ongoing airway
obstruction for observation and management.
COMPLICATIONS
Surgical complications
• Infection
• Bleeding, with or without aspiration
• Delayed healing
• Pneumonia
• Airway obstruction can occur from closure of cleft structures, edema (subglottic, flap,
tongue), increased oral secretions, posterior displacement of the tongue, or overlooked
throat pack. A long traction suture is placed in the tongue and tied loosely; if needed,
traction on the tongue suture stimulates respiration and clears the secretions. The use of an
oral pharyngeal airway is not recommended.
REFERENCES
1. Mossey PA, Little J, Munger RG, et al. Cleft lip and palate. Lancet. 2009;374(9703):1773–
1785.
2. Vlastos IM, Koudoumnakis E, Houlakis M, et al. Cleft lip and palate treatment of 530
children over a decade in a single center. 2009;73(7):993–997WW. Vander Poorten V,
Ostyn F, Van Kerckhoven W, et al. The Leuven staged supraperiosteal retropositioning
repair: Long-term velopharyngeal function in non-syndromic cleft palate. B-ENT.
2006;2(Suppl 4):35–43.
3. Nasser M, Fedorowicz Z, Newton JT, et al. Interventions for the management of submucous
cleft palate. Cochrane Database Syst Rev. 2008;23(1):CD006703.
ADDITIONAL READING
• “A Practice of Anesthesia for Infants and Children" By Charles J Cote, Jerrold Lerman, I.
David Todres. Saunders/Elsevier (2009).
• Hypothermia
• Pierre Robin syndrome
CLINICAL PEARLS
• Syndromes may make intubation difficult; consider performing an awake fiberoptic
intubation.
• Airway obstruction after extubation requires careful attention.
• Pain control during the postoperative period may be accomplished by nerve blocks.
Nasopalatine and palatine nerve blocks can be performed for soft and hard palate surgery;
infraorbital blocks for cleft lip surgery.
CLOSING CAPACITY
Kenneth R. Moran, MD
BASICS
DESCRIPTION
• Closing capacity is the smallest lung volume that is required to prevent closure of small
airways or alveoli. Closing Capacity (CC) = Residual Volume (RV) + Closing Volume (CV)
• The ability to recognize patients at risk for decreased functional residual capacity (FRC) or
increased CC can be useful to predict the degree to which intraoperative management will
affect airway closure, shunt, and Alveolar-arterial (A-a) gradient.
• Bronchioles distal to the 11th generation are <1 mm and do not have rigid cartilaginous
support to keep them open. These distal airways are subject to opposing forces that can
prevent or maintain patency (1):
– Outward elastic recoil of the chest wall (preventing airway collapse) and the opposing
inward pull of the lung parenchyma; the sum of these opposing forces determine the
intrapleural pressure (Ppl) at varying lung volumes. Note: The FRC is equal to the volume
at which the Ppl is zero.
– Surfactant maintains small airway patency by decreasing surface tension and collapse.
– If the CC is greater than the total lung volume at any given point (inhalation or
exhalation), premature airway closure results in distal lung segments that continue to
receive perfusion, but are no longer ventilated. The shunting of unoxygenated blood from
these segments into the arterial circulation can contribute to hypoxemia.
• CC describes the lung volume at which any further exhalation results in airway closure. CV
is the volume of air that can still be exhaled from the point of CC until only RV remains,
during maximal exhalation. CV is usually less than the functional residual capacity (and
expiratory reserve volume) in a healthy young adult in the standing position.
• FRC is the resting point at the end of normal exhalation where elastic recoil of the chest
equals inward lung recoil. It is the volume of air that remains in the lungs at the end of a
normal tidal volume (TV) exhalation; FRC = ERV + RV.
– RV is the volume of air left in the lung after a maximal expiration. During forced
expiration, before exhalation to RV, small airway closure begins to occur as the CC is
reached.
• CC versus FRC.
– CC < FRC. Small airways remain patent during normal TV. In young healthy patients,
lung volume at the end of resting exhalation (FRC) is greater than CC (Figure 1).
FIGURE 1. Normal pulmonary function and its relationship to closing capacity. CC is represented by the dotted line.
– CC > FRC. If pathological or mechanical changes result in a reduction in FRC or an

increase in CC, airway closure may occur during normal TV breathing (Figure 2).
FIGURE 2. A graphical representation of respiratory function in a person with decreased FRC and/or increased CC. Note
how normal TV breaths result in lung volumes below CC. CC is represented by the dotted line.
• Since CC = CV + RV, changes in RV affect FRC and CC equally (FRC = ERV + RV). Thus,
either a decrease in ERV or an increase in CV closes the gap between FRC and CC. An
increase in CC signifies that airway closure occurs at higher lung volumes; in other words,
while exhaling toward RV, closure occurs earlier.
– CV increases with age, smoking, and COPD (2); factors that affect lung parenchyma
elasticity. These airways become dependent on greater lung volumes to keep them open;
as a result the CC rises (1). Additionally, it should be noted that CV is not dynamic like
ERV and FRC and is unaffected by body positioning.
– ERV (and FRC) is decreased in obesity, head down positioning, and general anesthesia as a
result of decreased lung compliance. This is caused by pressure from adipose tissue on the
lungs, diaphragm, and abdomen (3).
ANATOMY
• Bronchioles
• Alveoli
• Ribs
• Muscles of respiration
– Diaphragm
– Intercostal muscles
– Scalene muscles
– Sternocleidomastoid muscles
• Age, smoking, and lung disease can lead to a decrease in lung recoil (the force pulling the
lung into itself) and an increase in lung compliance.
• Changes in collagen fibrils and elastin in the lungs account for the increase in compliance
and permit the lungs to inflate to larger volumes with less pressure. This results in larger
lung volume requirements to keep small airways open and increases CC (1). Early airway
closure, like atelectasis, can result in ventilation/perfusion (V/Q) mismatch where areas of
unventilated lung may continue to receive perfusion. Areas of perfusion without ventilation,
also known as shunt, can contribute to hypoxemia.
• Aging increases both RV and CV. While changes in RV affect CC and FRC equally, an
increase in CV will increase CC toward FRC (Figure 3).
• CC, while supine, increases to equal FRC in one’s mid-forties and becomes greater than FRC,
even when standing, in one’s mid-sixties. Eventually, exhalation of normal TV can bring
lung volumes below CC resulting in airway closure during normal breathing (4).
• Obesity does not affect the CC. It, however, diminishes chest and lung compliance, which
ultimately decreases FRC. This reduction in FRC results from a reduction in ERV; RV is not
affected (3). An obesity-associated reduction in FRC can result in lung volumes below the
CC and early airway closure.
• Decreased FRC from supine positioning and general anesthesia can result in early airway
closure when FRC falls below CC (CC > FRC).
• General anesthesia reduces FRC by 0.4–0.5 L (5)[A]; this is presumed to occur from a loss of
respiratory muscle tone and decreased chest wall compliance. Additionally, laying supine
can reduce FRC by up to 1 L. When the FRC is reduced in this manner below CC, air
trapping and shunting occurs. This has been hypothesized to be the cause of increased A-a
gradient [P(A-a)O2] during surgery (6). This effect is further enhanced in patients with a
baseline diminished FRC or elevated CC. Position and anesthesia do not affect the CC;
however, they reduce the FRC, bringing it closer to the CC.
• PEEP is often implemented to increase the FRC and improve the A-a gradient [P(A-a)O2] (5)
[A]. However, its use is limited since PEEP affects upper lung zones greater than lower
zones. Conversely, airway closure occurs to a greater degree in the lower lung zones. In
addition, an increase in intrathoracic pressure from PEEP may impede venous return and
result in deterioration of cardiac output.
• “Alveolar recruitment” may be achieved by applying a limited number of double TV breaths
in an attempt to reopen closed airways and alveoli. An inflation pressure up to 30–40 cm
H2O may be required (7)[A]. This must be done with caution as hemodynamic instability
can result from an increase in intrathoracic pressure and decreased venous return.
• Sitting a patient upright, or reverse Trendelenburg, >30° may increase FRC. This is useful
when trying to maximize respiratory function in the immediate postoperative period
including extubation.
• FRC remains decreased into the postoperative period. With reduced FRC, lung volumes are
more likely to fall below CC during resting TVs, contributing to post-operative hypoxemia.
EQUATIONS
• CC = CV + RV
• FRC = ERV + RV
REFERENCES
1. Wahba WM. Influence of aging on lung function—Clinical significance of changes from age
twenty. Anesth Analg. 1983;62:764.
2. ilic-Emili J, Torchio R, D’Angelo E. Closing volume: A reappraisal (1967–2007). Eur J Appl
Physiol. 2007;99:567–583.
3. Jubber AS. Respiratory complications of obesity. Int J Clin Pract. 2004;58:573.
4. Leblanc P, Ruff F, Milic-Emili J. Effects of age and body position on “airway closure” in
man. J Appl Physiol. 1970;28:448–451.
5. Hedenstierna G, Edmark L. The effects of anesthesia and muscle paralysis on the
respiratory system. Intensive Care Med. 2005;31:1327–1335.
6. Wahba RWM. Perioperative functional residual capacity. Can J Anaesth. 1991;38:384–400.
7. Rothen HU, Sporre B, Engberg G, et al. Re-expansion of atelectasis during general
anesthesia: a computed tomography study. Br J Anaesth. 1993;71:788–795.
8. Nield MA, Hoo GWS, Roper JM, et al. Efficacy of pursed-lips breathing—A breathing
pattern retraining strategy for dyspnea reduction. J Cardiopulm Rehabil Prev.
2007;27:237–244.
ADDITIONAL READING
• Alveolar-arterial gradient
• Spirometry
• V/Q matching
CLINICAL PEARLS
• An increase in CC signifies that airway closure occurs at higher lung volumes. In other
words, while exhaling, closure occurs earlier.
• Premature small airway closure occurs as a result of decreased FRC and/or increased CC. It
results in unventilated distal segments of lung that contribute to shunt and hypoxemia.
• It is important to recognize patients at risk for early distal airway closure, such as those with
advanced age, obesity, lung disease, or smoking history.
• Patients with advanced COPD use pursed lip breathing to stabilize small airways and
maintain their patency (8)[A]. Recognizing this breathing pattern can help identify patients
with advanced lung disease.
COCAINE ABUSE
BASICS
DESCRIPTION
• Cocaine is one of the oldest known psychoactive substances. Coca leaves have been chewed
and ingested for thousands of years and the purified chemical, cocaine hydrochloride, has
been a substance of abuse for more than 100 years (1).
• Cocaine is available as a street drug in the form of a fine, white, crystalline powder. It is
known as “coke,” “C,” “snow,” “flake,” or “blow.” It is frequently mixed with amphetamine
or heroin; the latter combination is known as a “speedball.”
• Today, it is used, legitimately, for its combined local anesthetic and vasoconstrictive effects
(e.g., eye and ENT procedures and laceration repair in the emergency department); and is a
Schedule II drug. It has been largely replaced by other local anesthetics that provide the
same effects without the addictive potential.
• Mechanism of action. Blocks the reuptake of norepinephrine into the sympathetic nerve
terminals; thus creates a sympathomimetic state (2).
• Classification. Local anesthetic; ester
• Pharmacokinetics
– Peak plasma levels are attained within 1–3 minutes when inhaled or administered
intravenously.
– Plasma half-life ranges from 60 to 90 minutes
– Metabolism is via plasma esterases. By-products include benzoylecgonine, ecgonine
methyl ester (EME), and norcocaine. Some metabolites can be detected in the urine 3–5
days after ingestion.
• Routes of administration include oral, intravenous, and transmucosal.
• CNS
– Acute effects: Euphoria and heightened perception of space or time, irritability,
restlessness, hyperthermia, and seizures (2).
– Chronic effects: Physical dependence and addiction develop rapidly. Focal neurological
deficits and coma have been reported; potential causes include vasoconstriction (transient
ischemic attacks) and cerebral hemorrhage.
– Withdrawal symptoms include fatigue, mental depression, and drug cravings.
• Cardiac system
– Acute effects: Tachycardia, hypertension, and coronary artery spasm can result in
myocardial ischemia and/or myocardial infarction. Prolonged QT interval and ventricular
arrhythmias can also result (3).
– Chronic effects: Left ventricular hypertrophy, systolic dysfunction, and dilated
cardiomyopathy.
• Respiratory system
– Acute effects: Nonspecific respiratory complaints may be reported. Nasal bleeding and
perforation of the nasal septum can result from snorting cocaine. “Crack lung” is a form of
acute lung injury that has been reported after cocaine abuse (4).
– Chronic effects: Diffuse alveolar infiltrates, alveolar damage, pulmonary infarction, and
noncardiogenic pulmonary edema have been reported.
• Low birth weight and premature delivery
• Fetal intrauterine growth retardation (IUGR) has been attributed to decreased uteroplacental
perfusion.
• Cognitive impairment and attention deficits are frequently encountered in children born to
cocaine-abusing mothers.
• Cocaine abuse among school children should not be overlooked. Recent data suggest
declining numbers of 30-day prevalence of cocaine abuse among 8th, 10th, and 12th
graders from its peak use in the late 1990s, as well as significant declines in past-month use
among 10th and 12th graders from 2008 to 2009 (1).
• Anesthetic implications of acute cocaine toxicity include the following:
– Cardiac. An increased risk of perioperative myocardial ischemia, congestive heart failure
(CHF), and ventricular arrhythmias.
– CNS. An increased minimum alveolar concentration (MAC) requirement of inhaled
anesthetic.
• Preoperative evaluation
– Obtain a detailed and complete history of substance abuse in every patient.
– In patients with a positive history of abuse, associated comorbidities such as hypertension,
coronary artery disease (CAD), arrhythmias, and CHF should be assessed.
– Examine the nares
– Labs. Urine drug screening can detect metabolites for up to 72–96 hours based on the half-
life of the metabolite being tested.
• Previously, cancellation was recommended for elective surgery in the event of a positive
drug screening due to the potentially increased risk of perioperative myocardial ischemia.
Recent evidence suggests that general anesthesia for elective procedures is possibly safe if
the patient lacks symptoms and signs of acute cocaine toxicity on physical examination and
has a QT interval <500 ms (5).
• Perioperative care
– Exercise caution when using beta-blockers in the context of acute cocaine toxicity.
Unopposed alpha activity can result in coronary vasoconstriction.
– Myocardial ischemia may be managed with short-acting beta-blockers (esmolol) and
mixed alpha and beta-blockers (labetalol) to treat cocaine-induced myocardial ischemia.
– Hypotension during the course of the anesthetic is usually resistant to treatment with
indirect-acting vasopressors (e.g., ephedrine). It is better treated with direct-acting
vasopressors (e.g., neosynephrine).
– If a nasal intubation is planned, be aware that the nasal mucosa can be atrophic and there
is an increased prevalence of nasal perforation among cocaine abusers.
– Regional anesthesia may be complicated by the following:
Combative behavior. Adequate sedation should be provided.
Altered pain perception
Ephedrine-resistant hypotension with spinal or epidural anesthesia. Treatment should
include intravenous fluid bolusing and direct-acting alpha agonists.
REFERENCES
1. National Research Report [http://www.nida.nih.gov/researchreports/cocaine]. Rockville,
MD: National Institute of Drug Abuse.
2. lkassabany NM. Evidence Based Practice of Anesthesiology. 2nd ed. Fleisher LA, editor.
Philadelphia, PA: Elsevier; 2010.
3. Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med.
2001;345(5):351–358.
4. Baldwin GC, Choi R, Roth MD, et al. Evidence of chronic damage to the pulmonary
microcirculation in habitual users of alkaloidal (“crack") cocaine. Chest.
2002;121(4):1231–1238.
5. Hill GE, Ogunnaike BO, Johnson ER. General anaesthesia for the cocaine abusing patient. Is
it safe? Br J Anaesth. 2006;97(5):654–657.
ADDITIONAL READING
• Hernandez M, Birnbach DJ, Van Zundert AA, Anesthetic management of the illicit-
substance-using patient. Curr Opin Anaesthesiol. 2005;18:315–324.
• Kuczkowski KM. The cocaine abusing parturient: A review of anesthetic considerations. Can
J Anaesth. 2004;51(2):145–154.
• Marijuana abuse
• Alcohol abuse
• The addicted anesthesia provider
CODES
ICD9
• 304.20 Cocaine dependence, unspecified
• 305.60 Cocaine abuse, unspecified
ICD10
• F14.10 Cocaine abuse, uncomplicated
• F14.20 Cocaine dependence, uncomplicated
CLINICAL PEARLS
• Cocaine abuse is often a mixed substance abuse problem. Inquire about other common drugs
of abuse and their respective adverse effects in the perioperative period.
• Cocaine abusers are at increased risk for HIV and viral hepatitis. This risk stems not only
from sharing contaminated needles but also from engaging in risky behaviors as a result of
intoxication.
• The perioperative setting can be very helpful in providing drug counseling and referral to
addiction clinics and behavioral intervention. Do not waste this opportunity.
• Crack is the free base of cocaine that can be smoked. It is named after the sound it makes
during manufacture and smoking. The onset of action is very quick and the peak effect is 1–
3 minutes. The resulting euphoria (the cocaine high) is the result of release of dopamine in
the CNS. It is often mixed with other addictive substances. “Speedballing” is mixing cocaine
with heroine that will obviously have more adverse effects.
COLLOIDS
Seth R. Cohen, DO
Raymond M. Planisic, MD
BASICS
DESCRIPTION
• Colloid solutions are comprised of large molecules dissolved in a crystalloid solution; when
administered these molecules help maintain intravascular oncotic pressure.
• They are divided into two groups
– Natural colloids, such as albumin
– Semisynthetic colloids, including gelatins, dextrans, and hydroxyethyl starches
• The goal of fluid administration is to improve organ perfusion through optimization of
volume status (1)[A]. Colloids can be utilized perioperatively to aid volume expansion.
• Total body water (TBW)
– Comprises 60% of body weight and is measured in kilograms.
– Two-thirds is intracellular fluid (ICF)
– One-third is extracellular fluid (ECF); of which 80% is interstitial, while the remainder is
intravascular.
– Varies with age, sex, pathologic conditions, and other factors.
• Starling forces define flow from intravascular to interstitial/extravascular space.
Intravascular oncotic pressure opposes the filtration or hydrostatic process (see equations).
Net driving force or net filtration is determined by the following factors (pressures are
measured in mm Hg).
– Capillary hydrostatic pressure (Pc) favors filtration across the capillary endothelium into
the interstitium.
– Interstitial hydrostatic pressure (Pi) drives fluid back into the capillaries and therefore
opposes filtration of capillary fluid into the interstitial fluid.
– Capillary oncotic pressure prevents movement of solvent and small ions across the
capillary membrane, thereby opposing filtration.
– Interstitial oncotic pressure prevents movement of solvent and small ions across the
capillary membrane, favoring filtration.
– Filtration coefficient is comprised of capillary surface area and capillary hydraulic
conductance. Increased water permeability is demonstrated by an increased value.
– Reflection coefficient functions to account for the small permeability of albumin and other
proteins. Protein permeability results in greater than expected oncotic pressure in
interstitial fluids.
• Crystalloids are composed of ionized salts and water-soluble molecules dissolved in water.
– The salts and molecules provide electrolytes and osmolarity but not oncotic pressure.
– Crystalloids can freely diffuse across intravascular endothelial walls into the interstitium.
– In theory, ~20–30% of crystalloid solution infused will remain intravascular.
• Colloids are composed of large molecules that provide oncotic pressure and are suspended in
a crystalloid solution. The molecules do not easily cross semipermeable membranes.
– Molecular weight (MW) of the colloid is proportional to size; larger molecules are less
easily filtered (higher reflection coefficient).
– Those molecules that are not filtered by the kidneys are eventually taken up by the
reticuloendothelial system or excreted through the gut.
– Balanced solutions (isotonic) have less adverse effects than normal saline (hyperchloremic
metabolic acidosis).
• Albumin (MW 69 kDa) is made from pooled human plasma that has been heated (60°C for
10 hours), screened for viruses, and ultrafiltered.
– Monomer; all molecules have the same size.
– Available in a 5% (isooncotic) for volume expansion and 25% (hyperoncotic) solutions for
hypoalbuminemic states (1)[A].
– Expanding effects may last between 16 and 24 hours.
• Gelatins are produced from bovine collagens. While they provide high osmotic pressure,
their low molecular size allows them to be rapidly filtered by the glomeruli; overall they
produce similar volume expansion to crystalloids.
– Least likely of the colloids to affect hemostasis.
– Half-life has been reported to be 3.5–4 hours.
– New generation gelatins (e.g., Polygeline, Plasmagel) have been developed and have
higher molecular size (greater oncotic pressure), but are not commonly used in the US.
• Dextrans are highly branched polysaccharide molecules produced by bacteria containing
dextran sucrose that grows on sucrose medium.
– Available in 10% dextran 40 (MW 40 kDa) and 6% dextran 70 (MW 70 kDa). Dextran 70
resembles human albumin in regard to MW.
– Dextran 40 promotes microvascular blood flow in vascular surgery by decreasing red
blood cell (RBC) aggregation, but is rapidly filtered by the kidneys and not used for
volume expansion.
– Dextran 70 is capable of up to 100–150% volume expansion with maximal expansion
reached ∼1 hour after infusion. Dextran 70 has expanding effects that last between 6 and
12 hours.
• Hydroxyethyl starches are made of amylopectin modified through hydrolysis and
hydroxyethyl substitution.
– Capable of up to 100% volume expansion.
– With greater substitution, the molecule becomes more resistant to degradation in the body
and the duration of its expansion effects also increase compared to other colloids.
– Hespan is presented in normal saline, while Hextend comes in a balanced electrolyte
solution (1).
– Believed to have anti-inflammatory properties and to preserve intestinal microvascular
perfusion in endotoxemia.
– Does not appear to interfere with coagulation at doses <50 mL/kg.
– Molecules <50,000 kDa are excreted by the urine within 24 hours; the larger molecules
are slowly degraded enzymatically to molecules small enough to be excreted.
• The most commonly accepted indications of colloid administration is for the treatment of
hypoalbuminemic states in the presence of salt/water overload (1) and replacing blood loss
prior to blood administration (2). Hypoalbuminemia can result from reduced production
(liver disease) or increased loss (renal disease). Serum albumin normally comprises ∼50–
60% of plasma proteins. It functions as a carrier of intermediate metabolites, trace metals,
drugs, dyes, fatty acids, hormones, and enzymes, and hence affects the transport,
inactivation, and/or exchange of tissue products.
• Adverse effects of colloids
– Increased vascular permeability is often seen in the setting of surgical tissue trauma,
hypoperfusion states, trauma, sepsis, and burns. This can result in oncotic molecules
entering the interstitial compartment and edema formation (net driving force favors fluid
movement out of the intravascular compartment).
– The use of colloids in trauma patients may be associated with an increased mortality,
especially in patients with traumatic brain injury (1).
– Volume overload
• Gelatins
– Greatest risk of anaphylactic reactions.
– Theoretical risk of Creutzfeldt–Jacob disease (CJD) (2).
• Dextrans
– Can cause coagulopathies from reduced platelet adhesiveness and dilution of factor VIII as
well as fibrinolysis.
– Can interfere with the ability to cross-match blood, by coating the RBC surface. If
administered, the blood bank should be informed.
– May result in acute renal failure due to accumulation of molecules in the renal tubule.
– Anaphylaxis can be reduced by pretreating with dextran 1, which acts as a hapten to bind
antibodies.
• Hespan
– Coagulopathies can occur from reduced circulating factor VIII and von Willebrand factor
levels and impaired platelet function; manifests as a prolonged PT and PTT.
– Pruritus
– Anaphylaxis
– Renal impairment, higher creatinine levels, oliguria, and acute renal failure in patients
who were critically ill with existing renal impairment.
– Can increase amylase levels, which is typically not clinically significant.
– May increase the erythrocyte sedimentation rate.
• Controversy exists over the use of colloids for volume resuscitation. Outcome studies have
not supported its use over crystalloids.
• Arguments for the use of colloids
– Venodilation from anesthetics can decrease preload and exacerbate hypovolemic states. If
necessary, colloids can be used for rapid expansion of plasma volume, while limiting total
volume load and peripheral edema (2). Traditionally, intraoperative blood loss has been
replaced with 3 mL crystalloids or 1 mL colloids for every 1 mL blood loss (3).
– Theoretically can increase oncotic pressure and provide greater volume expansion than
crystalloids.
– Do not require special preparation and are immediately available while awaiting blood
products.
– May be utilized in Jehovah’s witnesses (though some object to albumin).
– Less peripheral and pulmonary edema with associated impaired function. In particular,
during intra-abdominal procedures, intestinal edema may result from excessive fluid
administration, which has been associated with significant postoperative complications (3)
[A].
• Arguments against colloids
– Recent Cochrane review and Saline versus Albumin Fluid Evaluation (SAFE) Study
Subgroup analysis have found a possible increase in mortality in using colloids in trauma,
especially patients with traumatic brain injury (1)[A].
– Cochrane subgroup analysis has also linked colloid use with an increased risk of death in
hypoalbuminemic and burn patients (4).
– The use of crystalloids remains the mainstay in acute resuscitation of the trauma patient,
per advanced trauma life support (ATLS) guidelines (5).
EQUATIONS
Jv = k[(Pc – Pi) – σ(πc – πi)], where Jv = vascular flow, k = filtration coefficient, Pc =
intravascular hydrostatic pressure, Pi = interstitial hydrostatic pressure, σ = reflection
coefficient of the colloids, π c = intravascular colloid pressure, πi = interstitial colloid
pressure (4).
REFERENCES
1. Vercueil A, Grocott MP, Mythen MG. Physiology, pharmacology, and rationale for colloid
administration for the maintenance of effective hemodynamic stability in critically Ill
patients. Transfus Med Rev. 2005;19:93–109.
2. Grocott MP, Mythen MG, Gan TJ. Perioperative fluid management and clinical outcomes in
adults. Anesth Analg. 2005;100:1093–1106.
3. Chappell D, Jacob M, Hofmann-Kiefer K, et al. A rational approach to perioperative fluid
management. Anesthesiology. 2008;109:723–740.
4. Finfer S, Bellomo R, McEvoy S, et al. Effect of baseline serum albumin concentration on
outcome of resuscitation with albumin or saline in patients in intensive care units: Analysis
of data from the saline versus albumin fluid evaluation (SAFE) study. Br Med J.
2006;333(7577):1044.
5. Van Den Elsen MJ, Leenen LP, Kesecioglu J. Hemodynamic support of the trauma patient.
Curr Opin Anaesthesiol. 2010;23:269–275.
CLINICAL PEARLS
• Although colloids are more expensive, they can produce a quicker restoration of
intravascular volume status.
• The SAFE study showed no benefit or increased mortality in use of albumin versus saline in
an intensive care unit (ICU) setting (5)[A].
• Adverse effects of colloid use include renal impairment, decreased hemostasis, anaphylactic
reactions, and pruritus (1,4)[A].
• Choice of fluids remains controversial and pros/cons must be weighed with each fluid type
and clinical situation.
• Some authors have advised the use of crystalloid to replace fluid losses from insensible
losses and urinary output, while replacing blood loss and protein-rich fluid shifts with
colloids (4).
• Monitors to assess volume status. Central venous pressure (CVP) and pulmonary artery
occlusion pressure (PAOP) are most commonly used to guide volume status, but do not
always reliably predict fluid response. Other measures include cardiac output or index,
pulse pressure variation, stroke volume variation, systolic pressure variation, and
esophageal Doppler. Lactate levels and base deficit are signs of tissue perfusion (5)[B].
• The ideal colloid should be:
– Capable of remaining in the intravascular compartment
– Non-toxic, non-immunogenic
– Isotonic
– Easy to store
– Inexpensive
COLONOSCOPY
Edna Ma, MD
BASICS
DESCRIPTION
General
• A colonoscopy is an endoscopic procedure performed with a fiberoptic camera to examine
the colon, from the anus to the distal portion of the small bowel (e.g., terminal ileum).
• Colonoscopies are indicated for colorectal cancer screening, positive fecal occult blood, GI
hemorrhage, removal or biopsy of small polyps, change in bowel habits (associated with
inflammatory bowel disease or malignancy), or decompression (as with colonic pseudo-
obstruction).
• Colonoscopies can be performed under topical anesthesia with or without conscious
sedation (benzodiazepines and opioids) or deep sedation (typically propofol).
Position
Lateral decubitus
Approximate Time
15–45 minutes
EBL Expected
None to minimal, unless associated with underlying condition (e.g., GI hemorrhage or
coagulopathy).
Hospital Stay
• The majority of colonoscopies are outpatient procedures.
• For inpatients, the duration of the hospital stay depends on the underlying conditions.
• Endoscopic colonoscope
• Irrigation
• Suction
• India ink for tattooing polyp site
EPIDEMIOLOGY
Prevalence
• Incidence of colon cancer increases with age, beginning around 40 years of age, and is
higher in men than in women (60.4 in men versus 40.9 in women, per 100,000, per year)
(1).
• Propofol sedation is utilized in ∼25% of routine endoscopic procedures, of which the
majority are performed by anesthesia providers.
• In 2003, Medicare charges for code 00810 were 106 per case; this compared to an average
of 400 per case from commercial insurers (2).
• In Medicare beneficiaries, the number of colonoscopy cases performed by anesthesia
providers more than doubled between 2001 and 2003 to 700,000; this corresponded to
$80,000,000 in charges (2).
Prevalence
The lifetime risk of being diagnosed with colorectal cancer is 5.9% for men and 5.5% for
women. This amounts to ∼145,290 new cases and 55,290 deaths annually.
Morbidity
• Colorectal cancer survival is correlated to the stage of the disease at the time of diagnosis.
Approximately 65% of patients present with advanced disease.
• Colonoscopy is a low-risk surgical procedure, but it has the potential for perforation and
bleeding.
• Anesthetic risks include those associated with sedation, allergies, and nausea.
Mortality
• Colorectal cancer is the third most common cancer in both men and women and the third
leading cause of cancer-related mortality in men and women in the US (3).
• Five-year survival for cancer limited to the bowel wall at the time of diagnosis approaches
90%. When lymph nodes were involved, the 5-year survival dropped to 35–60%; and in the
presence of metastatic disease it became less than 10% (4).
• Efficiency, safety, and patient satisfaction must be provided; standard ASA monitoring as
well as airway equipment and emergency medications must be available.
• Patients arriving for routine screening colonoscopies often present after having bowel
preparations and they may be dehydrated, particularly for cases scheduled later in the day.
• Patients suspected of having a history of colon cancer may have mild anemia. The anemia
may be more severe depending on the extent of disease and may warrant transfusion.
• Risk of aspiration is more significant for patients with a history of obstruction (including
pseudo-obstruction) as bowel contents may travel in a retrograde direction.
• Decreases in functional residual capacity (FRC) are associated with cephalad displacement
of the diaphragm, which is more pronounced during insufflation of the colon and in patients
with severe obstruction or impaction.
SYMPTOMS
Anemia (occult blood, indicating proximal colon involvement, or “bright red blood per
rectum” [BRBPR], suggesting distal colon lesions). This can manifest as pallor or fatigue, or in
more severe cases, with lightheadedness, shortness of breath, or chest pain.
History
• A full anesthetic evaluation is necessary; patients who present for anesthetic management
often have significant comorbidities.
• Maintain a high index of suspicion for colon cancer in elderly patients that present with a
change in bowel habits, a history of fatigue or weight loss, particularly if there is a strong
family history of colorectal cancer.
Signs/Physical Exam
• A thorough airway exam is important in the event that the airway needs to be supported or
secured.
• Auscultation of the heart and lungs at a minimum is necessary for each patient.
MEDICATIONS
• Patient specific; related to patient comorbidities.
• Chemotherapeutic agents in patients with a history of colon cancer.
Labs/Studies
• Preoperative laboratory studies for routine screening and ambulatory cases are not typically
needed. If available, however, they should be reviewed.
• For inpatients, a hemoglobin level, coagulation panel and electrolyte values may have
already been obtained and should be reviewed; consider ordering if appropriate.
Concomitant organ dysfunction may occur if metastatic colon cancer is present. Primary
organs involved include the liver, lung, and bones.
TREATMENT
Premedications
• Anxiolytics, analgesics as needed. Short acting medications (e.g. midazolam, fentanyl)
should be utilized.
• GI prophylactic medications include acid reduction agents.
• Realistic sedation goals should be discussed, including the possibility of recall.
• If a patient has severe anemia, a blood transfusion may be necessary.
INTRAOPERATIVE CARE
• Monitored anesthesia care (MAC) is commonly provided for screening and outpatient
procedures using propofol; common adjuvants include midazolam and fentanyl. The goal is
to maintain spontaneous ventilation.
• General anesthesia (GA). Despite maintaining spontaneous ventilation and not
instrumenting the airway, some anesthetists consider the depth of “sedation” needed for a
colonoscopy as falling under the criteria of a general anesthetic. Inpatients may need their
airway secured with an endotracheal tube.
Monitors
• IV access
• MAC: Supplemental oxygen with nasal cannula or face mask. Titration of sedation can be
performed with benzodiazepines, opioids, propofol, or ketamine.
• GA: Spontaneous ventilation, laryngeal mask airway, or endotracheal tube.
Maintenance
• Sedation is typically performed with IV medications and titrated to maintain spontaneous
ventilation.
• Volatile agents may be administered via a face mask or an endotracheal tube.
• MAC and deep sedation: Re-orient the patient.
• GA with an endotracheal tube: Standard extubation criteria.
FOLLOW-UP
BED ACUITY
• The majority of colonoscopies are done on an outpatient basis.
• Comorbid conditions should dictate the level of care for inpatients.
• Intensive care unit (ICU) patients may have their procedure performed at the bedside to
avoid transport.
ANALGESIA
Not typically needed
COMPLICATIONS
• Surgical-related
• Perforation from biopsy instrumentation
• Bleeding from polypectomy site
• Postpolypectomy syndrome (also known as transmural burn syndrome)
• Infection from inadequate sterilization equipment
• Anesthetic-related
• Airway obstruction and desaturation
• Nausea
PROGNOSIS
Survival is directly related to early detection, cancer type, and stage. Tumors that have not
invaded the muscular mucosa (TNM stage T1–2, N0, M0) have a 5-year survival of ∼90% (5).
REFERENCES
1. Report: Number 1. AHCPR Publication No. 97-0302. Agency for Health Care Policy and
Research, Rockville, MD. http://www.ahrq.gov/clinic/colorsum.htm
2. isenberg J, Brill JV, Ladabaum U, et al. Sedation for gastrointestinal endoscopy: New
practices, new economics. Am J Gastroenterol. 2005;100:996–1111.
3. Cancer Trends Progress Report (http://progressreport.cancer.gov), in 2004 dollars, based
on methods described in Medical Care. 2002;40(8 Suppl):IV-104–117.
4. Jeffery M, Hickey BE, Hider PN. Follow-up strategies for patients treated for non-metastatic
colorectal cancer. Cochrane Database Syst Rev. 2002;(1).
5. esch CE, Benson AB 3rd, Somerfield MR, et al. American Society of Clinical Oncology.
Colorectal cancer surveillance: 2005 update of an American Society of Clinical Oncology
practice guideline. J Clin Oncol. 2005;23(33):8512–8519.
6. Colorectal cancer surveillance: 2005 update of an American Society of Clinical Oncology
practice guideline.
7. Standards of Practice Committee. Sedation and anesthesia in GI endoscopy.
Gastrointestinal Endoscopy. 2008;68(5):815–826. www.theasahq.org
• Upper gastrointestinal endoscopy
• Propofol
CODES
ICD9
V76.51 Special screening for malignant neoplasms of colon
ICD10
Z12.11 Encounter for screening for malignant neoplasm of colon
CLINICAL PEARLS
• Colonoscopies can be performed with topical anesthesia with or without conscious sedation,
or with MAC, deep sedation, or GA.
• “Who is qualified to give propofol?” is a topic that has been addressed by several
committees and even legislative bodies.
• Access to anesthesia providers is a key factor.
• Payor policies also affect the rate of anesthesia provider utilization in different regions of
the country.
• Most insurance carriers and Medicare require that “supporting documentation should
identify patient-specific reasons such as reports from prior endoscopies indicating difficulty
in completing the procedure; or unusual discomfort during the procedure; or evidence of an
unstable medical condition.”
• The routine assistance of an anesthesia provider for average-risk patients undergoing
standard upper and lower endoscopic procedures is believed to be cost-prohibitive.
• A full preoperative history and evaluation as well as consent should be attained on all
patients.
COMBINED SPINAL-EPIDURAL (CSE)
BASICS
DESCRIPTION
• The combined spinal-epidural analgesia (CSE) technique is used to deliver local anesthetic
(LA) (+/– adjuvant medications) into both subarachnoid and epidural spaces in one
multistep procedure.
• Advantages of the CSE technique include the following:
– Rapid onset of analgesia
– Minimal drug dosing
– The flexibility of continuous epidural analgesia (Figure 1).
FIGURE 1. CSE technique: The Tuohy needle is inserted into the epidural space (top left) and a spinal needle is inserted
through it. The pencil-point spinal needle may deform the dura considerably before puncturing it (top middle). After
injection through the spinal needle, it is withdrawn, and an epidural catheter is inserted (bottom left), and the epidural
needle is withdrawn (bottom right). (Adapted from Eisenach JC. Combined spinal-epidural analgesia in obstetrics.
Anesthesiology. 1999;91(1): 299–302).
• CSE kits. A wide variety of commercially available kits can be used. Although they vary by
institution and manufacturer, they contain the following basic standard items:
– Hollow bore epidural needle: To identify and access the epidural space and to function as
an “introducer” needle by which the spinal needle is inserted. Most commonly, a Tuohy
needle (16–18 gauge) is utilized.
– Loss of resistance syringes: Available in glass or plastic.
– Spinal needle: A long pencil-point (≤27 gauge) needle
– Epidural catheter
• Technique
– Usually, the epidural needle is inserted at a lower lumbar level (at the level of the cauda
equina), to minimize injury to the spinal cord. Identification of the epidural space relies
on tactile sensation, with a subtle change in resistance identified by the injection of either
saline or air; known as the “loss of resistance” technique. Identification of the
subarachnoid space. The spinal needle is passed through the hollow epidural needle. No
additional introducer is needed.
– Identification of the subarachnoid space depends on the return of cerebrospinal fluid.
Medications are then injected and the spinal needle is removed.
– Indwelling epidural catheter insertion. The catheter is threaded through the epidural
needle, usually with 4–5 cm of catheter lying in the epidural space. It allows for
medication delivery either as repeat boluses or continuous infusion. Typically, an
epinephrine-containing test dose is used to detect intravascular injection once the epidural
catheter is positioned.
• Subarachnoid medications
– Opioids. Sufentanil (5–10 μg) or fentanyl (20–35 μg) can be used to provide rapid
analgesia (usually within 5 minutes) for the first stage of labor, and will last for ∼90
minutes. Long-acting drugs such as preservative-free morphine are obviated by the ability
to deliver a continuous epidural infusion. Furthermore, intrathecal injection of morphine
is associated with unacceptably slower analgesia, and delayed-onset respiratory
depression occurring 6–12 hours after the injection, making it an unnecessary addition to
a CSE. Meperidine has LA-like effects that would make it an ideal drug for subarachnoid
injection; however, has been associated with severe hypotension and is rarely is used in
modern practice.
– LA. Combining Bupivacaine 2.5 mg with intrathecal opioid will prolong the duration of
analgesia and decrease the failure rate of CSE in the later stages of labor. A number of
small studies have demonstrated inferior analgesia with hyperbaric solutions when
compared to isobaric preparations.
– Adjuncts. The addition of epinephrine 200 μg or clonidine 50 μg can further increase
duration of analgesia. The increased risk of medication error and compounded side effect
profiles (including increased motor block with epinephrine or sedation and hypotension
with clonidine) have limited the use of multiple additives to intrathecal solutions.
• Continuous epidural infusions can be initiated shortly after the CSE is completed and
maternal hypotension and fetal adverse effects have been ruled out. If equipment and
patient understanding allows, patient-controlled epidural analgesia can be started using
parameters typical for any other post-operative patient.
ANATOMY
• The patient can be positioned in the sitting or lateral decubitus position for the procedure.
• Similar to the technique used to place an epidural catheter alone, the Tuohy needle is
inserted into the skin and traverses the
– Subcutaneous fat and tissue
– Supraspinous ligament
– Interspinous ligament
– Ligamentum flavum
– Enters into the epidural space
• Using a needle-through-needle technique, the spinal needle is inserted into the Tuohy needle
to pierce the dura.
• Postdural puncture headache (PDPH). Various investigators have shown that the use of a
pencil-point spinal needle for a CSE does not result in an increased incidence of PDPH.
• “Wet tap.” Accidental puncture of the dura with an epidural needle can be managed by
threading a soft epidural catheter into the intrathecal space, in order to minimize the risk
for PDPH. The catheter can be used for continuous spinal analgesia during labor or surgery.
Clear labeling of the catheter as “INTRATHECAL” is imperative to avoid overdose.
Obviously, infusion rates must be adjusted for continuous intrathecal, rather than epidural
infusion. It is postulated that local inflammation of the dura around the catheter aids in
sealing of the puncture, when the catheter is removed 24–48 hours after placement.
• Total spinal anesthesia. Rare event most often due to medication error or inadvertent
placement of the epidural catheter in the intrathecal space. This can be detected when a
dense spinal blockade occurs following test dose.
• LA toxicity. No additional risk of direct LA toxicity is involved with CSE when compared to
epidural alone.
• Inadvertent intrathecal catheter. Entrance of the epidural catheter into the intrathecal space
is unlikely without dural puncture by the Tuohy needle, given the comparatively smaller
size of the hole produced by the spinal needle.
• Pruritus. Spinal opioids are associated with pruritus in >80% of cases.
• Hemodynamics.
– Maternal hypotension can result from spinal opioids in up to 20% of patients.
– Fetal bradycardia (transient) can occur in up to 5% of patients. The mechanism is believed
to result from the abrupt decrease in circulating catecholamines that follows the rapid and
intense analgesia of CSE. This leads to an increase in uterine contractions with resultant
bradycardia until a new equilibrium is established.
• Respiratory. Maternal respiratory depression is uncommon, but has been reported to occur
in 0.1% of patients.
• Inadequate analgesia, unrecognized failed or patchy epidural
• Less common procedural complications can include persistent back pain, infection
(meningitis, epidural abscess), and epidural hematoma.
• Nerve injury. No additional risk is conferred with the use of CSE besides those inherent in
either the spinal or epidural components themselves.
• Mortality. No differences were found when CSE was compared to either a spinal or epidural
placement.
• Indications. Labor analgesia, C-section, abdominal surgery, and lower extremity procedures
when rapid onset of block and titratablility of level and density is required. The level of
blockade can be adjusted by increasing the epidural infusion rate.
• Contraindications. No additional contraindications when compared to epidural or spinal
analgesia. This includes local infection or bacteremia, prior spine surgery at that level,
anticoagulation and proven allergy to any component of the CSE. Use of pencil-point, rather
than cutting needle with CSE (or simply epidural analgesia alone), should be considered in
patients with history of PDPH.
REFERENCES
1. Collis RE, Davies DW, Aveling W. Randomised comparison of combined spinal-epidural and
standard epidural analgesia in labour. Lancet. 19953;345(8962):1413–1416.
2. Choi DH, Kim JA, Chung IS. Comparison of combined spinal epidural anesthesia and
epidural anesthesia for cesarean section. Acta Anaesthesiol Scand. 2000;44(2):214–219.
3. Eisenach JC. Combined spinal-epidural analgesia in obstetrics. Anesthesiology.
1999;91(1):299–302.
4. Dennison B. Combined subarachnoid and epidural block for caesarean section. Can J
Anaesth. 1987;34(1):105–106.
5. Ferouz F, Norris MC. Baricity, needle direction, and intrathecal sufentanil for labor
analgesia. Anesthesiology. 1997;86:592–598.
6. Holmstrom B, Laugaland K, Rawal N. Combined spinal-epidural block versus spinal and
epidural block for orthopedic surgery. Can J Anesth. 1993;40:601–606
• Epidural
CLINICAL PEARLS
• CSE analgesia offers many of the advantages of each of its component techniques.
• Patient satisfaction is high with the technique due to its rapid onset of almost complete
analgesia in the 1st stage of labor.
• The CSE technique can be used to increase the block height, or supplement a patchy
subarachnoid block for surgery.
• Special concerns for informed consent: Disclosure of both maternal and fetal risks as
mentioned above.
COMPLEX REGIONAL PAIN SYNDROME (CRPS) TYPE I
Andrew Fond, MD
Eric S. Hsu, MD
BASICS
DESCRIPTION
• Formerly known as reflex sympathetic dystrophy (RSD), complex regional pain syndrome I
(CPRS Type I) is a chronic neuropathic pain disorder characterized by the following:
– A nonspecific extremity injury
– No definable nerve injury
– Autonomic nervous system (ANS) involvement with features such as local edema as well
as altered sweating, skin color, and temperature.
– Signs of neuropathic pain such as intense burning pain, hyperalgesia, and allodynia.
• It differs from CRPS Type II only in that it lacks a documented or definable nerve injury.
EPIDEMIOLOGY
Prevalence
• A calculated at-risk incidence of ∼5.5 per 100,000 person years.
• 50,000 anticipated new cases in the US annually.
• Postfracture incidence reaches ∼1–2%.
Prevalence
• Prevalence of ∼21 per 100,000 person years
• Estimated female:male ratio of 3:1
• Mean age of diagnosis 36–42 years of age
Morbidity
• Permanent disability: 31%
• Need to make working adjustments: 28%
• Crush injuries
• Strains and sprains
• Fractures
• Surgery, especially after trauma
• May develop after virtually any injury
• Altered cutaneous innervation (1)
– Following the initial injury, there is decreased C-fiber and A Delta-fiber density in the
affected limbs of CRPS Type I patients compared with nonpainful control sites on the
same extremity and compared with healthy controls.
• Peripheral nervous system sensitization
– After tissue trauma, primary afferent fibers in the injured area release several
neuropeptides that increase background firing of nociceptors and increase firing in
response to nociceptive stimuli; this contributes to hyperalgesia and allodynia.
• Central nervous system sensitization
– Persistent or intense noxious stimuli resulting from tissue damage appear to trigger
increased excitability of nociceptive neurons in the spinal cord.
• Inflammatory mediators
– Increased levels of local, systemic, and CSF proinflammatory mediators.
– Decreased systemic levels of anti-inflammatory cytokines
• CNS (brain) plasticity
– There is a reduction in size of the representation of the CRPS-affected limb in the
somatosensory cortex compared with the unaffected side.
– The degree of somatotopic reorganization correlates with CRPS pain intensity and degree
of hyperalgesia.
– Psychological factors
– Greater preoperative anxiety may prospectively predict acute CRPS symptomatology after
total knee arthroplasty.
– Emotional arousal has a greater impact on pain intensity in CRPS than in non-CRPS
chronic pain, possibly via association with catecholamine release.
• Calcitonin injection was shown in one study to decrease the frequency of CRPS in
hemiplegic patients after stroke.
• Vitamin C 500 mg/day reduced the incidence of CRPS after wrist fractures in clinical
studies.
• CRPS Type I is a clinical diagnosis formulated by bedside history and physical examination.
Clinicians may use technical testing procedures to corroborate or objectively document their
clinical impressions.
• The modified diagnostic criteria for CRPS were published in 2007 (2).
– Pain is continuing and disproportionate to any inciting event.
– For clinical use, patient must report 1 symptom in 3 or more of the following categories.
Sensory: Hypesthesia and/or allodynia
Vasomotor: Temperature asymmetry (>1°C) and/or skin color changes or asymmetry.
Sudomotor/Edema: Edema and/or sweating changes or asymmetry
Motor/Trophic: Decreased range of motion and/or motor dysfunction or trophic changes
(hair, nail, skin)
– There must be 1 sign in 2 or more of the following categories upon physical examination:
Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or
temperature sensation and/or deep somatic pressure and/or joint movement)
Vasomotor: Evidence of temperature asymmetry (>1°C) and/or skin color changes
and/or asymmetry
Sudomotor/Edema: Evidence of edema and/or sweating changes and/or sweating
asymmetry
Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction
(weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
– There is no other diagnosis that better explains the signs and symptoms in CRPS.
• Three-phase bone scintigraphy may help to demonstrate osseous changes and uptake during
the subacute period (up to 1 year). However, there is no gold standard to compare with the
findings.
• A pathological uptake in the metacarpophalangeal or metacarpal bones is thought to be
highly sensitive and specific for CRPS.
• Plain radiographs and x-ray bone densitometry: Spotty and localized bone demineralization
has been observed only in chronic stages of CRPS.
• Quantitative sensory testing (QST) is a psychophysical testing of thermal pain and vibratory
thresholds that may help to assess the function or dysfunction of myelinated and
unmyelinated afferent fibers. However, there is no sensory profile that is characteristic for
CRPS.
• Autonomic function can be evaluated by the following points:
– Infrared thermometry measures the skin temperature difference between the affected and
normal limbs at resting and controlled modulation of sympathetic function.
– Quantitative sudomotor axon reflex test (QSART) can assess the function of sudomotor
(sweating) reflex loops. Swelling can be quantified by measuring water displacement.
• Posttraumatic neuralgia
• Diabetic and other small fiber neuropathies
• Entrapment neuropathy
• Thoracic outlet syndrome
• Vascular insufficiency
• Infection such as cellulitis
• Reynaud’s disease
TREATMENT
• Focused around pain management (pharmacologic and interventional), rehabilitation, and

psychological therapy (4).
• Pharmacologic interventions
– Tricyclic antidepressants (TCA) are a first-line agent. Although there are no controlled
studies specifically for CRPS, they are the best-studied group of pharmacological agents in
various neuropathic pain syndromes. Amitriptyline 10–75 mg PO per day; nortriptyline
10–75 mg PO per day; desipramine 10–75 mg PO per day. All TCAs have similar side
effects including sedation and anticholinergic effects.
– The efficacy of selective serotonin reuptake inhibitors (SSRI) in neuropathic pain states is
not well documented.
– Anticonvulsants such as gabapentin and pregabalin have been studied for postherpetic
neuralgia and diabetic neuropathy. Gabapentin 900–3600 mg/day PO divided into t.i.d.
dosing was shown to provide benefit of sensory deficit symptoms in addition to mild pain
relief. Alternatively, pregabalin (Lyrica) 150–600 mg/day PO divided into BID or TID
dosing can be used. Anticonvulsants are commonly used off-label in CRPS as a first-line
agent. Side effects include somnolence, dizziness, and peripheral edema.
– Opioids are used as second-line agents to provide analgesia and facilitate functional
rehabilitation. The use of opioids in neuropathic pain revealed efficacy when compared to
placebo. There is no long-term study of opioids in neuropathic pain or CRPS. Tramadol,
morphine sulfate, and oxycodone have been studied in treatment of neuropathic pain.
– NSAIDS have not been studied in CRPS. It may control mild-to-moderate pain in clinical
practice as a second-line agent for inflammation and edema.
– Corticosteroids: Oral prednisolone 10 mg TID has been studied in the acute (<13 weeks)
stage of CRPS.
– N-methyl-D-aspartate receptors antagonists have been studied to reduce central
sensitization. Although ketamine has provided favorable outcomes in case reports, well-
controlled studies for ideal dosing in CRPS are still pending.
– Clonidine transdermally administered may prevent the release of catecholamines via
presynaptic actions.
– Lidocaine 5% patch is approved for postherpetic neuralgia and has been used anecdotally
in CRPS.
– Calcitonin 100–300 IU/day intranasally may be effective. Clonodronate 300 mg IV QD or
aldrenoate 7.5 mg IV QD have both demonstrated improvement in pain, swelling, and
range of movement in acute CRPS.
– Gamma-aminobutyric acid (GABAB) agonists: Intrathecal baclofen up to 450 μg/day has
been used for the treatment of dystonia associated with CRPS.
• Interventional therapy
– Epidural clonidine may provide greater pain reduction at higher dosages (700 μg)
compared to lower dosages (300 μg) in CRPS, but may be associated with sedation and
hypotension. Epidural local anesthetics and/or steroids have not been studied in the
treatment of CRPS Type I.
– Peripheral nerve blocks in CRPS Type I do not provide diagnostic or therapeutic benefit as
in CRPS Type II.
– Paravertebral sympathetic ganglion blocks: Stellate (cervicothoracic) ganglion block for
the upper extremity and lumbar sympathetic block for the lower extremity can help to
differentiate if pain has a strong sympathetically mediated component or if it is
sympathetically independent (level 4 evidence).
– Intravenous regional anesthesia (IVRA) or intravenous regional sympatholysis (IVRS) to an
isolated extremity blocked with a tourniquet (level 4 evidence). Regional administration
of IV guanethidine, bretylium, or reserpine depletes noradrenaline in the postganglionic
axon.
– Epidural spinal cord stimulation (level 4 evidence). May be effective for pain control in
certain patients; does not improve return of function.
– Chemical neurolysis or radiofrequency neuroablation; lacks strong evidence to support its
efficacy.
– Surgical sympathectomy (level 4 evidence). Best results if within 12 months between
injury and intervention. However, there is limited evidence on efficacy and long-term pain
relief.
• Physical therapy and occupational therapy are important in trying to restore and maintain
function and range of motion (level 4 evidence).
• Cognitive-behavioral therapy (CBT) together with physical therapy revealed beneficial
effects in CRPS patients.
• Biofeedback technology provides a patient with visual and/or auditory feedback regarding
physiologic functions including muscle tension levels, perspiration, extremity temperature,
and brain wave pattern. It teaches patients how to alter these functions through a variety of
relaxation techniques, including progressive muscle relaxation, imagery, diaphragmatic
breathing, and autogenic techniques.
• Mind-body medicine: Mirror therapy provided pain reduction in a case series of CRPS Type
I.
FOLLOW-UP
• CRPS patients still have significantly higher levels of pain and dysfunction at 5 years after
injury compared to reference patients with similar precipitating injuries who did not
develop CPRS (5).
• Up to 33% of patients may reach full recovery when examined at 5 years.
• Factors that may contribute to poorest outcome include an affected upper extremity and the
inciting event being other than a fracture.
REFERENCES
1. ruehl S. An update on the pathophysiology of complex regional pain syndrome.
Anesthesiology. 2010;113(3):713–725.
2. arden RN, Bruehl S, Stanton-Hicks M, et al. Proposed new diagnostic criteria for complex
regional pain syndrome. Pain Med. 2007;8(4):326–331.
3. Hsu ES. Practical management of complex regional pain syndrome. Am J Ther.
2009;16(2):147–154.
4. Singh G, et al. The value of interdisciplinary pain management in complex regional pain
syndrome type I: A prospective outcome study. Pain Physician. 2004;7(2):203–209. de Mos
Marissa, et al. Outcome of the complex regional pain syndrome. Clin J Pain.
2009;25(7):590–597. www.ninds.nih.gov
• www.worksafebc.com
• Complex regional pain syndrome II (CPRS II)
• Assessment of acute pain
CODES
ICD9
• 337.20
• 337.21 Reflex sympathetic dystrophy of the upper limb
• 337.22 Reflex sympathetic dystrophy of the lower limb
ICD10
• G90.50 Complex regional pain syndrome I, unspecified
• G90.511 Complex regional pain syndrome I of right upper limb
• G90.512 Complex regional pain syndrome I of left upper limb
CLINICAL PEARLS
• The exact pathophysiologic mechanisms of CRPS are not entirely clear but are likely
multifactorial in nature and linked to peripheral and central sensitization.
• Other compounding factors in CRPS Type I may involve genetic factors, inflammation,
altered sympathetic and catecholaminergic function, reduced representation of affected limb
in the somatosensory cortex, and psychophysiologic interactions.
• There is no gold standard for the diagnosis of CRPS Type I; currently it is based on clinical
presentation, physical examination, and the aid of available tests.
• A multidisciplinary approach in CRPS Type I must involve timely diagnosis, pain
management, physical and occupational therapy, functional restoration, and psychosocial
therapy.
• Interventional pain management in CRPS Type I may consist of sympathetic blockade, a trial
and evaluation for implantation of electrodes for spinal cord stimulation, and deep brain
stimulation (neuromodulation).
COMPLEX REGIONAL PAIN SYNDROME (CRPS) TYPE II
Farooq A. Qureshi, MD
Eric S. Hsu, MD
BASICS
DESCRIPTION
• Formerly known as causalgia, complex regional pain syndrome (CRPS Type II) is a chronic
neuropathic pain condition characterized by the following:
– A trauma or injury to an extremity
– Nerve injury to the extremity, that is usually distal to the initial injury
– Autonomic nervous system (ANS) dysfunction that can lead to allodynia, hyperalgesia,
and trophic changes (skin color, temperature, hair and nail growth, and abnormal
sweating)
• It differs from CRPS Type I only in that there needs to be a definable nerve injury for CRPS
Type II.
EPIDEMIOLOGY
Prevalence
• CRPS Type I develops more often than CRPS Type II (1).
• Following peripheral nerve injury: ranges from 2–14% (mean 4%).
• Following military nerve root injuries:
– Men < 34 years: 10–15%
– Men > 34 years: 47%
Prevalence
• Approximately 4 per 100,000 persons
• CRPS Type II usually occurs in one extremity
• Male/female ratio of 1:3
May develop after any nerve injury including traumatic injury, amputation, surgery, and
regional anesthesia
• The mechanism of disease is multifactorial and includes the following (2):
– Altered cutaneous innervations
– Peripheral and central sensitization
– Inflammation
– Altered somatosensory representation in the brain
– Altered sympathetic and catecholaminergic function
– Genetic factors
– Psychophysiological interactions
• Pathogenesis. The inciting injury leads to decreased C-fiber and A delta-fiber density at the
site of injury. Primary afferent fibers in the injured area release several neuropeptides that
increase background firing of nociceptive stimuli, and decrease the firing threshold for
thermal and mechanical stimuli. Increased local and systemic levels of proinflammatory
cytokines such as Tumor Necrosis Factor (TNF)-α, interleukin-1β, interleukin-2, and
interleukin-6 are seen. Additionally, decreased systemic levels of the anti-inflammatory
cytokine interleukin-10 also occur. Persistent noxious input leads to central sensitization
involving N-Methyl-D-Aspartate (NMDA) receptors.
• Sympathetically mediated pain (SMP). A coupling between the sympathetic noradrenergic
neurons and primary afferents in the periphery of the body may occur at the site or along
the lesioned nerve. Noradrenaline, released by the sympathetic nerve fibers, may activate
and/or sensitize the afferent neurons and lead to SMP. Alternative coupling of sympathetic
neurons to non-nociceptive afferent (e.g., mechanical and temperature) neurons may
contribute to the mechanical or cold allodynia in CRPS Type II.
• Sympathetically independent pain: The later stages of the syndrome are not responsive to
sympathetic blockade.
• Genetics. Studies suggest that there may be an association with the angiotensin-converting
enzyme gene (non-major histocompatibilitycomplex (MHC) axis) as well as the HLA loci A3,
B7, DQ1(06), DR2 (15), and DR13.
• Psychology. The widely proposed myth “CRPS personality” does not appear to be
substantiated by current studies. No differences in psychological patterns were found in
those patients with radius fracture who developed CRPS Type II in comparison to patients
who recovered without developing CRPS.
Regional anesthesia and nerve blocks may minimize flare-ups in patients with a prior history
of CRPS Type II who are scheduled for surgery on the affected extremity. Placement should
occur prior to surgery or in the immediate postoperative period whenever SMP is a prominent
feature.
• International Association for the Study of Pain (IASP) Diagnostic Criteria for CRPS Type II
(1995):
– The presence of continuing pain, allodynia, or hyperalgesia after a nerve injury, not
necessarily limited to the distribution of the injured nerve with which the pain is
disproportionate to any inciting event.
– Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor
activity in the region of pain.
– The diagnosis is excluded by the existence of any other condition that would account for
the degree of pain and dysfunction.
– CRPS Type II is diagnosed when there is identifiable nerve injury.
• Diagnosis is based on history and physical exam findings. There is no gold standard
procedure or test to confirm CRPS. Some useful tests that aid in diagnosis include the
following:
– Electromyelogram and nerve conduction study may help to confirm the diagnosis of any
definite nerve injury that complements the history in CRPS Type II.
– Three-phase bone scintigraphy that demonstrates pathologic uptake in the
metacarpophalangeal or metacarpal bones is highly sensitive and specific, but changes are
not seen until the later stages.
– Quantitative sensory testing is a standardized psychophysical testing of thermal and
thermal pain thresholds and vibratory thresholds help to assess the function of large fiber,
myelinated small fiber, and unmyelinated small afferent fibers.
– Autonomic function testing includes infrared thermometry, laser Doppler flowmetry,
infrared thermography, and a quantitative sudomotor axon reflex test.
• Post-traumatic neuralgia
• Diabetic and other small fiber neuropathies; entrapment neuropathy
• Thrombophlebitis
• Deep vein thrombosis
• Thoracic outlet syndrome
• Vascular insufficiency
• Infection such as cellulitis
• Neuroma formation
• Syringomyelia
TREATMENT
• Should be multidisciplinary and aimed at providing both pain relief and functional
restoration and rehabilitation. These include pharmacological, interventional,
neuromodulation, rehabilitation, and alternative therapies (3).
• Pharmacologic therapies are empiric and target the predominantly neuropathic symptoms.
Randomized controlled trials are lacking.
– Tricyclic antidepressants (TCA): First-line agents. Although there is no good outcome
evidence, they remain the best-studied group of pharmacological agents in neuropathic
pain. All TCAs have similar side effects: Sedation, anticholinergic effect, and should be
cautiously used in patients with a known history of arrhythmias. Amitriptyline 10–75 mg
PO QD; nortriptyline 10–75 mg PO QD; desipramine 10–75 mg PO QD
– Serotonin–norepinephrine reuptake inhibitors (SNRI): First-line agents. Controlled studies
are lacking, but they are approved for painful diabetic neuropathy and fibromyalgia.
Duloxetine 30–120 mg PO QD
– Anticonvulsants: Although they are off-label for CRPS, they are considered first-line
agents. Side effects include somnolence, dizziness, and peripheral edema. Gabapentin
900–3600 mg/day divided into TID dosing; pregabalin 150–600 mg/ day divided into BID
or TID dosing (4).
– NSAIDS: Second-line agents and have not been extensively studied, but may help with
inflammation and edema.
– Corticosteroids: Oral prednisolone 10 mg TID has been studied in the acute (<13 weeks)
stage of CRPS.
– Opioids are effective in postoperative and cancer pain. The use of opioids in neuropathic
pain revealed efficacy when compared to placebo. There are no long-term studies on the
efficacy of opioids for CRPS.
– Gamma-aminobutyric acid (GABAB) agonists: Intrathecal baclofen up to 450 μg/day has
been used for treatment of dystonia associated with CRPS.
– Bisphosphonates: Clodronate 300 mg IV QD or alendronate 7.5 mg IV QD may improve
pain, swelling, and range of movement in acute CRPS.
– Topical agents: Second-line and off-label use in CRPS.
Clonidine patch for localized area of hyperalgesia and pain
Lidocaine 5% patch to affected area 12 hours on/12 hours off.
Diclofenac 1.3% patch to affected area BID
Capsaicin 0.075% cream QID
• Interventional therapies include peripheral, neuraxial, and sympathetic nerve blocks (5).
– Peripheral nerve blocks can be performed for each specific nerve presumed to be involved
in CRPS Type II over the upper or lower extremity. The brachial plexus block may be
considered if more than one peripheral nerve is suspected. No plexus block can be
recommended for CRPS Type II involving the lower extremity.
– Epidural techniques. Continuous epidural infusion with local anesthetics and opioids in
coordination with intensive physical and occupational therapy and functional
rehabilitation may be performed as an inpatient. Epidural clonidine can provide greater
pain reduction at higher dosages (700 μg) compared to lower dosages (300 μg) in CRPS;
however, this may be associated with significant side effects (sedation, hypotension).
Epidural steroid injections have not been studied in the treatment of CRPS Type II.
– Sympathetic nerve blocks such as a stellate ganglion block or lumbar sympathetic block
(level 4 evidence) can help to differentiate if pain has a strong SMP. Eighty-five percent of
the patients report a positive acute effect, but fewer patients experience long-term relief.
There is no definitive protocol for selecting candidates for stellate and lumbar sympathetic
blockade.
– IV regional anesthesia: Level 4 evidence. Use of IV bretylium or reserpine to deplete
noradrenaline in the postganglionic axon to an isolated extremity blocked with a
tourniquet.
• Neuromodulation techniques may be considered and utilized when patients reach the
plateau in responding to nerve blocks; involve advanced interventional techniques.
– Spinal cord stimulation has been shown to significantly reduce pain levels as well as
improve functional status and quality of life.
– Peripheral nerve stimulation: Especially advantageous for CRPS Type II as there has been
definite nerve injury.
– Surgical sympathectomy (level 4): Best results if performed within the first year of injury.
Limited evidence on efficacy.
• Rehabilitation methods include (6)
– Physical therapy and occupational therapy are important in trying to improve function
and range of motion (level 4).
FOLLOW-UP
Outcome studies:
• CRPS patients have significantly higher symptoms and signs of pain and injury than
reference patients with the same precipitating injury who did not develop CPRS at 5 years
(7).
• Thirty-three percent of patients reach full recovery when examined at 5 years.
• Patients in the poorest outcome group often had their upper extremity affected, inciting
event other than a fracture, and cold extremities.
REFERENCES
1. eldman PH, Reynen HM, Goris RJ. Signs and symptoms of reflex sympathetic dystrophy:
Prospective study of 829 patients. Lancet. 1993;342:1012–1016.
2. Bruehl S. An update on the pathophysiology of complex regional pain syndrome.
Anesthesiology. 2010;113(3):713–725.
3. Hsu ES. Practical management of complex regional pain syndrome. Am J Therapeutics.
2009;16(2):147–154.
4. Rowbotham MC. Pharmacologic management of complex regional pain syndrome. Clin J
Pain. 2006;22:425–429.
5. Nelson DV, Brett RS. Interventional therapies in the management of complex regional pain
syndrome. Clin J Pain. 2006;22:438–442.
6. Singh G, et al. The value of interdisciplinary pain management in complex regional pain
syndrome type I: A prospective outcome study. Pain Physician. 2004;7(2):203–209.
7. de Mos Marissa, et al. Outcome of the complex regional pain syndrome. Clin J Pain.
2009;25(7):590–597.
ADDITIONAL READING
• www.ninds.nih.gov
• www.worksafebc.com
• Complex regional pain syndrome (CRPS) Type I
CODES
ICD9
• 354.4 Causalgia of upper limb
• 355.71 Causalgia of lower limb
ICD10
• G56.40 Causalgia of unspecified upper limb
• G56.41 Causalgia of right upper limb
• G56.42 Causalgia of left upper limb
CLINICAL PEARLS
• A definable injury of the peripheral nerve is required for the diagnosis of CRPS Type II in
addition to the common symptoms and signs seen in CRPS Type I.
• The exact pathophysiologic mechanisms of CRPS Type II are not entirely clear but are likely
multifactorial in nature and linked to peripheral and central sensitization following nerve
injury that leads to inflammation and sympathetic nervous system dysfunction.
• There is no gold standard test except the documentation of nerve injury for diagnosis of
CRPS Type II. Diagnosis criteria are based on clinical presentation, physical examination,
and the aid of available tests.
• Treatment of CRPS Type II should be immediate and focus toward restoration of full
function of the affected extremity. This goal is best achieved by an interdisciplinary team
involving pain management, physical and occupational therapy, and psychosocial support
and therapy.
• Interventional pain management in CRPS Type II may consist of sympathetic blockade,
diagnostic and therapeutic peripheral nerve blocks, and a trial implant of electrodes for
peripheral nerve stimulation and/or spinal cord stimulation as neuromodulation.
CONGENITAL DIAPHRAGMATIC HERNIA
Ranu Jain, MD
BASICS
DESCRIPTION
• Congenital diaphragmatic hernia (CDH) is a failure of a portion of the fetal diaphragm to
fully develop. The defect allows abdominal contents to enter the thorax, often interfering
with normal lung growth.
• CDH can present as a neonatal life-threatening emergency.
EPIDEMIOLOGY
Prevalence
Live births: ∼1:2000 to 1:5000
Prevalence
• More common in males
• Left-sided CDH is more common
• In an otherwise healthy neonate with CDH, the maternal risk of recurrence for future
pregnancies is only 2%.
Morbidity
Related to the degree of pulmonary hypoplasia and comorbidities (e.g., cardiac, spinal, etc)
Mortality
• Ranges from 40% to 62% (decreased in otherwise healthy children).
• Mortality has been correlated with the initial Alveolar-arterial oxygen difference, (A-a)
gradient, after surgical repair.
– <400 mm Hg = likely survival
– 400–500 mm Hg = intermediate chances
– >500 mm Hg = unlikely to survive
• Those presenting later in childhood (Morgagni’s hernia), or even adulthood, have an
extremely good outcome, with low or no mortality.
• Cause remains unknown
• There does appear to be a genetic link and an increased risk if a sibling or a parent had the
condition.
• CDH results from a failure of fusion of peripheral and central elements of the diaphragm.
• Respiratory. Pulmonary hypoplasia occurs secondary to compression by abdominal contents.
There is an abnormal division of airways that results in a decreased number of bronchi,
alveoli, and pulmonary arterial branches. Additionally, there is surfactant deficiency and
premature muscularization of pulmonary vessels. Severity is related to the time during
gestation when herniation occurred (usually during the 8th week).
– Mechanical abnormalities result from the herniation of abdominal contents shifting into
the mediastinum; causes the mediastinum to shift to the opposite side of the defect.
– Circulating vasoactive mediators increase, as does the body’s sensitivity. This further
worsens the pulmonary hypertension associated with CDH.
• Reduction in the herniated viscera and closure of the diaphragmatic defect should be
emergently performed following birth. However, surgical treatment can be delayed to
stabilize infants with pulmonary hypoplasia and persistent pulmonary hypertension of the
newborn (PPHN). Preoperative stabilization with delayed repair has become the standard of
care.
• Physiologic considerations include hypoxemia, hypercarbia, acidemia, pulmonary
hypertension and associated right-to-left shunting, possible pneumothorax, and malrotation.
• Goals
– Adequate gas exchange and prevention of worsening metabolic or respiratory acidosis
while avoiding ventilator-associated lung injury.
– Avoidance of aspiration
– Adequate pain control
– Maintain normothermia, volume status, and electrolyte balance.
SYMPTOMS
• Cyanosis
• Tachycardia
• Tachypnea, retractions, grunting, severe respiratory distress
• A small subset of patients (∼5%) present primarily with bowel obstruction and minimal
respiratory distress.
History
• Birth history
• Prematurity
• Weight
• Pulmonary status: Oxygen requirements, intubation history. If intubated, note the ventilator
settings and size of endotracheal tube.
• Other congenital anomalies (cardiac abnormalities are present in ∼25% of cases)
• History of blood product transfusions
• Family history of congenital anomalies or malignant hyperthermia
• History of extracorporeal membrane oxidation (ECMO)
Signs/Physical Exam
• Intrathoracic bowel sounds
• Scaphoid abdomen, barrel-shaped chest
• Auscultation of the lungs typically reveals poor air entry on the left (with a left
posterolateral hernia), and shifting of cardiac sounds over the right chest.
TREATMENT HISTORY
• Minimally invasive fetal surgeries have been attempted (e.g., tracheal balloon occlusion) to
promote the growth of hypoplastic lung tissue, but it has not shown improved survival.
• Ex utero intrapartum therapy (EXIT) procedures may be performed for severely hypoplastic
lungs with very large CDH.
• ECMO. Morbidity occurs secondary to anticoagulation and intracranial bleeding. Indications
include
– Estimated gestational age >35 weeks
– Absence of intracranial hemorrhage
– Absence of uncorrectable cyanotic congenital heart disease
– Absence of uncorrectable associated anomalies
– Parental consent
• Nitric oxide can promote smooth muscle relaxation and short-term improvements in arterial
oxygenation. Its use is controversial; it may be helpful in the initial stabilization, but does
not reduce the need for ECMO or decrease mortality.
• Permissive hypercapnia to a PaCO2 of 60 mm Hg may decrease ventilator support and
barotrauma as well as dilate the pulmonary vasculature; in the setting of pulmonary
hypoplasia, this can be beneficial. However, it remains controversial.
• High frequency oscillatory ventilation (HFOV). May be utilized if conventional ventilation
fails to reverse hypercapnia and hypoxemia. It avoids injury to the lung and preserves end
expiratory lung volume without overdistension.
MEDICATIONS
• Sedation and muscle relaxation are used in intubated patients to avoid ventilator
dyssynchrony and decrease the release of catecholamines, which may increase pulmonary
vascular resistance.
• IV fluids and total parenteral nutrition (TPN) should be continued in the OR.
Labs/Studies
• Amniocentesis and karyotyping for chromosomal abnormalities or low levels of alpha-
fetoprotein.
• Prenatal ultrasound can reveal polyhydramnios; the heart may be shifted to the opposite
side of the hernia, and intestinal loops may be seen in the chest.
• Chest radiograph. Typical findings in a left-sided posterolateral CDH include air-filled or
fluid-filled loops of the bowel in the left hemithorax and shift of the cardiac silhouette to
the right, with or without pneumothorax.
• Echocardiogram to assess myocardial function and determine whether the left ventricular
mass is significantly decreased.
• Ultrasound of the brain to evaluate for intraventricular bleeding, hypoxic–ischemic changes,
and major intracranial anomalies.
• CNS: Neural tube defects or hydrocephalus
• Craniofacial, extremity, or spinal abnormalities
• Genitourinary anomalies (6–8%)
Surgical treatment can be delayed to stabilize pulmonary hypoplasia and PPHN.
CLASSIFICATIONS
• The Bochdalek hernia, also known as a posterolateral diaphragmatic hernia, can occur on
the left or right. It accounts for >95% of cases.
• Morgagni’s hernia, also known as a retrosternal or parasternal hernia can occur through this
right, anterior defect (known as the foramen of Morgagni). Infants may be asymptomatic;
however, repair is still recommended to avoid the risk of a strangulated intestine. Accounts
for ∼2% of cases.
• Diaphragmatic eventration describes cranial displacement of part, or all, of an otherwise
intact diaphragm into the chest cavity. This rare type of CDH occurs due to incomplete
muscularization of the diaphragm or failure of phrenic nerve innervation, and can be found
unilaterally or bilaterally. Minor forms of diaphragm eventration are asymptomatic;
however, severe cases will present with respiratory distress similar to Bochdalek hernia.
TREATMENT
Premedications
Patient may be intubated, sedated, and/or paralyzed.
• Postoperative intubation may be needed.
• Postoperative ECMO support may be needed.
• Epidural for postoperative analgesia may be needed.
INTRAOPERATIVE CARE
• Epidural for postoperative pain control
Monitors
• Pulse oximeter probes at preductal (right-hand) and postductal (either foot) sites are helpful
for assessing right-to-left shunt at the ductus arteriosus level. In PPHN, the preductal PaO2
is higher.
• Arterial line should be placed for frequent blood gas measurements.
• Patients are considered an aspiration risk. They should have their stomach suctioned before
induction, followed by a rapid sequence with succinylcholine or rocuronium; alternatively,
an awake intubation may be appropriate.
• Prior to the start of surgery, patients should have adequate IV access and blood products
available in order to treat possible intraoperative blood loss.
• An epidural can be placed after intubation. Transcaudal, lumbar, or thoracic sites are all
options to provide chest wall/pleural or abdominal analgesia.
Maintenance
• Opioids and/or volatile anesthetics with neuromuscular blockade. Nitrous oxide is avoided
because it can diffuse in the viscera and exaggerate lung compression.
• Ventilator. Rates of 30–60 breaths/minute while maintaining the PIP <25 cm H2O to
minimize barotraumas.
– A PaO2 >50 mm Hg can provide for adequate oxygen delivery at the tissue level. Higher
concentrations may require increased ventilator support and barotrauma.
– A lower FI02 is preferred to avoid retinopathy of prematurity. Optimal FI02 maintains the
preductal SpO2 between 95% and 100%.
• Fluids. Active warming of the patient, IV fluids, and/or blood products should be done to
avoid hypothermia.
– Dextrose-containing fluids are preferred due to the decreased glycogen stores in the
neonate.
– The amount of insensible losses will depend on the size of the defect.
– Blood loss is typically minimal.
• Hematocrit. Should be maintained between 30% and 35%; fetal hemoglobin has an
increased affinity to oxygen and a decreased sensitivity to 2,3-DPG that can exacerbate
cellular hypoxia.
• Chest tube drainage is necessary when a tension pneumothorax is present.
• Postoperative intubation is needed in infants with increased airway pressures and/or
pulmonary hypertension.
• Pain control with IV narcotics or epidural
FOLLOW-UP
BED ACUITY
NICU or PICU
• Blood gas analysis to assess oxygenation and ventilation, as well as possible postoperative
acidosis.
• CBC to evaluate hematocrit after surgical blood loss and intraoperative volume shifts.
• Ventilator settings: Low peak pressures to avoid injury to the normal lung.
• Pneumothorax on the unaffected side should be suspected if the infant is hypotensive and
hypoxic.
COMPLICATIONS
• Hypoventilation
• Pneumothorax
• Hypothermia
• All the above conditions could lead to right-to-left shunting either through the ductus
arteriosus or an abnormal shunt (e.g., ASD, etc).
REFERENCES
1. de buys Roessingh AS, Dinh-Xuan AT. Congenital diaphragmatic hernia: Current status and
review of the literature. Eur J Pediatr. 2009;168(4):393–406.
2. Langer JC. Congenital diaphragmatic hernia. Chest Surg Clin N Am. 1998;8(2):295–314.
3. Moya FR, Lally KP. Evidence-based management of infants with congenital diaphragmatic
hernia. Semin Perinatol. 2005;29(2):112–117.
4. Finer NN, Tierney A, Etches PC, et al. Congenital diaphragmatic hernia: Developing a
protocolized approach. J Pediatr Surg. 1998;33(9):1331–1337.
• Pneumothorax
CODES
ICD9
756.6 Anomalies of diaphragm
ICD10
Q79.0 Congenital diaphragmatic hernia
CLINICAL PEARLS
• CHD presents as a life-threatening emergency; nonetheless, respiratory and cardiac
stabilization should be ensured prior to surgical correction. This may entail the use of
ECMO and/or nitric oxide. ECMO is recommended for neonates with reversible respiratory
failure.
• Prognosis is related to the degree of hypoplasia and the pulmonary muscular abnormalities,
which result in decreased lung compliance and risk of hypoventilation.
CONGESTIVE HEART FAILURE
John F. Coleman, MD
Wei Dong Gao, MD, PhD
BASICS
DESCRIPTION
• Congestive heart failure (CHF) can result from a syndrome of ventricular or valvular
function abnormalities, as well as improper neurohormonal regulation, leading to
inadequate blood flow and pressure to meet the body’s metabolic demands (1).
• CHF presents in one of three ways:
– Tissue hypoperfusion and hypoxia; fatigue, dyspnea, decreased exercise tolerance
– Fluid retention
– Coincidentally during the evaluation of another disorder
EPIDEMIOLOGY
Prevalence
Age group, per 1,000 (2):
• 65–74 years: 9.2 male, 4.7 female
• 75–84 years: 22.3 male, 14.8 female
• 85 years and older: 41.9 male, 32.7 female
Prevalence
Adults 20 and older: 5,800,000 in the US (3,100,000 males, 2,700,000 females) (2)
Morbidity
• In 2006, accounted for 1,106,000 hospital discharges in the US (3,4).
• Perioperative all-cause 30-day readmission is 17.1% versus 10.8% for coronary artery
disease (CAD).
Mortality
• One-year mortality rate: 1 in 5 (3,4)
• Any-mention death rate: 98.2 per 100,000 deaths; 103.7 for white males, 105.9 for black
males, 80.3 for white females, 84.4 for black females
• Perioperative all-cause mortality: 8% versus 3.1% for CAD.
• Cardiac: Hypertension (HTN), myocardial infarction, CAD, valvular disease (1,5)
• Metabolic: Diabetes mellitus, dyslipidemia
• Demographics: Family history, age
• Lifestyle: Obesity and tobacco use
• Medications: Toxins (e.g., chemotherapy)
• HF is a progressive disorder that can affect systolic and diastolic function, independently or
simultaneously (6,7).
• Systolic dysfunction is encompassed by a decline in the pumping capacity of the left
ventricle (LV) after an index event. This event causes a loss of myocytes and/or a decreased
ability of the myocytes to generate force.
• Diastolic dysfunction is the abnormal filling and relaxation of the LV resulting from
decreased compliance or impaired relaxation. LV relaxation is an energy-requiring process
and will be negatively affected by ischemia. When the LV has normal ejection fraction (EF)
and there are signs and symptoms of HF, it is termed “normal ejection fraction heart
failure”
• Compensatory mechanisms maintain cardiac output. These include the following:
– Modifications of the adrenergic system and retention of salt and water.
– Activation of vasodilatory molecules to offset vasoconstriction/increased afterload by the
adrenergic system.
– Neurohumoral and cytokine system activation causing LV remodeling and CHF
progression; involves changes in myocyte biology, myocyte loss, matrix degradation, and
alterations in LV geometry.
• Maintain cardiac output and prevent myocardial ischemia by avoiding acute changes in
right ventricle (RV) and LV preload and afterload, heart rate, and myocardial oxygen
balance. Mild HTN is better tolerated than hypotension.
• Hemodynamic consequences of HF include decreased cardiac output, increased LV end-
diastolic pressure (EDP), peripheral vasoconstriction, retention of sodium and water, and
decreased oxygen delivery.
SYMPTOMS
• Dyspnea, paroxysmal nocturnal dyspnea, orthopnea, cough
• Chest pain
• Exercise intolerance, fatigue, weakness
• Anorexia and nausea
• Nocturia
• Cognitive dysfunction
History
• Baseline functionality (7,8)
• History of CAD, cardiac surgery, abnormal blood pressure; NYHA or ACC/AHA
classification.
• Diabetes and blood glucose levels
• Use of tobacco, alcohol, and illicit drugs.
• Pacemaker and internal cardiac defibrillator (ICD) settings and interrogation.
Signs/Physical Exam
• Vital signs, height, and weight (8)
• Tachypnea, rales, pleural effusions, cyanosis
• Resting tachycardia and S3 heart sound; jugular venous distension
• Hepatomegaly, ascites, peripheral/dependent edema
MEDICATIONS
• Beta-blockers counteract the neurohumoral effects of HF to decreased myocardial oxygen
consumption, while improving ventricular systolic function and reversing ventricular
remodeling (1,9).
• Angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin receptor
blockers (ARBs) prevent and decrease ventricular remodeling; may cause hyperkalemia.
Also have been associated with refractory hypotension during general anesthesia.
• Diuretics decrease preload. Should be held in the immediate preoperative period.
• Digoxin offers rate and rhythm control and positive inotropy in those patients who remain
symptomatic on beta-blockers, ACE inhibitors, and diuretics.
• Vasodilators decrease afterload and wall tension.
• Statins may offer some benefit to patients with CAD in that they have pleiotropic (nonlipid
lowering) effects of decreased inflammation and stabilization of atheromatous plaques.
Labs/Studies
• Electrolytes, BUN, and creatinine (8)
• CBC
• TSH, liver function
• Chest x-ray (CXR) (cardiomegaly, pulmonary edema, pneumonia)
• ECG (myocardial infarction and ischemia, left ventricular hypertrophy (LVH), conduction
abnormalities or dysrhythmias)
• Echocardiography (EF%, LV structure/function, valvular pathology)
• Digoxin level
• Brain natriuretic peptide (BNP) (for new diagnosis to risk stratify only)
• Pacemaker and ICD interrogation
• Cardiac catheterization, noninvasive testing
• Neurological: Cerebrovascular disease, stroke and transient ischemic attacks (TIAs)
• Cardiovascular: HTN, arrhythmias, peripheral vascular disease, anemia
• Pulmonary: COPD
• Metabolic: Diabetes mellitus, hyperlipidemia
• Decompensated HF
• Unstable arrhythmias
CLASSIFICATIONS
• New York Heart Association (NYHA)
– I – not limited by symptoms
– II – somewhat limited by dyspnea
– III – dyspnea during a mild workload
– IV – dyspnea at rest or little exertion
• American College of Cardiology/American Heart Association (ACC/AHA)
– A – high risk but without symptoms
– B – structural heart disease without signs/symptoms
– C – prior or current symptoms
– D – refractory HF requiring specialized interventions
TREATMENT
Premedications
• Anxiolysis should be titrated cautiously; monitor for hypoxia.
• Beta-blockers should be continued perioperatively. Randomized controlled trials have shown
improved outcome in high-risk cardiac patients by preventing arrhythmias and ischemia.
INTRAOPERATIVE CARE
All types have been used successfully. Both general and neuraxial techniques result in
sympatholysis in patients with high compensatory sympathetic tone; can result in profound
hypotension that should be anticipated and treated aggressively.
Monitors
• Invasive monitoring is dependent on the severity of disease, surgical procedure, and
emergency surgery.
• Arterial lines can aid with beat-to-beat blood pressure monitoring and frequent lab draws.
Worsening Alveolar-arterial (A-a) gradient or a-A ratio as well as metabolic acidosis/base
excess can indicate worsening pulmonary edema, fluid overload, and/or myocardial pump
or valvular dysfunction.
• Central venous monitoring can aid with assessing ventricular filling and fluid status. A
pulmonary artery catheter can provide additional information of mixed venous oxygen
saturation (an indicator of worsening cardiac output), systemic vascular resistance (SVR),
and LVEDP; can guide and assess inotropic, vasodilator, and diuretic therapy
intraoperatively and postoperatively.
• Transesophageal echocardiography (TEE) can aid with monitoring ventricular filling,
ventricular wall motion, valve function, and EF. Limited by clinical expertise, availability,
and intraoperative use.
• Both IV and inhalational agents can be utilized for induction, and should be titrated
carefully.
• Propofol causes vasodilation and hypotension; consider lower doses, and more time for
onset of action.
• Etomidate has favorable hemodynamic effects but can cause some decrease in blood
pressure in patients with ventricular dysfunction or HF.
• Ketamine can be useful in the setting of poor ventricular function (EF <30%) due to its
sympathomimetic effects. It also has the potential to cause negative inotropic effects in the
patient with ventricular dysfunction or cardiomyopathy.
• Opioids, lidocaine, and other IV anesthetics can blunt the sympathetic stimulation with
laryngoscopy and intubation to prevent tachycardia and HTN.
• High-dose opioids in combination with other IV anesthetics cause a dose-dependent cardiac
depression likely due to blunting of the already elevated sympathetic tone.
Maintenance
• Both inhalational and/or IV balanced anesthesia techniques can be utilized; they include
inhaled volatile and nitrous oxide, opioid, and neuromuscular blockers. Sympatholysis can
be accentuated and compounded in patients with a high sympathetic tone, such as in HF
patients. Therefore, it is important to consider smaller doses and to titrate to desired effects.
• Positive pressure ventilation (PPV) and positive end-expiratory pressure (PEEP) may
decrease pulmonary congestion and improve arterial oxygenation (decrease atelectasis and
shunting of alveolar–capillary units).
• Fluids should be carefully titrated to optimize preload (Frank–Starling curve) while avoiding
RV and LV overload and pulmonary congestion.
• Since HF patients have down regulation of B1 receptors, a combination of inotropic agents
with different mechanism of action may sometimes be needed (i.e., epinephrine +
milrinone).
• Standard extubation criteria apply; however, patients may be less capable of meeting them.
• Prevent and immediately treat tachycardia, hypotension/HTN, and increased/decreased
contractility if present. Hypotension can be a sign of myocardial ischemia and/or worsening
HF.
• Supplemental oxygen should be administered.
• Treat shivering and hypothermia.
FOLLOW-UP
BED ACUITY
• Intensive care unit (ICU) for patients with acute or worsening HF, invasive monitoring, or
vasopressors and inotropic support.
• Patients requiring furosemide and/or vasodilators (i.e., nitroglycerine) for pulmonary edema
should be observed in an acute setting.
• Consider supplemental oxygen
• If medication treatment fails, consideration should be made for a mechanical ventricular
assist device, biventricular pacemaker for resynchronization therapy, coronary artery bypass
or surgical ventricular remodeling, or even heart transplantation may be considered (9).
COMPLICATIONS
Worsening HF/acute exacerbations can be a sign of myocardial ischemia, arrhythmias,
electrolyte disturbances, anemia, and hypotension (10).
REFERENCES
1. roban L, Butterworth J. Perioperative management of chronic heart failure. Anesth Analg.
2006;103:557–575.
2. Heart Disease and Stroke Statistics 2010 Update, American Heart Association. Fleisher LA.
Implications of preoperative heart failure. Anesthesiology. 2008;108:551–552.
3. ammill BG, et al. Impact of heart failure on patients undergoing major noncardiac surgery.
4. Schocken DD, et al. Prevention of heart failure. Circulation. 2008;117:2544–2565.
5. Mann DL, et al. Mechanisms and models in heart failure: The biomechanical model and
beyond. Circulation. 2005;111:2837–2849.
6. Mancini D, Burkhoff D. Mechanical device-based methods of managing and treating heart
failure. Circulation. 2005;112:438–448.
7. Wojciechowski P. Perioperative optimization of the heart failure patient. Int Anesthesiol
Clin. 2009;47(4):121–135.
8. Jessup M, et al. 2009 Focused update: ACCF/AHAe guidelines for the diagnosis and
management of heart failure in adults. Circulation. 2009;119:1977–2016.
9. Fonarow GC, Abraham WT, Albert NM, et al. Factors identified as precipitating hospital
admissions for heart failure and clinical outcomes: Findings from OPTIMIZE-HF. Arch
Intern Med. 2008;168:847.
ADDITIONAL READING
• ACC/AHA guidelines for the diagnosis and management of heart failure in adults.
• Noninvasive testing as recommended by the ACC/AHA guidelines on perioperative
cardiovascular evaluation and care for noncardiac surgery.
• High-output cardiac failure
• Afterload
• Preload
• Left ventricular end diastolic pressure
• Lusitropy
CODES
ICD9
428.0 Congestive heart failure, unspecified
ICD10
I50.9 Heart failure, unspecified
CLINICAL PEARLS
• Assess the severity of HF and other organ involvement in order to plan appropriate
anesthetic technique.
• Elective surgery should be postponed in patients with acutely decompensated HF.
• Patients with CHF have a high risk for perioperative morbidity and mortality.
• The primary goal of anesthesia care for patients with HF is maintaining cardiac output by
optimizing both preload and afterload, preventing cardiac ischemia, and avoiding cardiac
dysrhythmias throughout the perioperative period.
CONTEXT-SENSITIVE HALF-TIME
Elizabeth Rebello, MD
BASICS
DESCRIPTION
• Context-sensitive half-time is a pharmacokinetic parameter that differs from elimination
half-life.
• It is defined as the time required for the plasma drug concentration to decline by 50% after
terminating an infusion. It takes into account:
– Multicompartment systems
– The concepts of distribution as well as elimination
– Duration of infusion
• The concept of context-sensitive half-time has improved the understanding of the
pharmacokinetic behavior of anesthetic drugs after constant infusion.
• Until computer simulations proved otherwise, the elimination half-life of a drug, or the time
necessary for the concentration in the plasma to decrease by one-half of its original value,
was often used to describe the duration of a drug’s clinical effect (1).
• One-compartment pharmacokinetic model. The elimination half-life provides a useful and
suitable description of the rate of drug disposition on a one-compartment model. It reflects
metabolic capacity. However, it is of limited value in depicting the pharmacokinetics of
drugs with a multicompartment model (1).
• Multicompartment pharmacokinetic model. The context-sensitive half-time provides a useful
and suitable description of the rate of drug disposition in a multicompartment model.
Hence, it is useful in describing IV anesthetics and analgesics.
– Gradients. The concentration gradient between the compartments is the driving force
upon which plasma drug concentration differs in extent and direction over time.
– Continuous infusion. When a drug with a multi-compartment pharmacokinetic model is
given via a steady-state infusion, central compartment drug levels:
Immediately increase
Decline after a short administration interval because of redistribution into peripheral
compartments
Gradually fall after equilibrium has been reached with peripheral compartments,
secondary to drug metabolism or elimination (2,5). This assumes that the infusion does
not exceed the body’s metabolic/elimination rate.
– Discontinuation of infusion.
If equilibrium between the compartments has occurred, the plasma concentration will
decline over time from metabolism and elimination. Eventually, the drug will move from
the peripheral compartment back into the plasma; by doing so, it maintains the plasma
concentration of the drug and extends its pharmacological effect (2,3).
If equilibrium between the central and peripheral compartments has not occurred at the
time that the infusion is stopped, drug in the plasma will continue to redistribute as well
as be metabolized and eliminated. Eventually, the gradient will favor movement from
the peripheral compartment to the plasma (extends pharmacologic effect).
• Context-sensitive half-time is
– A pharmacokinetic parameter that is independent from elimination half-life (2). For a
multicompartment pharmacokinetic model, it is a more suitable descriptor of the rate of
drug disposition than the elimination half-life.
FIGURE 1. Context-sensitive half-times as a function of infusion duration. (Reproduced with permission from Hughes MA,
Glass PSA, Jacobs JR. Context–sensitive half-time in multicompartment pharmacokinetic models for intravenous anesthetic
drugs. Anesthesiology. 1992;76:334–341.)
– A function of the duration of the drug administration (Figure 1); it increases as duration
increases.
– Not a constant number; the relative effect of distributive processes on the plasma
concentration fluctuates over time and differs for each drug
– A tool by which different drugs may be compared and can aid with selecting an
appropriate choice for an infusion (6).
ANATOMY
• Central compartment: Plasma
• Peripheral compartment: Muscle, fat, etc.
Concurrent disease states may affect the context-sensitive half-time and recovery time
• The concept of context-sensitive half-time has increased the understanding of appropriate
drug selection for an infusion and has developed the practice of total intravenous anesthesia
(TIVA) as a standard type of anesthesia (5). Context-sensitive half-times are now defined in
drug development literature of IV analgesics and anesthetics to demonstrate that a drug
may be used as an infusion (4,5).
– Propofol. The context-sensitive half-time is not significantly prolonged even at a long
duration. This demonstrates one of the characteristics of propofol that makes it a suitable
drug for continuous infusion.
– Fentanyl. The context-sensitive half-time is significantly prolonged after 2 hours. Less
suitable for a constant infusion at long duration.
– Sufentanil. The context-sensitive half-time is not prolonged at a long duration. Suitable for
a continuous infusion.
– Alfentanil. Longer context-sensitive half-time as compared to sufentanil.
– Remifentanil. Context-sensitive half-time is independent of infusion duration and very
suitable for constant infusion.
– Midazolam. Longer context-sensitive half-time than propofol.
– Dexmedetomidine. Short context-sensitive half-time with infusions of short durations;
increases significantly with infusions of long (>8 hour) duration (7).
– Ketamine. Moderately short context-sensitive half-time, however, can become greater than
propofol over time with increased infusion duration.
• Limitations. The context-sensitive half-time may not always be a clinically relevant
parameter (2,8):
– Inhaled anesthetics: Desflurane, sevoflurane, isoflurane, and enflurane have small context-
sensitive half-times (<5 minutes) and do not increase significantly with increasing
duration (8).
– Does not directly describe how long it will take a patient to recover from IV anesthetics;
the site of action of IV anesthetics is in the brain, not in the plasma (6).
• Recovery describes awakening and being capable of maintaining spontaneous ventilation.
– Dependent on factors such as the discrepancy between the plasma drug concentration at
the termination of an infusion and the plasma concentration below which awakening
occurs (9).
– The effect-site decrement time, or the time required for any specified decrement in effect-
site concentration, may be a better predictor of recovery (9).
– May be affected by drug interactions and concurrent disease states (10).
• Intravenous anesthetics affect SSEPs to a lesser extent than volatile anesthetics. Infusions of
various drugs and combinations of drugs are commonly utilized with or without volatile
agents/nitrous oxide. They include: Propofol, etomidate, barbiturates, ketamine, opioids,
benzodiazepines, and other drugs (clonidine, dexmedetomidine, droperidol). Choice is often
dictated by hemodynamic parameters, side-effects, and context-sensitive half-time.
REFERENCES
1. Shafer SL, Varvel JR. Pharmacokinetics, pharmacodynamics, and rational opiod selection.
2. Hughes MA, Glass PSA, Jacobs JR. Context –sensitive half-time in multi-compartment
pharmacokinetic models for intravenous anesthetic drugs. Anesthesiology. 1992;76:334–
341.
3. Keifer J, Glass P. Context-sensitive half-time and anesthesia: How does theory match
reality? Curr Opin Anaesthesiol. 1999;12(4):443–448.
4. Bailey JM. Context-sensitive half-times. What are they and how valuable are they in
anesthesiology? Clin Pharmacokinet. 2002;41(11):793–799.
5. Glass PSA, Half-time or half-life: What matters for recovery from intravenous anesthesia?
6. Schnider TW, Shafer SL. Evolving clinically useful predictors of recovery from intravenous
anesthetics. Anesthesiology. 1995;83:902–905.
7. eeves JG, Glass SA, Lubarsky DA. Intravenous nonopioid anesthetics. In: Miller RD, ed.
Miller’s Anesthesia, 6th ed. Philadelphia: Elsevier Churchill Livingstone, 2005;317–378.
8. Bailey JM. Context sensitive half-times and other decrement times of inhaled anesthetics.
Anesth Analg. 1997;85:681–686.
9. Bailey JM. Technique for quantifying the duration of intravenous anesthetic effect.
10. Schrag S, Mohl U, Hirsch M, et al. Recovery from opiod anesthesia: The clinical
implications of context-sensitive half-times. Anesth Analg. 1998;86:184–190.
• Somatosensory evoked potentials/motor evoked potentials (SSEP/MEPs)
CLINICAL PEARLS
• Context-sensitive half-time is the time required for the plasma drug concentration to decline
by 50% after terminating an infusion.
• It takes into account the effects of distribution and metabolism on drug disposition.
• The context-sensitive half-time has improved our understanding of the pharmacokinetics of
anesthetics drugs after a continuous infusion. Additionally, it has complemented the basis
for drug selection when administering an infusion and has encouraged the use of TIVA as a
standard practice in anesthesia.
• Context-sensitive half-time does not directly describe how long it will take a patient to
recover from IV anesthetics.
CONTINUOUS POSITIVE AIRWAY PRESSURE
Rachel Helle, DO
BASICS
DESCRIPTION
• Continuous positive airway pressure (CPAP) is a form of noninvasive positive pressure
ventilation (NPPV). CPAP
– Provides a constant level of pressure to the airway throughout the respiratory cycle.
– Can be delivered via a nasal mask, nasal pillow, or full face mask with straps.
– Does not require endotracheal intubation.
– Levels are typically 5–12 cm H2O.
– Requires a conscious, cooperative patient, an adequately fitted facemask, and
hemodynamic stability
• CPAP is contraindicated in patients that:
– Require endotracheal intubation
– Are unable to adequately eliminate CO2
– Have acute facial trauma
– Have impaired swallowing
– Have gastrointestinal bleeding
• It is most commonly utilized by patients in the outpatient setting with obstructive sleep
apnea. For inpatients, it is utilized for chronic obstructive pulmonary disease (COPD)
exacerbations or cardiogenic pulmonary edema.
• CPAP creates a back pressure within the airway to recruit fluid-filled or collapsed alveoli
and increase effective lung inflation. In doing so, it
– Increases the functional residual capacity (FRC). Initially, CPAP affects only functional
alveoli, but with time will recruit unventilated alveoli.
– Can improve oxygenation by optimizing V/Q matching; improves ventilation to previously
atelectatic alveoli.
– Increases lung compliance by allowing alveoli to remain open.
– Reduces the work of breathing by forcing air into the lungs so inspiratory muscles require
less effort to generate negative pressure.
– Does not aid with CO2 elimination.
• CPAP is applied to a spontaneously breathing patient; it cannot provide mandatory or
assisted breaths. Patients determine their own respiratory rate, inspiratory time, and tidal
volume; it is effort independent. It requires a tight-fitting mask with no air leaks in order to
function appropriately.
• BiPAP (bi-level positive airway pressure) is similar to CPAP with two levels of pressure: A
higher pressure for inspiration and a lower pressure for expiration, both of which are above
the ambient pressure.
• Discomfort with CPAP
– Patients perceive an increased work of breathing.
– The straps and mask may be uncomfortable.
– Airflow can dry their eyes.
– The device may interfere with normal sleep.
• Complications of CPAP
– Skin breakdown
– Gastric distension. It is typically avoided in patients with recent gastric or esophageal
surgery; however, it has not been shown to increase the incidence of anastomotic leakage
following gastric bypass.
– May be associated with stress ulcers
– May cause barotrauma if pressures are too high (pressures <25 cm H2O are typically
safe).
• Increases mortality in patients with postextubation hypoxemic respiratory failure following
a course of prolonged mechanical ventilation, possibly due to a delay in reintubation.
• Laryngospasm. 100% oxygen using CPAP splints the airway and stretches laryngeal muscles,
attenuating the contraction of actin and myosin fibrils. Initiate CPAP as soon as possible
(<15 seconds) because the longer a muscle is in spasm, the stronger the contraction
becomes and the more difficult it is to overcome. CPAP will not break complete
laryngospasm because forced inflation of the pharynx distends the piriform fossa on either
side of the larynx and presses the aryepiglottic folds more firmly against each other. Oxygen
will fill the stomach instead of the lungs.
• In postoperative patients, CPAP is as effective as incentive spirometry in reducing atelectasis
and improving gas exchange.
• Possibly decreases morbidity. CPAP use has been shown to reduce the incidence of
reintubation, pneumonia, and sepsis, as well as decrease the duration of intensive care unit
(ICU) stay.
• Maintenance of upper airway patency. CPAP during induction or extubation helps maintain
patency, particularly in children.
• Obesity. Application of CPAP (6 cm H2O) for 5 minutes prior to induction, followed by 5
minutes of mechanical ventilation with PEEP in sedated patients has been suggested to be
superior to PEEP alone (5).
• Postlung resection. CPAP improves lung efficiency with gas exchange without undesired side
effects; it does not increase the pleural air leak or dead space to tidal volume ratio. It has
also been shown to reduce the incidence of reintubation and mortality.
• One lung ventilation. May be useful for the non-dependent and non-ventilated lung.
– It causes diversion of blood flow to the dependent (perfused) lung.
– 5–10 cm of H2O reduces shunt to nonventilated lung ratio, allowing for increased
oxygenation.
– Not useful in patients undergoing video-assisted thoracoscopy, as it can impede
visualization.
• Acute cardiogenic pulmonary edema. Earlier improvement and resolution of dyspnea,
respiratory distress, and metabolic abnormalities when compared to treatment with
standard oxygen therapy.
• Bridge from invasive to spontaneous ventilation in patients who pass weaning trials, but are
at risk for failing extubation in the ICU setting.
– Risk factors include
More than one comorbid condition
COPD
Congestive heart failure
APACHE score >12
Age >65 years
Ineffective cough
Excessive secretions
Previous weaning failures
Upper airway obstruction
– A favorable response to CPAP is typically apparent within the first hour.
– Absence of improvement strongly suggests the need for tracheal intubation.
• Obstructive sleep apnea (OSA). CPAP may be used at home during sleep to prevent
redundant upper airway tissue from causing a “variable extrathoracic" obstruction. Soft
tissue collapse obstructs the airway, leading to hypoventilation and stridor (snoring). With
positive pressure inhalation, the redundant tissue is “pushed out of the way" allowing air to
enter the lung.
– CPAP is indicated for episodes of nocturnal hypoxemia or retention of CO2 that are
diagnosed following a sleep study.
– Successful use of CPAP in an obese patient suggests that the patient can be ventilated with
a mask.
– CPAP may prevent postoperative atelectasis in the morbidly obese patient.
– Patients on CPAP at home should be instructed to bring their CPAP machines into the
hospital when they present for surgery.
• Patients are weaned from CPAP by gradually reducing the CPAP pressure and/or increasing
the amount of time each day without the pressure support.
REFERENCES
1. Antonelli M, Conti G. Noninvasive positive pressure ventilation as treatment for acute
respiratory failure in critically ill patients. Crit Care. 2000;4(1):15–22.
2. Keenan SP, Sinuff T, Cook DJ, et al. Which patients with acute exacerbation of chronic
obstructive pulmonary disease benefit from noninvasive positive-pressure ventilation? A
systematic review of the literature. Ann Intern Med. 2003;138(11):861–870.
3. Epstein SK. Weaning from mechanical ventilation. Respir Care. 2002;47(4):454–466.
4. Campbell RS, Davis BR. Pressure-controlled versus volume controlled ventilation: Does it
matter? Respir Care. 2002;47(4):416–424.
5. Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations
of chronic obstructive pulmonary disease. N Engl J Med. 1995;333(13):817–822.
6. Gray A, Goodacre S, Newby DE, et al. Noninvasive ventilation in acute cardiogenic
pulmonary edema. N Engl J Med. 2008;359(2):142–151.
7. Aquilό R, Togores B, Pons S, et al. Noninvasive ventilatory support after lung resectional
surgery. Chest. 1997;112(1):117–121.
8. Esteban A, Frutos-Vivar F, Ferguson ND, et al. Noninvasive positive-pressure ventilation for
respiratory failure after extubation. N Engl J Med. 2004;350(24):2452–2460.
ADDITIONAL READING
• Longnecker DE, Brown D, Newman M, et al. Anesthesiology. New York, NY: McGraw Hill;
2008.
• Positive-end expiratory pressure (PEEP)
• Obesity hypoventilation syndrome (OHS)/ Pickwickian syndrome
• Laryngospasm
• Atelectasis
CLINICAL PEARLS
• CPAP is commonly used in the operative setting to maintain airway patency during mask
ventilation and to terminate laryngospasm.
• Frequently used at home by those with obstructive sleep apnea.
• Patients who use home CPAP should be instructed to bring their machines to the hospital
prior to surgery.
• CPAP is effective in reducing atelectasis and improving oxygenation in postoperative
patients.
• NPPV and CPAP are used to manage acute and chronic respiratory failure in many patients,
and some patients with heart failure.
• The use of CPAP should not delay tracheal intubation in patients in acute respiratory failure.
• Noninvasive ventilation can preserve normal swallowing, feeding, speech, cough, and
physiologic air warming and humidification.
CONTROLLED HYPOTENSION
BASICS
DESCRIPTION
• Controlled hypotension is also known as deliberate or induced hypotension. It is an
anesthetic technique (first described in 1917 by Dr. Cushing) that is implemented to reduce
bleeding and the need for blood transfusions, as well as provide a “bloodless” surgical field
in certain scenarios.
– It is specifically mentioned in the ASA’s Practice Guidelines for Perioperative Blood
Transfusion and Adjuvant Therapies.
• Deliberate hypotension is achieved by utilizing one (or a combination of) drugs and/or
volatile agents to deliberately lower a surgical patient’s BP. Agents are titrated to achieve
one of the following endpoints:
– Reduction in the baseline mean arterial pressure (MAP) of 30%
– Goal MAP of 50–65 mm Hg
– Reduction in the systolic arterial pressure to 80–90 mm Hg (1)[A].
Physiology Principles
• Controlled hypotension is postulated to reduce blood loss by decreasing arterial and venous
bleeding. It is most commonly utilized in orthopedic, neurosurgical, plastics, and vascular
cases to improve surgical visualization, reduce operative time, and total blood loss.
• BP can be measured by either a noninvasive BP cuff or invasive arterial catheter (allows
beat-to-beat monitoring).
• Reductions in BP and MAP to the above-specified range can be achieved by reducing cardiac
output, preload, and/or afterload.
• There are several drugs and techniques that can be utilized; they are categorized as primary,
secondary, or both.
– Primary methods can be used alone; they include regional anesthesia, volatile agents,
sodium nitroprusside, remifentanil, nitroglycerin, trimethaphan, alprostadil, and
adenosine.
– Secondary methods are used adjunctively to limit the dosages needed or attenuate adverse
effects of other drugs or techniques. They include ACE inhibitors (captopril), clonidine,
dexmedetomidine, opioids, and propofol (1)[A].
– “Both” describes agents that can be used alone or in combination and include beta-
blockers (labetalol, esmolol, propranolol), calcium-channel blockers (verapamil, diltiazem,
nicardipine), and fenoldopam.
• Hemodynamics. Vasodilators can decrease afterload and improve left ventricular function as
well as decrease cardiac work and oxygen consumption. Additionally improved LV ejection
can reduce the LVEDV/LVEDP and possibly improve coronary perfusion (however, this must
be balanced against decreased diastolic blood pressure; see below).
ANATOMY
• BP measurements are typically performed in the upper extremities utilizing either a NIBP
cuff or an arterial line.
• The NIBP cuff can be used in the lower extremities. The arterial catheter is usually placed in
a radial artery but other options exist such as ulnar, femoral, and dorsalis pedis sites.
However, systolic BP readings in the leg can run 10–20% higher than the brachial artery
pressures.
• Although there are potential benefits, the anaesthetist needs to weigh them against the risks
in each individual patient.
• General risks include impaired perfusion and hypoxia of vital organs and microcirculatory
dysregulation. This is often difficult to discern as adequate oxygen delivery is an ever-
moving target that is altered by BP, hemoglobin content, oxygen saturation, tissue
extraction, and utilization.
– Cerebrum. CPP = MAP − ICP; where CPP is cerebral perfusion pressure, ICP is
intracranial pressure.
– Myocardium. No ideal number exists in regard to optimal cardiac perfusion pressures.
Coronary perfusion is equal to the diastolic blood pressure minus the left ventricular end
diastolic pressure.
Controlled hypotension can decrease the DBP but can also decrease afterload and
myocardial oxygen consumption.
As discussed above, LVEDV/LVEDP may be decreased and can offset decreases in
coronary perfusion pressure as well.
Additionally, because the LV is only perfused during diastole, the heart rate also becomes
an important factor.
– Renal concerns
Studies in patients with no preexisting renal disease have demonstrated that
autoregulation generally remains intact with a MAP between 80 and 180 mm Hg
More recent information suggests that the kidneys do not seem to incur damage with
MAPs of 50–60 mm Hg
Renal compensatory mechanisms appear to be well preserved at MAPs to 60 mm Hg for
>200 minutes (2)[B]
One study showed that MAPs of 50 mm Hg for approximately 120 minutes resulted in
decreased urine flow rate, effective renal blood flow, osmolar clearance, and endogenous
creatinine clearance; however, all parameters returned to normal after cessation of
anesthesia (3)[B].
– Hepatic concerns. The extent of autoregulation is unknown. Studies in patients with no
preexisting hepatic disease have suggested that MAPs between 50 and 60 mm Hg did not
appear to result in ischemia or affect autoregulation. Liver enzymes do not typically
increase, and when they are elevated they returned to normal after 14 days (4)[B].
• Patients with end-organ disease are at increased risk for ischemia or hypoperfusion
– Cerebral disease
With chronic hypertension, the cerebral autoregulation curve is shifted to the right
One well-controlled study by Williams-Russo et al (5), however, demonstrated no long-
term cognitive dysfunction in patients with end-organ disease (44% of 117 patients had
baseline HTN) at MAPs between 45 and 55 mm Hg suggesting that at these pressures the
metabolic requirements of the brain are met (4)[A]
Carotid stenosis results in maximal dilation distal to the lesion; thus, drops in BP cannot
be compensated by further vasodilation to maintain flow
– Cardiac disease
Chronic and significant hypertension alter the autoregulation range
Significant stenotic valve lesions have a fixed cardiac output and drops in SVR or the
reflexive tachycardia that may occur with controlled hypotension are not well tolerated
Atherosclerotic vessels are perfusion-dependent; vessels are maximally vasodilated just
distal to the lesion (similar to carotid stenosis)
– Renal. Acute on chronic renal dysfunction can result from intraoperative hypoxia or
hypotension.
• The major indication for imposing controlled hypotension is to reduce bleeding:
– Provides a favorable and clear surgical field and may increase the quality and speed of a
surgical procedure (6)[B].
– Decreases the need for blood product transfusion. This is generally welcomed secondary to
the concerns of infection and adverse systemic reactions (7)[A].
• Appropriate adjuncts should be implemented to aid in monitoring end-organ perfusion and
function as well as volume status. They include, but are not limited to
– Hemodynamic variables such as pulse pressure waveform variation in pulse oximetry and
arterial line waveforms aid with assessing volume status
– EKG rhythm analysis to asses myocardial perfusion and oxygenation
– ETCO2 reduces from “dead space” pathophysiology (decreases in BP reduce alveolar
perfusion and exhalation of CO2)
– Urine output is an indicator of renal perfusion
– BIS/EEG/SSEP/MEP monitoring to assess neural perfusion and oxygenation
– Blood gas analysis (pH, CO2, HCO3, base deficit) can indicate metabolic acidosis from
anaerobic metabolism (lactate production).
– CVP trends can aid with volume assessment
– Mixed venous O2 aids with assessing oxygen delivery and utilization at the tissue level.
• Of note, none of these methods guarantee end-organ perfusion but are adjunctive to clinical
impression.
• Hemodynamics
– The effect of controlled hypotension on HR, SVR, and ischemia varies based on the drug or
drugs used to achieve the hypotensive state. The overriding concern is ischemia, and
trying to gauge the level of hypotension that can safely be handled by patients with
preexisting cardiac conditions is sometimes difficult. Patient-specific decisions are
certainly warranted in this case.
EQUATIONS
• BP = CO × HR; BP is blood pressure, CO is cardiac output, and HR is heart rate
– Normal = 120/80 mm Hg
• MAP = [(2 × DBP) + SBP]/3; where MAP is mean arterial pressure, DBP is diastolic blood
pressure, and SBP is systolic blood pressure
– Normal = 70–110 mm Hg
• CPP = MAP – RAP (or ICP if greater); where CPP is cerebral perfusion pressure, MAP is
mean arterial pressure, RAP is right atrial pressure, and ICP is intracranial pressure
– Normal = between 70–90 mm Hg
REFERENCES
1. Tobias JD. Controlled hypotension in children: A critical review of available agents.
Paediatric Drugs. 2003;4(7):439–453.
2. Toivonen J, Kaukinen S, Oikkonen M, et al. Effects of deliberate hypotension induced by
labetalol on renal function. Eur J Anaesthesiol. 1991;8:13–20.
3. Lessard MR, Trepanier CA. Renal function and hemodynamics during prolonged isoflurane-
induced hypotension in humans. Anesthesiology. 1991;74:860–865.
4. Fukusaki M, Miyako M, Hara T, et al. Effects of controlled hypotension with sevoflurane
anaesthesia on hepatic function of surgical patients. Eur Acad Anesthesiol. 1999;16:111–
116.
5. Williams-Russo P, Sharrock NE, Mattis S, et al. Randomized trial of hypotensive epidural
anesthesia in older adults. Anesthesiology. 1991;91(4):926–935.
6. Enderby GEH. The advantages of controlled hypotension in surgery. Br Med Bull.
1958;14(1):49–51.
7. Choi WS, Samman N. Risks and benefits of deliberate hypotension in anaesthesia: A
systematic review. Int J Oral Maxillofac Surg. 2008;37(8):687–703.
ADDITIONAL READING
• Textbook of Neuroanaesthesia and Critical Care. 1st Edition, 2000. Edited by Basil F. Matta,
David K. Menon, and John M. Turner.
• Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 21th Edition, 2011. Edited
by Laurence Brunton, Bruce Chabner, and Bjorn Knollman.
• Scoliosis
• Perioperative blindness
• Blood transfusion infection
CLINICAL PEARLS
• For surgical procedures that may benefit from controlled hypotension, the risks for the
individual patient should be assessed.
• Patients at risk for end-organ damage should be discussed with the surgeon.
• Ensure that a reliable method of determining BP is used.
COOLING OF THE HEART
January Y. Tsai, MD
BASICS
DESCRIPTION
• Myocardial cooling is used to limit ischemic injury during cardiac arrest or surgical
procedures requiring cessation of blood flow to the myocardium. Examples include
– On pump coronary artery bypass grafting (OPCABG)
– Open valve repair or replacement
– Cardiac aneurysm repair
– Ascending aorta or aortic arch repair
• The therapeutic effects stem from reducing the metabolic rate and hence optimizing the
myocardial O2 supply:demand ratio.
• Myocardial O2 consumption results from:
– Mechanical/contractile processes (~80% of O2 consumption)
– Basal O2 consumption (~20% of O2 consumption)
– Electrical/conduction processes (~0.5% of O2 consumption) (1)
• Myocardial O2 consumption varies as a function of temperature and contractility
– 37°C NSR at rest: 6–8 mLO2/100 g/min
– 37°C NSR heavy exercise: 70 mLO2/100 g/min
– 37°C VF: 4 mLO2/100 g/min
– 37°C Empty beating: 3 mLO2/100 g/min
– 37°C Asystole: 1–2 mLO2/100 g/min
– 15°C Empty beating: 0.4 mLO2/100 g/min
– 15°C Asystole: 0.3 mLO2/100 g/min (2)
• Cooling of the heart decreases mechanical/contractile processes as well as cell
“housekeeping” activities, while maintaining cell membrane integrity (Na+–K+ ATP
synthase). Additionally,
– ATP consumption: Decreases
– Heart rate: Decreases
– Cardiac output: Decreases by 7%/1°C
– Stroke volume: Unchanged
– Arterial pressure: Unchanged
– Enzyme Q10: Reaction rate halves for every 10°C decrease in temperature; normally ∼2
(3)
• The putative molecular basis of myocardial protection consists of
– Reduced inflammation
– Modified cell death signaling pathways
– Preserved mitochondrial protein gene expression
– Decreased EKR1/2 enzyme phosphorylation
– Decreased COX-2 expression
– Upregulation of Akt transcription factor in cardiomyocytes with preserved cell survival (4)
• Cardioplegia solution is utilized to halt electrical activity with consequent therapeutic arrest
of cardiomyocyte contractility. Cold cardioplegia (∼4°C) containing a high potassium (K+)
concentration of 20–30 mmol/L is administered to prevent cellular repolarization; it is
delivered via the coronary sinus (retrograde), aortic root (antegrade), and/or coronary ostia.
Since the resting potential of the ventricular myocardium is about –84 mV at an
extracellular K+ concentration of 5.4 mmol/L, raising the K+ concentration to 16.2 mmol/L
increases the resting potential to –60 mV, a level at which muscle fibers are inexcitable to
ordinary stimuli. Theoretically, cold cardioplegia solution decreases O2 consumption from
6–8 mLO2/100 g/ min to 0.3 mLO2/100 g/min.
• Systemic physiologic effects of hypothermia include
– Cold diuresis
– Alkalosis
– Hypokalemia
– Increased infection risk
– Mild coagulopathy
– Hyperglycemia
• Effects of inadequate cooling include
– Myocardial ischemia
– Arrhythmia
– Cardiac stunning
– Difficulty weaning from CPB
• Causes of inadequate cardioplegia administration include
– Improper cannula placement (right atrium instead of CS)
– Significant aortic insufficiency
– Severe occlusive coronary disease physically hindering distribution of cardioplegia
solution
– Infrequent cardioplegia administration
– Inadequate volume of solution
– Incorrect potassium concentration
• Significant aortic insufficiency
– Retrograde flow through the aortic valve prevents adequate antegrade cardioplegia
delivery to the coronary arteries.
– May require retrograde cardioplegia via the CS.
– In a study of 84 consecutive patients undergoing CABG, TEE allowed accurate calculation
of the severity of aortic regurgitation, which was significantly associated with the need for
retrograde cardioplegia administration (5).
• Ventricular fibrillation
– Likely with profound hypothermia (<25°C)
– Abnormal conduction may require pacing.
• Myocardial protection through decreasing the metabolic rate is crucial with preexisting
coronary disease.
• Cooling of the heart can occur concurrent with systemic cooling:
– External cooling with ice pack or a heat exchange device
– Endovascular cooling
– Infusion of cold intravenous fluids
– Gastric lavage
– Urinary bladder lavage
• Temperature measurement
– Locations include nasopharynx, esophagus, bladder, and rectum.
• Body size
– May affect duration of cooling and rewarming times
• TEE
– Bicaval and midesophageal four-chamber views are useful for evaluating cardiac
contractility, segmental wall motion, and to assist retrograde cannula placement.
– Inadequate delivery of cold cardioplegia solution may occur due to physical occlusion of
the coronary arteries may require retrograde administration.
REFERENCES
1. raunwald E. The determinants of myocardial oxygen consumption. Thirteenth Bowditch
Lecture, XXIV International Congress of Physiological Sciences, Washington, D.C., August
30, 1968.
2. essen M, Abd-Elfattah AS, Wechsler AS. Neonatal myocardial oxygen consumption during
ventricular fibrillation, hypothermia, and potassium arrest. Ann Thorac Surg. 1996;61:82–
87.
3. Hamamoto H, Sakamoto H, Leshnower BG, et al. Very mild hypothermia during ischemia
and reperfusion improves postinfarction ventricular remodeling. Ann Thorac Surg.
2009;87:172–177.
4. Drescher C, Diestel A, Wollersheim S, et al. How does hypothermia protect cardiomyocytes
during cardioplegic ischemia? Eur J Cardiothoracic Surg.
2011;doi:10.1016/j.ejcts.2010.12.006.
5. Moisa RB, Zeldis SM, Alper SA, et al. Aortic regurgitation in coronary artery bypass
grafting: Implications for cardioplegia administration. Ann Thorac Surg. 1995;60(3):665–
668.
6. Tissier R, Chenoune M, Ghaleh B, et al. The small chill: Mild hypothermia for
cardioprotection? Cardiovasc Res. 2010;88:406–414.
• Cardioplegia
• Hypothermia
CLINICAL PEARLS
• Hypothermia combined with cardioplegia is commonly used for cardioprotection.
• Optimal temperature remains unknown.
• Systemic hypothermia can have neuroprotective effects.
• TEE assists retrograde CS cannula placement.
• Mild hypothermia (32–35°C) is beneficial for cardioprotection with STEMI or resuscitation
after cardiac arrest when instituted expeditiously (6).
– The cardioprotective effects of hypothermia are greatest when cooling is initiated within
20 minutes after the onset of ischemia.
– Following coronary artery occlusion, infarct size was progressively reduced with
decreasing temperature from 39.5 to 35.4°C (3). Overall, hypothermic myocardial
protection decreased metabolic requirements and minimized ischemic insult.
COR PULMONALE
BASICS
DESCRIPTION
• Cor pulmonale consists of right ventricular (RV) impairment or failure in the absence of left
ventricular (LV) disease. It is secondary to acute or chronic abnormalities of the pulmonary
circulation, lungs, or thorax and is sometimes referred to as “pulmonary” heart failure.
• It can be diagnosed by noninvasive assessment of RV function using EKG and invasively via
pulmonary artery catheterization; however, for both of these modalities, diagnostic criteria
are not standardized.
EPIDEMIOLOGY
Incidence
• Unknown; poorly studied in the population of patients undergoing general anesthesia.
• RV failure occurs in ~30% of patients after left ventricular assist device placement (LVAD).
Prevalence
Greater in patients with underlying pulmonary disease that contributes to chronic hypoxic
states
Morbidity
• Cor pulmonale and pulmonary hypertension (PH) are associated with a 13.1-fold increase in
perioperative morbidity and mortality when undergoing noncardiac surgery compared to
cross-matched patients without PH (1).
– More likely to develop congestive heart failure (OR = 11.9)
– Susceptible to more hemodynamic instability and respiratory failure
– Patients were shown to need longer ventilator support, stay longer in the intensive care
unit (ICU), and have higher readmission to the hospital within 30 days of surgery.
Mortality
• Despite equivalently smooth operative courses, PH patients had increased in-hospital deaths
compared to matched controls (9.7% vs 0%); systolic pulmonary artery pressure (PAP)
served as an independent predictor of mortality (2).
• These patients also had significantly more frequent postoperative heart failure and delayed
extubation.
• Cor pulmonale and RV failure can be either acute or chronic.
• Acute etiologies include thromboembolic disease, cardiac tamponade, RV ischemia, and
acute chest syndrome with sickle cell disease
• Chronic etiologies include chronic obstructive pulmonary disease, obstructive sleep apnea,
valvular disease, congenital heart disease, PH, and collagen-vascular disease
PATHOPHYSIOLOGY
• Similar to the LV, the RV stroke volume is affected by preload (central venous pressures),
afterload (pulmonary artery pressures and pulmonary vascular resistance), and contractility.
• In contrast to the LV, the RV has ~1/6th the muscle mass, decreasing its ability to pump
effectively against an increased afterload. It functions more as a volume pump than a
pressure pump.
• Elevations in RV afterload can result in
• Acute: Dilation of the RV
• Chronic: Hypertrophic response to improve contractile forces against the increased tension;
recall LaPlace’s law. This results in decreased compliance and impaired diastolic filling.
• In low cardiac states, compensation is primarily with a tachycardic response due the the
RV’s limited ability to respond with greater contractile force. The RV is more prone to overt
failure when faced with decreased preload (vasodilatory states), increased afterload
(hypoxia, hypercarbia, coughing, bucking), or decreased contractility (ischemia,
anesthetics).
• Hypoxemia. The degree of hypoxemia and inability to maintain arterial oxygenation is
directly associated with the development of PH and RV failure. Hypoxia induces pulmonary
vasoconstriction (increased PVR), which in turn increases the risk of RV strain and failure.
• Arrhythmias
• Atrial (more common) or ventricular arrhythmias can develop.
• Inhaled beta-agonists may induce tachycardias.
• Systemic beta antagonists may worsen bronchospastic status, thus creating further
complications.
• Hepatic congestion secondary to venous congestion is common, usually evident by
elevations in transaminases and INR. This may partially subside with optimization of cor
pulmonale.
• Patients should be optimized prior to elective surgery. Control infections and bronchospastic
diseases prior to administering anesthesia.
• Pulmonary hygiene should be focused on the clearance of secretions and recruiting poorly
ventilated units of lung in order to optimize oxygenation and ventilation.
• Avoid acute increases in the PAP (hypoxia, hypercarbia, acidosis, increased sympathetic
states), or decreases in contractility.
• Volume optimization must be carefully assessed and addressed. Hypovolemia will decrease
preload and RV output; whereas fluid overload may exacerbate arrhythmias and RV strain.
SYMPTOMS
• Peripheral edema and ascites, often presenting as ankle edema and congestive hepatomegaly
• Distress during mild exertion or rest, not relieved by sitting upright (in contrast to
orthopnea present in patients with LV failure)
• Nonproductive cough
• Other classically associated symptoms of heart failure
History
• Dyspnea and tachypnea often overlap with underlying pulmonary disease.
• Severity of underlying disease: Exercise tolerance, need for bronchodilators, or supplemental
oxygen
• Exacerbations: Fatigue, worsening dyspnea, and increased oxygen requirements
Signs/Physical Exam
• Cardiac examination: A right-heave may be palpated along the left sternal border or in the
epigastrium; an augmented pulmonic component of the second heart sound; and associated
murmurs due to incompetence of the tricuspid valve (during systole) and/or pulmonic valve
exist (during diastole). Both murmurs are augmented by inspiration.
• Peripheral edema, jugular venous engorgement, and positive hepatojugular reflex
TREATMENT HISTORY
• Options are focused primarily on maintaining and restoring oxygenation and ventilation to
decrease PVR, volume status, and RV workload.
• Supportive therapy of oxygen is important to maintain a PaO2 >60 mm Hg or SpO2 >90%.
• Lung transplantation in severe disease
MEDICATIONS
• Anticoagulation for thromboembolic disease
• Heart failure regimens (diuretic therapy) may be needed to manage peripheral edema but
can also impair RV function (decreased preload and metabolic alkalosis).
• Calcium channel blockers (CCBs) are a first-line outpatient treatment, although many are
not candidates or responders to these. These agents can exacerbate perioperative
hypotension and can increase mortality risk in patients with systolic dysfunction.
• Phosphodiesterase inhibitors and endothelin antagonists
• While not FDA approved for this use, inhaled nitric oxide (iNO) and inhaled epoprostenol
have been used to treat acute crises (RV failure, hypoxemia, and PH).
Labs/Studies
• Arterial blood gas: Objectively assess the degree of respiratory insufficiency.
• Liver function tests: Dysfunction and coexisting coagulopathy
• EKG: Findings include RV enlargement, ventricular septal flattening “D-sign,” ventricular
dysmotility, and evidence of elevated estimated RV systolic pressure.
• Chest x-ray: A decrease in the retrosternal space on lateral films indicates RV hypertrophy. A
prominent main pulmonary artery and decreased vascular markings may be consistent with
PH.
• Echocardiogram: Right atrial and RV hypertrophy (peaked P waves in leads II, III, and aVF).
Right axis deviation and right bundle branch blocks can also be seen.
• Pulmonary function tests: Assess the response to bronchodilator therapy.
• Right atrial pressure tracing: Predominant A wave due to enhanced right atrial contraction
with decreased ventricular compliance.
• Right heart catheterization: Elevated PAP with normal pulmonary artery occlusion pressures
(representing normal left ventricular end-diastolic pressure, LVEDP).
• Cardiac MRI: While not widely available, can provide accurate information on RV function.
TREATMENT
Premedications
• Maintaining oxygenation and ventilation is imperative; thus, medications that may depress
ventilation (i.e., opioids) should be used judiciously.
• Inhaled beta-agonists may be needed to optimize pulmonary disease.
Increased risk of perioperative complications, morbidity, and mortality
INTRAOPERATIVE CARE
• Dependent on the procedure. As a sole technique, regional anesthesia has the benefit of
avoiding anesthetic induction, airway instrumentation, mechanical ventilation, and
extubation, as well as minimizing systemic opioids. However, supplemental sedation, failed
blocks, or complications of the block (e.g., high spinal and local anesthetic toxicity) need to
also be considered. Additionally, patients may not be able to lie flat during a procedure.
• Supplementing the general anesthetic with a regional technique has the benefit of
decreasing the need for systemic opioids.
• Caution should be exercised when performing regional techniques that can affect respiratory
parameters. Interscalene blocks can cause phrenic nerve palsies (C3, C4, C5); neuraxial
techniques to the T6 level can affect accessory muscles of respiration.
Monitors
• Invasive monitoring is dependent on the degree of patient dysfunction and the operative
procedure.
• Arterial line. Monitoring arterial line BP helps identify rapid changes in hemodynamics and
allows frequent blood gas measurements of PaO2 and PaCO2 (can aid with decision to
extubate).
• Central lines can assess RV pressures.
• Pulmonary artery catheters. May be used to assess the degree of patient illness, effect of
fluid shifts and changes in acid/base status from hypercarbia, laparoscopy, etc. by
monitoring the PAPs.
• An alternative to invasive monitoring includes transesophageal echocardiogram; however,
this monitor requires expertise and is usually employed only while the patient is intubated
• To minimize increases in PVR, patients should have an adequate depth of anesthesia prior to
instrumenting the airway.
• Supraglottic devices (i.e., LMA) may decrease airway stimulation; however, adequate
ventilation must be ensured to prevent respiratory acidosis.
• The RV can also be preload dependent against the fixed afterload of PH. Anesthetic selection
must avoid sympathetic spikes without dropping systemic vascular resistance.
Maintenance
• N2O is controversial with conflicting evidence on its effects on PVR. Monitoring the right
atrial or PAP can allow early identification of intolerance and allow discontinuation.
• Neuromuscular blockade (and other anesthetic drugs) should avoid histamine release.
• Fluids should be titrated judiciously; patients can be sensitive to hypovolemia and require a
sufficient preload to maintain the RV output. However, hypervolemia can overload the
Frank–Starling curve of the RV and lead to strain or failure and worsening venous
congestion.
• Extubation. Standard criteria apply; however, patients may be less capable of meeting them.
If adequate ventilation and oxygenation cannot be ensured, consider delaying extubation.
Deep extubation can result in inadequate ventilation and hypercarbia.
• A smooth emergence with minimal coughing is desired to prevent increased intrathoracic
pressure, RV afterload, and sympathetic input.
• Tracheal application of lidocaine may be helpful to minimize the response to airway
instrumentation.
REFERENCES
1. Kaw R, Pasupuleti V, Deshpande A, et al. Pulmonary hypertension: An important predictor
of outcomes in patients undergoing non-cardiac surgery. Respir Med. 2001;105:619–624.
2. Lai HC, Lai HC, Wang KY, et al. Severe pulmonary hypertension complicates postoperative
outcome of non-cardiac surgery. Br J Anaesth. 2007;99(2):184–190.
3. Lahm T, McCaslin CA, Wozniak TC, et al. Medical and surgical treatment of acute right
ventricular failure. J Am Coll Cardiol. 2010;56(18):1435–1446.
4. Jardin F, Viellard-Baron A. Acute cor pulmonale. Curr Opin Crit Care. 2009;15(1):67–70.
5. Veillard-Baron A, Jardin F. Why protect the right ventricle in patients with acute
respiratory distress syndrome? Curr Opin Crit Care. 2003;9(1):15–21.
ADDITIONAL READING
• Haddad F, Couture P, Tousignant C, et al. The right ventricle in cardiac surgery, a
perioperative perspective: I. Anatomy, physiology, and assessment. Anesth Analg.
2009;108(2):407–421.
• Haddad F, Couture P, Tousignant C, et al. The right ventricle in cardiac surgery, a
perioperative perspective: II. Pathophysiology, clinical importance, and management.
Anesth Analg. 2009;108(2):422–433.
• Obstructive sleep apnea
• Epidural
• Deep extubation
CODES
ICD9
• 415.0 Acute cor pulmonale
• 416.9 Chronic pulmonary heart disease, unspecified
ICD10
• I26.09 Other pulmonary embolism with acute cor pulmonale
• I27.81 Cor pulmonale (chronic)
CLINICAL PEARLS
• Management and support of cor pulmonale include the avoidance of hypercarbia, hypoxia,
and heightened sympathetic states.
• Further treatment requires application of physiologic principles through decreasing RV
afterload, while maintaining preload and contractility.
• Tachycardia is an appropriate compensatory response to RV dysfunction and should be
treated cautiously.
• Laparoscopy may be poorly tolerated; it is associated with hypercarbia and decreased
venous return due caval compression.
CORNEAL ABRASIONS
John L. Ard Jr., MD
T. Kate Huncke, MD
BASICS
DESCRIPTION
• Corneal abrasion is the most common ocular injury during nonocular surgery.
• It usually does not lead to permanent injury, but can be the cause of great pain and
discomfort in the postoperative period.
EPIDEMIOLOGY
Incidence
1.51 cases per 1,000 nonocular surgeries
Morbidity
• Usually resolves within 24–72 hours with proper treatment.
• In one study, 16% of corneal abrasions resulted in permanent injury.
• Direct trauma and chemical irritation (responsible for 20% of injuries):
– Face mask
– Anesthesia provider’s stethoscope, wrist watch, protective face shields, or badge
– Laryngoscope blade
– Airway placement
– Suction
– Central venous line insertions
– Laryngeal mask airway placement
– Drapes
– Patients hands or fingers as they rub their eyes after emergence with the index finger and
the pulse oximeter attached
– Patients lying laterally after emergence while still slightly sedated
• Lagophthalmos is the term to describe the inability to close the eyelids completely. Under
general anesthesia, incomplete closure (and taping) can result in dry eye; accounts for 80%
of injuries.
• Lateral or prone position
• Head and neck surgery. The surgical field is located near the eyes and increases the
possibility of trauma by the surgical team and inadvertent instillation of antimicrobial
preparation solutions (1)[A].
• Longer surgical duration; less common in procedures <1 hour (2)[A].
• Zygomaticomaxillary complex fractures are associated with minor (55%) and major (10%)
ocular injuries (3)[B]. Consider preoperative evaluation to ascertain baseline.
• Tear production. Decreases can result in drying of the corneal epithelium. It is affected in
certain populations:
– Diabetics have decreased tear production and increased corneal sensitivity (4)[B].
– Menopausal and postmenopausal women have decreased production due to serum
prolactin and sex hormone levels.
– Premature infants have decreased production until a mean postconceptual age of 8.5
months (5)[B].
– Women under the age of 41 have an increase in tear flow and lower tear osmolality; no
difference in corneal abrasions has been noticed, however (6)[C].
– Rheumatoid arthritis with Sjögren’s syndrome has decreased tear production.
• The cornea is the outer most layer of the eyeball. The external surface of the cornea is a
layer of delicate epithelium that is continuous with the conjunctiva.
• Dry eye. An inadequate supply of oxygen to the cornea produces edema and in the presence
of a dry environment, desquamation of the epithelial layer readily occurs, producing an
abrasion.
• General anesthesia:
– Reduces basal tear production
– Abolishes the blink reflex
– Decreases the tone of the orbicularis oculi that normally keeps the eyelid closed
– Abolishes Bell’s phenomenon (the eyeball turns upward during normal sleep)
• Manually close eyes and tape them shut as soon as the patient loses consciousness after the
induction of general anesthesia (7)[C]. Check to make sure the eye is completely closed. Eye
injury may occur if the patient opens their eyes prematurely beneath the tape or with
removal of the tape (8)[A].
• Intermittent checks to ensure that there is no inadvertent eyeball compression, particularly
in the lateral or prone position or head and neck surgeries.
• Op-sites or bio-occlusive dressings may be considered in prone, lateral, prolonged
procedures, or head and neck surgery. They offer protection as well as prevent drying and
exposure to contaminants (cleaning solutions).
• Water-based eye ointment. Studies have not shown that this significantly reduces the
incidence of injury. Additionally, patients may be more likely to rub their eyes to improve
visualization.
• Corneal protectors or shells may be considered when facial injuries or burns or the
procedure prevent taping or op-site.
• Soft contact lenses
• Protective goggles are rigid and prevent inadvertent compression of the cornea.
• Tarsorrhaphy sutures (suture the eyelids closed).
• Geliperm is a sterile, transparent, pliant hydrogel dressing that allows for continuous
observation of the eye (9)[C].
• Laser eye protection for the patient includes taping closed and placing wet sponges over the
eye, taping the sponges on the face, and placing a metal shield over it. Alternatively, laser
goggles can be placed.
DIAGNOSIS
• An urgent ophthalmology consultation for any patient who wakes up complaining of painful
eye or decreased vision.
• The ophthalmologist will examine the eye with fluorescein stain and a blue light.
• Conjunctivitis
• Red eye
• Acute angle-closure glaucoma
• Corneal ulcer
• Episcleritis
• Keratitis
• Scleritis
TREATMENT
• Small abrasions with moderate pain

– Topical antimicrobials like chloramphenicol 1% ointment: Two drops every 3 hours (10)
[C].
• Larger abrasions. In addition to chloramphenicol 1% ointment (10)[C]:
– Topical analgesics (NSAIDS) like diclofenac drops 0.1% solution: One drop four times
daily (10)[A]
– Oral analgesics (10)[A]
FOLLOW-UP
Re-evaluate in 24 hours; if there is improvement, there is no need to follow up unless

symptoms worsen again.
CLOSED CLAIMS DATA
• Eye injuries are 3% of total claims (11)[C].
– Corneal abrasions comprised the largest single group of eye injuries (25 of 71 eye injuries)
(11)[C].
– Sixteen percent of corneal abrasions resulted in permanent injury (11)[C].
REFERENCES
1. Siffring PA, Poulton TJ. Prevention of ophthalmic complications during general anesthesia.
Anesthesiology. 1987;66:569–570. [A]
2. atra YK, Bali IM. Corneal abrasions during general anesthesia. Anesth Analg. 1977;56:363–
365. [A]
3. amal BT, Pfahler SM, Lane KA, et al. Opthalmic injuries in patients with
zygomaticomaxillary complex fractures requiring surgical repair. J Oral Maxillofac Surg.
2009;67:986–989. [B]
4. ousen P, Cackett P, Bennett H, et al. Tear production and corneal sensitivity in diabetes. J
Diabetes Complications. 2007;21:371–373. [B]
5. kar Y, Cira A, Apaydin C, et al. The effect of prematurity on tear production. Curr Eye Res.
2004;28:145–151. [B]
6. raig JP, Tomlinson A. Effect of age on tear osmolality. Optom Vis Sci. 1995;72:713–717.
[C]
7. hite E, Crosse MM. The aetiology and prevention of peri-operative corneal abrasions.
Anesthaesia. 1998;53:157–161. [C]
8. now JC, Kripke BJ, Norton ML, et al. Corneal injuries during general anesthesia. Anesth
Analg. 1975;54:465–467. [A]
9. uddihy PJ, Whittet H. Eye observation and corneal protection during endonasal surgery. J
Laryngol Otol. 2005;119:556–557. [A]
10. ilson S, Last A. Management of corneal abrasions. Am Fam Physician. 2004;70:123–128.
[A]
11. ild WM, Posner KL, Caplan RA, et al. Eye injuries associated with anesthesia. A closed
claims analysis. Anesthesiology. 1992;76:204–208. [C]
12. artin D, Weingarten T, et al. Performance improvement system and postoperative corneal
injuries. Anesthesiology. 2009;111:320–326. [B]
ADDITIONAL READING
• Batra YK, Bali IM. Corneal abrasions during general anesthesia. Anesth Analg. 1977;56:363–
365.
• Cucchiara RF, Black S. Corneal abrasion during anesthesia and surgery. Anesthesiology.
1988;69:978–979.
• Perioperative blindness
CODES
ICD9
918.1 Corneal abrasion
ICD10
• S05.00XA Inj conjunctiva and corneal abrasion w/o fb, unsp eye, init
• S05.01XA Inj conjunctiva and corneal abrasion w/o fb, right eye, init
• S05.02XA Inj conjunctiva and corneal abrasion w/o fb, left eye, init
CLINICAL PEARLS
• Patching the eye is no longer thought to be helpful (9)[A].
• Topical mydriatics are not effective for treatment of corneal abrasions and are not
recommended (9)[B].
• Increasing awareness of corneal abrasions helps prevent the injury (12)[B].
• The injury may occur in the immediate postoperative period as well as the operating room.
CORONARY ARTERIES
Daniel Castillo, MD
BASICS
DESCRIPTION
• The coronary arteries deliver oxygen-rich blood to the myocardium.
• Epicardial coronary arteries run on the outer surface of the heart. When healthy, they are
capable of autoregulation to maintain an adequate coronary blood flow (CBF) that meets
oxygen demand.
• Subendocardial coronary arteries run deep within the myocardium.
• The coronary arteries are classified as “end-circulation,” since they represent the only source
of blood supply to the myocardium. Thus, blockage of these vessels can be critical since
there is typically very little redundant blood supply (unless collateral blood flow has
developed).
• Coronary blood flow (CBF) varies directly with the pressure difference across the coronary
bed (coronary perfusion pressure; CPP) and inversely with the resistance of the coronary
vasculature (CVR): CBF = CPP/CVR.
– The CPP equals the arterial driving pressure minus the back-pressure to flow across the
coronary bed.
For the left ventricle (LV), the driving pressure is the aortic pressure during diastole
(DBP).
Left ventricular end diastolic pressure (LVEDP) is utilized to measure the back pressure.
As its name implies, it is the pressure within the left ventricle at the end of diastole; it is
dependent on preload volume, ventricular compliance, and systolic function.
Thus, CPP of left ventricle = DBP − LVEDP
– Resting CBF is 225–250 mL/min or 4–5% of the cardiac output.
– There are pronounced systolic and diastolic coronary flow variations throughout the
cardiac cycle.
• Diastole. Arterial inflow primarily occurs during diastole; at least 75% of total CBF to the LV
occurs during diastole.
• Systole. Arterial inflow declines as venous outflow peaks, reflecting the compression of the
microcirculatory vessels. During systole, the strength of compression decreases blood flow
through subendocardial arteries of the LV to almost zero. Thus, the subendocardial system
of the LV is the most vulnerable site for myocardial ischemia.
• Myocardial oxygen consumption
– Myocardial oxygen extraction is near-maximal at rest (about 75% of arterial oxygen
content); by far the greatest oxygen extraction of all organs.
– The major determinants of oxygen demand are heart rate, contractility, and wall stress
(preload, afterload, wall thickness); heart rate is the most important among them.
– Since cardiac oxygen extraction is near-maximal under resting conditions, the primary
mechanism to meet increased oxygen demand is through enhanced delivery.
– The factors responsible for regulation of CBF are not well understood; various local
metabolic factors are implicated. Activation of beta-adrenoreceptors (sympathetic nervous
system) also leads to coronary vasodilatation.
ANATOMY
• The blood supply to the myocardium arises from the aorta behind the left and right aortic
valve leaflets through two main coronary arteries: The left main and the right coronary
artery (RCA).
• The left main coronary artery (LMCA) extends for a short distance before dividing into the
left anterior descending artery (LAD) and the circumflex coronary artery (LCX) (see Figure
1).
FIGURE 1. Coronary artery anatomy
• LAD
– Courses down the interventricular groove and gives rise to the septal and diagonal
branches.
– The septal branches vary in number, size, and course into the interventricular septum and
usually supply the anterior two thirds of the septum.
– One to three diagonal branches exist and distribute blood to the anterolateral aspect of the
heart.
– The LAD continues down the interventricular groove and usually passes all the way
around the apex of the LV.
• LCX
– Passes along the base of the LV within the coronary sulcus and terminates in the left
posterior descending branch.
– Its main vessels are the obtuse marginal branches (one to three in number) and supply the
lateral-free wall of the LV.
• RCA
– Arises from the anterior wall of the aortic root (also makes it prone to air entry on
termination of cardiopulmonary bypass).
– Passes down the right atrioventricular (AV) groove.
– Usually supplies the anterior and posterior walls of the right ventricle except for the apex
(supplied by LAD).
– Gives rise to the acute marginal branches that supply the anterior wall of the right
ventricle.
– Also supplies the right atrium including the sinoatrial (SA) node in about 55% (in 45% SA
node supplied by LCX), the AV node in about 90% (10% supplied by LCX), the posterior
third of the septum, the inferior wall, and the base of the LV.
• Coronary artery dominance
– In about 80–85% of individuals, the RCA gives rise to the posterior descending artery
(PDA) to supply the posterior inferior aspect of the LV; this pattern of blood supply is
called a right dominant system.
– In a left dominant system the LCX supplies the posterior–inferior aspect of the LV (about
10–15%).
– In a codominant system, both the RCA and the LCX supply the posterior–inferior aspect of
the LV (about 5–10%).
• Myocardial segments
– Consensus recommendations were published by the American Heart Association (AHA) on
how to define 17 myocardial segments (see Figure 2) (1). The standardization of the 17
segments facilitates communication about results from the wide variety of cardiac imaging
modalities currently in use for research and clinical applications.
– Despite tremendous variability in the coronary artery blood supply to myocardial
segments, the 17 segments were assigned to the 3 major coronary arteries.
FIGURE 2. American Heart Association consensus definitions of left ventricular segmentation. (Reused with permission
from ACC/AHA 2007 Guidelines on perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: Executive
Summary. Circulation. 2007;116:1971–1996.)
• Coronary collaterals
– An extensive network of coronary capillaries are normally present from the time of birth.
In normal hearts, the collaterals are not demonstrable by angiography due to their small
diameter. Only enlarged collaterals (due to myocardial oxygen deprivation) are visible on
angiography.
– These collaterals are not visualized on angiography in normal hearts due to their small
diameter. Only enlarged collaterals (due to chronic myocardial oxygen deprivation) are
visible on angiography.
• Blood supply of the papillary muscles
– Two papillary muscles tether the mitral valve to the wall of the heart. If the papillary
muscles are not functioning properly, mitral regurgitation may develop.
– The anterolateral papillary muscle usually receives blood supplies from two arteries (LAD
and LCX) and thus is more resistant to coronary ischemia.
– The posteromedial papillary muscle is usually only supplied by one coronary artery (PDA)
and thus more susceptible to ischemia.
• Coronary artery disease (CAD) is a condition in which a plaque builds up inside the
coronary arteries. It is the leading cause of death worldwide.
– Cardiac catheterization (angiography) is the gold standard to determine the anatomy of
the coronary blood supply in the individual patient. It can show whether CAD is present,
but it does not necessarily assess the functional significance of a lesion and comes with its
own morbidity/mortality risk (see chapter on cardiac catheterization).
– Alternatively, less-invasive imaging methods are on the rise to diagnose CAD: Computed
tomography angiography, cardiac magnetic resonance imaging, and positron emission
computed tomography (PET).
– Echocardiography and nuclear tests do not provide direct information about coronary
arteries. Wall motion abnormalities are correlated and extrapolated to likely artery
distribution.
• Patients with CAD are at increased risk for an adverse perioperative event.
• All patients should be evaluated preoperatively for the presence of cardiovascular risk
factors; the decision should be made whether further diagnostic studies and/or
interventions are warranted prior to surgery in accordance with the AHA/ACA guidelines
(2,3)[B].
• 12-Lead EKG
– Inferior leads (II, III, and aVF): Electrical function of the inferior heart muscle. The inferior
wall is usually supplied by the RCA.
– Lateral leads (aVL, I, V5, and V6): Electrical function of the lateral wall of the LV.
Ischemia or infarction is typically present here, as this represents the area of greatest
oxygen consumption (thick muscle, strong contractility/tension) and most tenuous supply
(hypertrophy, not perfused during systole). Typically supplied by branches of the LCX.
– Anterior leads (V3 and V4): Electrical function of the anterior wall of the heart. Usually
supplied by the LAD.
– Septal leads (V1 and V2): Electrical function of the intraventricular septum. Branches of
the LAD usually supply the anterior two third of the septum.
EQUATIONS
• CBF = CPP/CVR, where:
– CBF = coronary blood flow
– CPP = coronary perfusion pressure
– CVR = coronary vascular resistance
• CPP = (diastolic systemic blood pressure – LVEDP), where LVEDP = left ventricular end
diastolic pressure.
REFERENCES
1. AHA Scientific Statement. Standardized myocardial segmentation and nomenclature for
tomography imaging of the heart. Circulation. 2002;105:539–542.
2. ACC/AHA 2007 Guidelines on perioperative Cardiovascular Evaluation and Care for
Noncardiac Surgery: Executive Summary. Circulation. 2007;116:1971–1996.
3. 2009 ACCF/AHA Focused Update on Perioperative Beta Blockade Incorporated into the
ACC/AHA 2007 Guidelines on perioperative Cardiovascular Evaluation and Care for
Noncardiac Surgery. Circulation. 2009;120:e169–e276.
ADDITIONAL READING
• Ahmadi N, Nabavi V, Hajsadeghi F, et al. Mortality incidence of patients with non-
obstructive coronary artery disease diagnosed by computed tomography angiography. Am J
Cardiol. 2011;107(1):10–16.
• Hombach V, Merkle N, Bernhard P, et al. Prognostic significance of cardiac magnetic
resonance imaging: Update 2010. Cardiol J. 2010;17(6):549–557.
• Cardiac catheterization
CLINICAL PEARLS
• Coronary arteries are the only source of blood supply to the myocardium.
• There are significant blood supply variations between individuals.
• Blood flow to the subendocardium of the LV nearly ceases during diastole; the
subendocardium of the LV is most at risk for ischemia.
• Myocardial oxygen extraction is near-maximal at rest; an increase in oxygen demand must
be met primarily by an increase in blood flow at constant hemoglobin levels.
CORONARY ARTERY BYPASS GRAFTING (CABG), ON PUMP
Ali Salehi, MD
BASICS
DESCRIPTION
General
• Coronary artery bypass grafting (CABG) was first introduced by Dr. D.W. Gordon Murray in
1953. It has since evolved with advancements in cardiopulmonary bypass (CPB),
cardioplegia, and harvesting techniques.
• The procedure entails an incision, followed by a sternotomy with a standard saw, exposure
of the heart, and harvesting of graft conduits.
• Grafts. Generally, a left internal mammary artery (LIMA) and segments of the reversed
saphenous vein graft (SVG) are harvested. The LIMA is a preferred conduit because its
patency rate exceeds 90% at 10 years. Advantages of a SVG include easy accessibility,
availability, ease of harvest, and resistance to spasm (1). However, they have a higher
incidence of atherosclerosis and deficiency of nitric oxide production compared to arterial
grafts. The right internal mammary artery or radial artery can also be used depending on
the patient’s history and concerns for preventing lower extremity wound infections. In the
case of radial artery harvest, an “Allen test” should be performed preoperatively to confirm
collateral flow.
• The ascending aortic site is assessed by the surgeon prior to cannulation and clamping.
Epiaortic echocardiography is indicated when plaque is noted in the aortic arch or
descending aorta on transesophageal echocardiography.
• Anticoagulation with heparin (300–400 units/kg) is administered to achieve an activated
clotting time >400 seconds.
• Cannulation. Subsequently an arterial cannula is placed in the ascending aorta proximal to
the take-off of the innominate artery and a venous cannula is placed in the right atrium
through the right atrial appendage. Antegrade and retrograde cardioplegia catheters are
placed based upon the surgeon’s preference and clinical indication.
• CPB is initiated. The body is cooled to about 30–32°C. After adequate pump flow is achieved
(2–2.5 L/min/m2) and hemodynamics are optimized, cold cardioplegia is given and the
aorta is cross-clamped. Warm cardioplegia can be used in the setting of severe myocardial
dysfunction and low ejection fraction (EF).
• Bypass targets are then determined; an appropriate target is free of disease and easily
accessible. Distal anastomoses are done first and then proximal (aortic) anastomoses are
performed (before or after the removal of the aortic cross-clamp). When proximal
anastomoses are done after cross-clamp removal, a side clamp is placed on the ascending
aorta to allow perfusion of the heart while the surgeon completes the procedure.
• Rewarming. Gradual rewarming to 36°C begins after the last distal anastomosis.
• The patient will be separated from CPB by gradually turning down the pump flows to zero
and supporting myocardial contractility and BP by the use of inotropes and vasopressors, as
needed. Excess pump blood is retransfused to the patient and the BP controlled by
administration of vasodilators like nitroglycerin, if needed.
• Heparin reversal. Protamine (1 mg for every 100 units of heparin) is administered, followed
by venous and arterial cannulae removal. Pleural and mediastinal chest tubes and atrial and
ventricular pacing wires are placed. After adequate hemostasis is achieved, the chest is
closed.
Position
• Supine, frog legged, and arms tucked to the side
• Prep from chin to toes
• Patient’s ankles, knees, and elbows need to be padded carefully to avoid nerve injury.
Incision
Median sternotomy
Approximate Time
6–8 hours
EBL Expected
400–800 cc
Hospital Stay
5–7 days; varies based on comorbidities and complications
• Sternotomy saw
• CPB machine
• Cardioplegia
EPIDEMIOLOGY
Prevalence
In the US: 228,000 annually with an annual cost of 10 billion dollars (2).
Prevalence
Increases with age, male gender, diabetes, severity, and number of vessels involved.
Morbidity
Increased in patients with diabetes (blood glucose >150 mg/dL), renal disease (Cr >1.5
mg/dL), female gender, obesity, previous CVA, reoperation, and emergent surgery.
Mortality
1–3%; can reach 5% in certain patient populations (3).
• Patients often have several comorbidities.
• Understanding the stages of going “on” and “off pump,” potential complications, and close
communication with the surgical team are key.
SYMPTOMS
• Can be asymptomatic and diagnosed during a routine check-up
• Angina or angina equivalent; dyspnea, palpitation, fatigue, chest tightness, sweating, and
epigastric discomfort
History
Detailed cardiac history and documentation of any recent changes
Signs/Physical Exam
• Tachycardia, hypotension, and hypertension
• Congestive heart failure: Leg swelling, jugular venous distention, and crackles
• Arrhythmias
• Pericardial friction rub
• Systolic ejection murmur due to ischemic Mitral Regurgitation (MR) or rupture papillary
muscle
• Holosystolic murmur due to ischemic Ventricular septal defect (VSD)
MEDICATIONS
• Beta-blockers and statins should be continued perioperatively.
• Aspirin should be stopped 3–5 days prior to surgery except in high-risk patients (unstable
angina, recent myocardial infarction, MI).
• Clopidogrel should be stopped 7–10 days prior to surgery, if possible.
• ACE inhibitors, on the day of surgery, increase the incidence of hypotension on induction.
Labs/Studies
• Hgb/Hct and PT/INR/PTT
• Electrolytes, BUN/Cr and blood urea nitrogen, BUN/creatinine
• EKG (rhythm, heart block, bundle branch block, Q wave, ST-T changes, LVH)
• Echocardiogram (LV and RV function, wall motion abnormalities, valvular abnormalities,
patent foramen ovale)
• Coronary angiogram (extent of coronary involvement, other abnormalities, pulmonary
artery (PA) pressure if right heart catheterization done, cardiac output)
• Pulmonary function tests if pulmonary disease present
• Carotid duplex study in patients with a history of CVA, diabetes. or bruit on auscultation
• Chest CT in patients undergoing redo operation to determine the relationship of the major
blood vessels and cardiac chambers to the sternum.
Cerebrovascular, renovascular, peripheral vascular disease, as well as COPD/emphysema
TREATMENT
Premedications
Midazolam or fentanyl can treat anxiety prior to transporting the patient to the OR and can
be supplemented while placing the arterial line and other monitors. These medications should
be carefully titrated, if at all, in patients with pulmonary hypertension, unstable angina, or
heart failure.
• Blood consent in the event of transfusion
• Possibility of an intra-aortic balloon pump (IABP) post-CPB
• Need for prolonged intubation
• Explanation of possible postoperative complications
Third-generation cephalosporins and/or vancomycin within 60 minutes of incision
(institution dependent)
INTRAOPERATIVE CARE
Monitors
• Standard ASA monitors, large bore IVs, and Foley catheters
• Arterial line (beat-to-beat BP change, multiple lab work); typically placed preinduction
• Central line access (preferably a 9 Fr sheath) for administration of fluids, vasoactive, and
inotropic agents. It is also used to monitor central venous pressure (CVP) and float a Swan–
Ganz if indicated
• Transesophageal echocardiography to monitor myocardial function and assess volume status
and diagnosis of any other cardiac pathology
• Choice of induction agents depends on the patient’s hemodynamic status and comorbidities.
A balanced anesthetic technique using small doses of a short-acting narcotic and etomidate
is commonly used. In patients with significant LV dysfunction, higher doses of narcotics are
often used. Neuromuscular blocking agents without vagolytic or histamine releasing effects
are preferred; cisatracurium should be considered if there is impaired renal or hepatic
function.
• Inotropes may be started preinduction in patients with myocardial dysfunction and low EF
in order to maintain hemodynamics.
• Hemodynamic instability may require emergent “going on pump.”
Maintenance
• Balanced technique with volatile agents and short-acting narcotics facilitate early
extubation. Volatile agents can cause peripheral vasodilatation and decrease myocardial
contractility but can induce ischemic preconditioning and mitigate reperfusion injury (4).
• “On pump.” After CPB is instituted, the patient is cooled and anesthetic requirement
decreases. The perfusionist administers a low-dose volatile agent into the CPB circuit
throughout the bypass period. Awareness typically occurs during rewarming when the
anesthetic requirement increases and anesthesia is not properly supplemented. Additional
doses of benzodiazepines, narcotics, or propofol should be considered when rewarming is
initiated. Delivery of volatile agents from the anesthetic machine should be immediately
restarted by the anesthesiologist after separation from CPB and resumption of ventilation.
• Preparation for weaning. In anticipation of coming off bypass, adequate ventilation should
be established and any metabolic and hematologic abnormalities need to be optimized. With
warming, normal sinus rhythm will usually return; sometimes ventricular fibrillation will
ensue, requiring defibrillation with internal pads at 10–20 J to revert to sinus rhythm. If the
heart rate is <70 bpm, epicardial pacing wires should be considered.
• Most patients require some period of mechanical ventilation and inotropic support
postoperatively.
• In patients determined to be candidates for fast-tracking, it is better to use short-acting
narcotics and neuromuscular blocking agents. Excluding factors include long bypass time,
multiple comorbidities, complex procedures, hypothermia, coagulopathies, massive blood
transfusion or volume resuscitation, or need for prolonged inotropic support.
FOLLOW-UP
BED ACUITY
Intensive care unit (ICU) (preferably a cardiac unit) for ventilatory and inotropic support, as
well as volume resuscitation, transfusion, urine output, and hemodynamic monitoring.
ANALGESIA
• Pain on POD 1–2: Sternotomy incision; POD 3–7: Back pain, saphenous vein, or radial artery
harvesting sites.
• Narcotic PCA has shown to be effective, with eventual conversion to PO medications.
• NSAIDs, tramadol, and paracetamol have been used adjunctively and shown to decrease the
narcotic requirements (5).
COMPLICATIONS
• Reoperation within 24 hours 7%
• LV failure needing IABP or assist device 3–7%
• MI 5%
• Renal failure 3.5%
• Stroke 3.1%
• Mediastinities 0.6%
PROGNOSIS
LIMA grafts have a 90–95% patency in 10 years. Patency for radial artery and SVGs are 85–
90% and 75%, respectively.
REFERENCES
1. LU M, Chen JJ, Awan O, et al. Evaluation of bypass grafts and stents. Radiol Clin N Am.
2010;48:757–770.
2. Mangano DT, et al. Cardiovascular morbidity and CABG surgery-a perspective;
Epidemiology, cost and potential therapeutic solutions. J Card Surg. 1995;10(Suppl):366–
368.
3. Chaitman BR, Rosen AD, Williams DO, et al. The final 10-year follow-up, results from BARI
randomized trial. J Am Coll Cardiol. 2007;49(15):1600–1606.
5. Zuagg M, Lucchinetti E, Spahn DR, et al. Volatile anesthetics mimic cardiac
preconditioning by priming the activation of mitochondrial K(ATP) channels via multiple
signaling pathways. Anesthesiology. 2002;97:4–14.
6. Konstantatos A, Silvers AJ, Myles PS. Analgesia best practice after cardiac surgery.
Anesthesiol Clin. 2008;26:591–602.
ADDITIONAL READING
• Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia, 4th
ed. Philadelphia: Lippincott Williams & Wilkins; 2008:230–260.
• Cardioplegia
• Awareness under anesthesia
CLINICAL PEARLS
• Following anesthetic induction, if the patient becomes hemodynamically unstable,
consideration to go onto pump should be emergently performed.
• Fast-tracking extubation postoperatively should be considered whenever possible.
CORONARY ARTERY BYPASS GRAFTING, OFF-PUMP
(OPCABG)
Ali Salehi, MD
BASICS
DESCRIPTION
General
• The complications of cardiopulmonary bypass surgery (CPB) include a systemic
inflammatory response that is associated with increased risk of stroke, perioperative
myocardial infarction (MI), heart failure, and renal failure.
• Off-pump coronary artery bypass grafting (OPCABG) dates back to the 1950s. Interest in the
procedure has grown in North America since the 1990s.
• Criteria for patients to be a candidate for OPCABG include the following:
– Low ejection fraction (EF <30%)
– Advanced pulmonary disease
– Renal failure
– Advanced aortic atherosclerosis
– One or two vessel disease
• The procedure begins similarly to on-pump cases: Incision, sternotomy, exposure of the
heart and harvesting of graft conduits (left internal mammary artery (LIMA), saphenous
vein, or radial artery), and anticoagulation with heparin. Heparin dosing (150–200
units/kg) and target activated clotting time (ACT; 250–300 seconds) are lower than with
on-pump CABG. However, some surgeons prefer an ACT similar to on-pump CABG due to
the potential for going on bypass.
• An apical suction cup is used to position the heart for better exposure of the target coronary
artery. An epicardial stabilizer is then applied to immobilize the area being anastomosed; it
allows the heart to continue beating, but can cause regional myocardial dysfunction.
• The LIMA to LAD anastomosis is usually done first because it does not require significant
manipulation of the heart and restores blood flow to a significant portion of the left
ventricle (LV). This may decrease the level of hemodynamic instability when the heart is
positioned to perform the subsequent grafts (left circumflex and right coronary artery). The
anastomosis is performed by incising the target artery and an intracoronary shunt is placed
to maintain distal perfusion until completed. Close communication between the anesthesia
team and the surgical team is essential at this time.
• Heparin reversal. After the completion of revascularization, protamine (usually a dose of 50
mg) is given for heparin reversal. If the ACT is still elevated, small additional doses (20–30
mg) are given.
• Shed blood is collected into a cell saver device, washed, and returned to the patient.
• Epicardial pacing wires are placed.
• Closure ensues after adequate hemostasis is achieved.
Position
• Supine, frog-legged, and arms tucked to the side
• Prep from chin to toes (can cause considerable hypothermia)
• Patient’s ankles, knees, and elbows need to be padded carefully to avoid nerve injury.
Incision
• Median sternotomy
• Minimally invasive techniques through a thoracotomy (MIDCAB) and robotic-assisted
procedures have also been performed, but are less common.
Approximate Time
4–6 hours
EBL Expected
300–600 cc
Hospital Stay
5–7 days on average; varies depending on comorbidities and complications
• Sternotomy saw
• Cardiopulmonary bypass machine (should be primed and ready if conversion is needed)
• Different cannulae (possible need for CPB)
• Off-pump retractor (allows attachment of apical suction and epicardial stabilizer)
• Apical suction cup
• Epicardial stabilizer
• Cell saver
EPIDEMIOLOGY
Morbidity
May have decreased length of stay and need for blood and blood product transfusion.
Mortality
Similar to on-pump CABG
• Significant comorbidities may exist.
• Manipulation and positioning of the heart can be associated with hemodynamic instability
and arrhythmias.
• Myocardial function should be monitored during the grafting period.
• Maintenance of body temperature
• Anesthetic technique should facilitate early extubation.
SYMPTOMS
• Can be asymptomatic and diagnosed during a routine check-up
• Angina or angina equivalent, dyspnea, palpitations, fatigue, chest tightness, sweating, and
epigastric discomfort
History
• Detailed cardiac history and documentation of any recent changes.
• Detailed neurological, renal, and pulmonary history due to the increased incidence of
peripheral vascular, cerebrovascular, and renovascular comorbidities as well as smoking in
this patient population.
Signs/Physical Exam
• Tachycardia, hypotension, and hypertension
• Congestive heart failure: Lower extremity swelling, jugular venous distention, and crackles
in the lungs
• Arrhythmias
• Systolic ejection murmur due to ischemic mitral regurgitation or ruptured papillary muscle
• Holosystolic murmur due to ischemic ventricular septal defect (VSD)
• Pericardial friction rub
• Due to post myocardial infarction pericarditis
MEDICATIONS
• Beta-blockers and statins should be continued into the perioperative period
• Aspirin should be discontinued 3–5 days prior to surgery unless in high-risk patients
(unstable angina, recent MI).
• Clopidogrel should be discontinued 7–10 days prior to surgery, if possible.
• ACE inhibitors. When taken on the day of surgery, there is a higher risk for hypotension at
induction.
Labs/Studies
• Hgb/Hct, PT/INR/PTT
• Electrolytes, BUN/creatinine
• EKG (rhythm, heart block, bundle branch block, Q wave, ST-T changes, LV hypertrophy)
• Echocardiogram (left and right ventricle function, wall motion abnormalities, valvular
abnormalities, patent foramen ovale)
• Coronary angiogram (extent of coronary involvement, other abnormalities, PA pressure if a
right heart catheterization was done, cardiac output)
• Pulmonary function tests in patients with pulmonary disease
• Carotid duplex study in patients with a history of CVA, diabetes, or bruit on auscultation
• Chest CT in patients undergoing redo operation to determine the relationship of the major
blood vessels and cardiac chambers to the sternum
• Renovascular disease
• COPD/emphysema
TREATMENT
Premedications
Midazolam or fentanyl can treat anxiety prior to transporting the patient to the OR and can
be supplemented while placing the arterial line and other monitors. Should be carefully
titrated, if at all, in patients with pulmonary hypertension, unstable angina, or heart failure.
• Blood consent for possible need of transfusion
• Possibility of placement of intra-aortic balloon pump perioperatively (preinduction to help
stabilize hemodynamics)
• Need for use of CPB due to hemodynamic instability
• Need for prolonged intubation postoperatively due to the patient’s comorbidities
• Explanation of possible postoperative complications
Third-generation cephalosporin and/or vancomycin within 60 minutes of incision (institution
dependent)
INTRAOPERATIVE CARE
General endotracheal anesthesia. Use of regional anesthesia for OPCABG has been reported,
but is not popular with many anesthesiologists (4).
Monitors
• Large bore IVs
• Foley catheter to monitor urine output
• Arterial line (beat-to-beat BP change, multiple lab work). Often placed preinduction.
• Central line access (preferably a 9FR sheath) for administration of fluids and vasoactive and
inotropic agents. It is also used to monitor CVP and float a Swan–Ganz, if indicated (left
heart failure, hemodynamic instability, and pulmonary hypertension).
• Transesophageal echocardiography to monitor myocardial function, assess volume status,
and diagnose other cardiac pathology. Most sensitive monitor to detect new regional wall
motion abnormalities or worsening of mitral regurgitation during cardiac positioning and
grafting. These changes are warning signs of an impending cardiovascular collapse.
• Choice of induction agents depend on the patient’s hemodynamic status and comorbidities.
A balanced anesthetic technique using small doses of a short-acting narcotic and etomidate
is commonly used; in patients with significant LV dysfunction, higher doses of narcotics are
often used. Neuromuscular blocking agents without vagolytic or histamine releasing effects
are preferred; cisatracurium should be considered if there is impaired renal or hepatic
function.
• Inotropes may be started preinduction in patients with myocardial dysfunction and low EF
in order to maintain hemodynamics.
Maintenance
• Balanced technique with volatile agents and short-acting narcotics (facilitate early
extubation). Volatile agents can cause peripheral vasodilatation and decrease myocardial
contractility but can induce ischemic preconditioning and mitigate reperfusion injury.
• Hemodynamics. Manipulation and turning of the heart to access the coronaries can result in
profound hypotension. This effect may be decreased by correcting all metabolic and
electrolyte abnormalities; maintaining euvolemia by administering fluids or blood if Hgb
<8 mg/dL; administering inotropes and vasopressors to support myocardial function and
maintain myocardial perfusion, especially in patients with a low EF; and decreasing the
heart rate to provide a quiet operating field (70–80 bpm).
• Temperature. In the absence of CPB, warming can be difficult. Consider warming the
operating room before patient arrival. Cover the patient during line placement and
induction. All fluids should be administered via a hotline. Sterile forced-air warming
blankets can be placed on the lower extremity after vein harvest grafting.
Patients can be extubated in the operating room or early in the intensive care unit (ICU). The
decision should be made after a discussion between the surgeon and the anesthesiologist.
Factors determining the feasibility of early extubation are normal LV function, little or no
inotropic support, no evidence of bleeding, limited volume resuscitation, normothermia,
hemodynamic stability, and a normal airway
FOLLOW-UP
BED ACUITY
• ICU bed for ventilator and inotropic support as well as volume resuscitation, transfusion,
urine output, and hemodynamic monitoring.
• Length of ICU stay could be very short for uncomplicated cases.
ANALGESIA
Same as on-pump CABG
COMPLICATIONS
Same as on-pump CABG
PROGNOSIS
• Outcome studies have shown that there is decreased enzyme release, bleeding, atrial
fibrillation, length of hospital stay, as well as the need for blood and product transfusion
(avoiding the systemic inflammatory response) (1,3).
• However, studies have not shown a difference in 30-day risk of death, stroke, MI, renal
failure, mediastinitis, or coma (1,3).
• There was no difference in neuropsychological outcome (1).
• One-year outcomes showed that saphenous graft patency is worse for off-pump, while LIMA
graft patency is the same (1,4).
• Off pump coronary artery bypass grafting in comparison to on pump CABG tend to have
fewer planned grafts completed (1).
REFERENCES
1. hroyer AL, Grover FL, Hattler B, et al. On-pump versus off-pump coronary artery bypass
surgery. N Engl J Med. 2009;361(19):1827–1837.
2. ijeysundera DN, Beattie WS, Djaiani G, et al. Off-pump coronary artery surgery for
reducing mortality and morbidity; meta-analysis of randomized and observational studies.
J am Coll Cardiol. 2005;46:872–882.
3. Puskas JD, Williams WH, Mahoney EM, et al. Off-pump versus conventional coronary
artery bypass grafting: Early and one year graft patency, cost and quality of life outcomes:
A randomized trial. JAMA. 2004;291:1841–1849.
4. Bainbridge D, Cheng DCH. Minimally invasive direct coronary artery bypass and off-pump
coronary artery bypass surgery: Anesthetic considerations. Anesthesiology Clin.
2008;26:437–452.
ADDITIONAL READING
• Hensley FA, Martin DE, Gravlee GP, ed. A Practical Approach to Cardiac Anesthesia, 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2008:230–260.
• Coronary artery bypass on pump
CLINICAL PEARLS
• Off bypass CABG decreases the systemic inflammatory response that is associated with
bypass as well as other complications. Studies have shown a decrease in blood transfusion
frequency, length of hospital stay, and bleeding.
• However, 30-day outcome data has not shown an improvement in several parameters at this
time.
CORONARY ARTERY DISEASE
BASICS
DESCRIPTION
• Coronary artery disease (CAD) is the presence of hardened and narrowed coronary arteries.
This architectural change is often the result of atherosclerosis, which describes the buildup
of plaque and cholesterol over years. Rare cases of genetic abnormality such as familial
hypercholesterolemia can result in CAD prior to age 40 years.
• CAD is the most common cause of ischemic heart disease, which is the leading cause of
death in the US.
• The spectrum of disease varies, and treatment should be tailored to symptoms and disease
distribution.
EPIDEMIOLOGY
Incidence
Increasing as healthcare availability, imaging techniques, and average life expectancy
increase.
Prevalence
1–1.5% of the total US population has ischemic heart disease.
Morbidity
• Ischemic cardiomyopathy (ICM) is the most common consequence of CAD.
• The TIMI (Thrombolysis in Myocardial Infarction) risk score looks at 7 factors to determine
risk.
– Age 65 years or older
– At least 3 risk factors for coronary artery disease
– Prior coronary stenosis of 50% or more
– ST-segment deviation on electrocardiogram at presentation greater than 0.5 mm
– At least 2 anginal events in prior 24 hours
– Use of aspirin in prior 7 days
– Elevated serum cardiac markers
As determined by number of risk factors, risk of all-cause mortality, new or recurrent MI, or
severe recurrent ischemia requiring urgent revascularization within the first 2 weeks are: 1 =
5%, 2 = 8%, 3 = 13%, 4 = 20%, 5 = 26%, 6/7 = 41%
Mortality
Ischemic heart disease is the leading cause of death in the US.
• Age: Males >45 years and women >55 years
• Family history
• High levels of LDL cholesterol
• Low levels of HDL cholesterol
• Hypertension (HTN)
• Diabetes
• Cigarette smoking
• Obesity
• Sedentary lifestyle
• Type A personality
• Postmenopausal
• High lipoprotein A levels
• Other diagnosed vascular diseases
PATHOPHYSIOLOGY
• Plaques consist of fat, cholesterol, calcium, white blood cells, and fibrin that cause arterial
hardening.
• Laminar flow within an artery is directly proportional to vessel radius to the fourth power;
therefore, narrowing of arteries with plaque can significantly decrease blood flow.
• The LV is more prone to ischemia than the right ventricle due to its thicker muscle and
increased afterload that results in decreased oxygen delivery and increased oxygen
consumption, respectively. When “stressed” from increases in heart rate, contractility,
afterload, or preload, ischemia may result due to the impaired oxygen supply.
• Ischemic cardiomyopathy (ICM) results from chronic hypoxia of the myocardium. Hypoxic
events cause tissue damage and scar tissue formation and can significantly reduce pump
function (decreased CO and ejection fraction). Arrythmia and angina are common at late
stages of ICM.
• Infarction can occur from myocardial oxygen supply–demand imbalance even without total
coronary artery occlusion. Commonly, plaque buildup causes near occlusion of coronaries,
but plaque disruption causes thrombus formation which more often leads to sudden cardiac
death (SCD).
• Preoperative evaluation is aimed toward assessing current myocardial function and
myocardium at risk for ischemia.
• Anesthesia and surgery can impair myocardial oxygen supply and delivery. The anesthesia
provider’s primary aim should be to maintain CO, coronary perfusion, and prevent cardiac
decompensation.
SYMPTOMS
• May be asymptomatic for decades as plaque builds up
• Shortness of breath, dyspnea on exertion, fatigue, angina, palpitations, lightheadedness
History
Family history, previous diagnosis of CAD, risk factors
Signs/Physical Exam
Congestive heart failure
TREATMENT HISTORY
• Previous cardiac evaluation
• Angioplasty, stent placement (bare metal versus drug eluting)
• Coronary artery bypass
MEDICATIONS
• Aspirin
• Beta-blockers (first-line therapy)
• Calcium channel blocker
• Omega-3 fatty acids
• Statin therapy
• Antihyperglycemics and insulin
Labs/Studies
• Preoperative labs are based on type of surgery, medications, severity of CAD.
• Diagnosis of CAD requires imaging: coronary angiogram, radionucleotide perfusion scans,
magnetic resonance imaging.
• Computed tomography (4).
Atherosclerosis of the aorta, carotid artery, and peripheral arteries is common.
• Unstable angina
• Severe disease without recent evaluation or appropriate medical management
• Recent MI or stroke
CLASSIFICATIONS
TIMI grade flow is a widely adopted scoring system from 0–3 referring to levels of coronary
blood flow assessed during percutaneous coronary angioplasty:
• TIMI 0 flow (no perfusion) refers to the absence of any antegrade flow beyond a coronary
occlusion.
• TIMI 1 flow (penetration without perfusion) is faint antegrade coronary flow beyond the
occlusion, with incomplete filling of the distal coronary bed.
• TIMI 2 flow (partial reperfusion) is delayed or sluggish antegrade flow with complete filling
of the distal territory.
• TIMI 3 flow (complete perfusion) is normal flow that fills the distal coronary bed
completely.
TREATMENT
Premedications
• Midazolam to prevent anxiety and increased sympathetic tone, as needed
• Narcotics for sympathetic stability and pain control, as needed
• Patients on beta blockers should have their doses continued in the perioperative period.
• Risk for intraoperative MI and SCD
• Risk for transfusion
INTRAOPERATIVE CARE
• Depends on surgical procedure and patient preference
• If possible, MAC is preferred (less expected hemodynamic perturbations)
• If a neuraxial technique is chosen, aspirin does not contraindicate placement
Monitors
• 5-lead EKG has increased sensitivity for LV ischemia.
• Arterial line allows beat-to-beat BP monitoring or minimally invasive CO monitoring.
• Central venous line may be considered to guide fluid administration and for fluid and/or
vasopressor delivery.
• Pulmonary artery catheter may be considered if the patient is at high risk for
decompensation to monitor right and LV function, volume status, cardiac output, and mixed
venous saturation
• Transesophageal echocardiography may be considered for hypertrophic cardiomyopathy and
management of perioperative events.
• Newer noninvasive CO monitors – NICOMs based on bioimpedance or bioreactance.
• Smooth, controlled induction to maintain vital signs and coronary perfusion within normal
limits.
• Narcotic-based inductions may have a more gradual and minimal impact on BP and cardiac
function, and may be preferable to the potentially harsher sedative-hypnotic only
inductions.
• Short-acting medications should be available to treat increases in heart rate (esmolol), HTN
(esmolol, nitroglycerin, calcium channel blockers, propofol), and hypotension
(phenylephrine, ephedrine).
Maintenance
• Volatile and/or IV anesthetics may be used; neither technique has shown superiority in
patients with coronary artery disease.
• Maintaining myocardial oxygen supply and decreasing demand are more important than the
specific anesthetic technique.
– Decrease the heart rate, while maintaining an adequate cardiac output.
– Monitor and maintain normal sinus rhythm
– Decrease contractility while maintaining adequate cardiac output; avoid and anticipate
sympathetic stimulation (e.g., incision, retraction, pain, adequate depth of anesthesia)
with narcotics and/or deepening the anesthetic
– Optimize the afterload; an adequate diastolic perfusion pressure is necessary to maintain
cardiac perfusion (CPP = DBP–LVEDP). However, increases in afterload require an
increase in myocardial oxygen consumption
– Optimize preload; an adequate intravascular fluid volume is necessary to maintain an
adequate stroke volume (Starling curve).
– Maintain the oxygen content of arterial blood with an adequate hematocrit, oxygen
saturation, and ventilator settings.
– Alternatively, support life in severe systolic dysfunction with inotropes and vasopressors
as needed.
• Normothermia. Measures to avoid hypothermia should be made; shivering can increase
myocardial oxygen consumption significantly
• Intraoperative ischemia should be monitored and treated utilizing the coordinated efforts of
the healthcare team, so as to optimize myocardial oxygen supply and demand.
Have narcotics, anxiolytics, antihypertensives, and beta-blockers available to maintain
postoperative vital sign stability
POSTOPERATIVE CARE
BED ACUITY
Depends on type of surgery and intraoperative events
• Cardiology consult may be warranted depending on perioperative cardiac events
• Medicine consult for the management of diabetes, hyperlipidemia, HTN, and diet control
COMPLICATIONS
• MI
• Death
REFERENCES
1. Antman EM, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method
for prognostication and therapeutic decision making. JAMA. 2000;284(7):835–842.
2. Shehata N, et al. Factors affecting perioperative transfusion decisions in patients with
coronary artery disease undergoing coronary artery bypass surgery. Anesthesiology.
2006;105(1):19–27.
3. Kulka PJ, et al. Coronary artery plaque disruption as cause of acute myocardial infarction
during cesarean section with spinal anesthesia. J Clin Anesth. 2000;12(4):335–338.
4. Rodríguez-Palomares JF, et al. Coronary angiography by 16-slice computed tomography
prior to valvular surgery. Rev Esp Cardiol. 2011; 64(4):269–276.
5. Ogata T, et al. Morphological classification of mobile plaques and their association with
early recurrence of stroke. Cerebrovasc Dis. 2010;30:606–611.
ADDITIONAL READING
• World Health Organization Department of Health Statistics and Informatics in the
Information, Evidence and Research Cluster (2004). The global burden of disease 2004
update. Geneva: WHO.
• http://www.timi.org/
• Postoperative chest pain
• Coronary stents
CODES
ICD9
• 414.00 Coronary atherosclerosis of unspecified type of vessel, native or graft
• 414.01 Coronary atherosclerosis of native coronary artery
ICD10
• I25.10 Athscl heart disease of native coronary artery w/o ang pctrs
• I25.110 Athscl heart disease of native cor art w unstable ang pctrs
CLINICAL PEARLS
• CAD is commonly caused by atherosclerosis.
• Severity of CAD must be confirmed by imaging studies and symptomatology. Multiple
classifications exist for atheroma that mitigates management.
• Previous stent placement may place the patient under increased risk for intraoperative
ischemia due to stress or inadequate antiplatelet treatment; especially within 4–6 weeks of
bare-metal stent and 1 year with DES.
• Decreasing myocardial oxygen demand and increasing myocardial oxygen supply are the
key principles of management.
• Acute or chronic functional decompensation must be supported with inotropes and
vasopressors when necessary, even if they cause increased myocardial oxygen consumption.
CORONARY ARTERY SPASM (PRINZMETAL ANGINA)
Victor L. Mandoff, MD
BASICS
DESCRIPTION
• Coronary artery spasm (CAS) describes vasospasm of the coronary arteries that can manifest
clinically as angina, arrhythmias, acute myocardial infarction, or sudden death.
• Typically it occurs
– In a cyclical pattern
– In clusters with symptom free quiescent episodes in between
– At rest
– After midnight to early morning
• It was first described by Dr. Myron Prinzmetal in 1959 as episodes of “temporary increased
tonus” (1) and is thus commonly referred to as Prinzmetal angina (also variant angina).
EPIDEMIOLOGY
Incidence
Observed in 4 out of 100 (4%) of patients undergoing cardiac angiography in the US.
Prevalence
• Patients are usually in their 50s
• Some studies suggest that it is more common in females
• People of Japanese ethnicity have a three-fold increase over Caucasians.
Morbidity
Acute myocardial infarction has been shown to occur in 3.5–6.5% of patients with a diagnosis
of CAS.
Mortality
• Prognosis depends on coexisting atherosclerotic disease. One-year survival in patients:
– Without atherosclerotic disease or with single vessel disease: 99%
– With multivessel atherosclerotic disease: 87%
• More common in patients with the following comorbidities:
• Smokers
• Hypercholesterolemia
• Migraine headaches
• Raynaud’s disease
• Cocaine users
• Can be triggered by administration of ergonovine, histamine, serotonin, and acetylcholine
(ACh)
• Anxiety or panic disorder
• Type A personality
• East Asian populations
PATHOPHYSIOLOGY
• Although the clinical manifestations of variant angina are similar to those of classical angina
(secondary to an imbalance in myocardial oxygen supply and demand), their pathogenesis
and treatment differ. Coronary spasm is an abnormal contraction of an epicardial coronary
artery, as opposed to plaque buildup or rupture (acute coronary syndrome).
• The exact mechanism is not completely understood and multiple theories exist that revolve
around vascular endothelial function combined with an increase in vascular smooth muscle
abnormalities and oxidative stress.
• Dysfunctional coronary artery endothelium. The endothelium normally plays an important
role in vascular tone regulation. Dysfunction is characterized by an impairment of the
balance between endothelium-derived relaxing factors and endothelium-derived constricting
factors (2).
• Hypercontractile response to ACh and intracellular calcium. ACh’s normal vasodilatory
effects appear to be impaired in the face of endothelial dysfunction, causing
vasoconstriction instead. Calcium’s effect may be the result of increased smooth muscle cell
mass and/or abnormalities in the Rho-kinase pathway.
• Increased oxidative stress. Smoking and insulin resistance have been shown to decrease
nitric oxide (NO) activity via oxygen-derived free radicals; this effect appears to be
diminished with antioxidants such as Vitamin E.
• Enhanced phospholipase C activity
• In patients with known CAS, avoid hyperventilation and histamine releasing drugs. Continue
perioperative calcium channel blockers and avoid nonselective beta-blockers.
• As with coronary artery disease (CAD), optimize coronary perfusion pressure, avoid
tachycardia, maintain normal sinus rhythm, and optimize preload, afterload, and
contractility.
SYMPTOMS
• Retrosternal pain or pressure
• Radiation to the neck, jaw, left arm, or left shoulder
• Can be associated with a loss of consciousness or arrhythmias
History
• May describe anginal pain typically at rest in clusters of two or three
• Occurs between midnight and early morning
• Resolves spontaneously or with nitroglycerin
Signs/Physical Exam
• May be absent between episodes
• No real pathognomonic sign
• Hypertension
• Tachycardia
• Transient arrhythmia or heart murmur
• Rales
• Jugular venous distension
• Peripheral edema
TREATMENT HISTORY
Coronary stenting may be performed in patients that are refractory to medical management.
Appears to be more effective when focal CAS, as opposed to multivessel spasm.
MEDICATIONS
• Nitrates include short-acting nitroglycerin and long acting isosorbide dinitrate.
• Calcium channel blockers such as amlodipine, nifedipine, diltiazem, and verapamil
• Selective beta-blockers are beneficial if there is coronary atherosclerotic stenosis.
Nonselective blockers can exacerbate spasm by inhibiting beta-mediated vasodilation,
unmasking alpha-adrenergic tone, and increasing vascular permeability to calcium.
Labs/Studies
• No specific labs are indicated preoperatively. May consider a CBC if anemia or infection are
suspected and electrolytes if diabetic or with renal disease.
• EKG. Baseline EKGs are commonly normal. During acute episodes, ST segment elevation is
more commonly seen than ST depression (which is more common in CAD). May resolve
completely when the patient is asymptomatic; however, T wave inversion has been shown
to persist for hours and even days (1). Heart block is associated with CAS of the right
coronary artery, whereas ventricular tachycardia is associated with CAS of the left anterior
descending artery.
• Initial workup of patients may have involved nuclear stress tests, Holter monitoring,
treadmill or echocardiogram stress testing, and coronary angiography. Angiography is
considered the gold standard and agents and techniques that induce spasm may have been
utilized (hyperventilation, ACh, ergonovine, methylergonovine).
• Pulmonary disease in smokers
• Vasospastic disorders: Raynaud phenomenon and migraines
• In patients with known or undiagnosed disease, elective cases should be delayed in the
event of an active anginal attack preoperatively.
• Diagnosed disease. Symptoms should resolve (angina, arrhythmias), maneuvers to improve
myocardial oxygen supply while decreasing demand should be implemented, and
assessment of cardiac function may be considered.
• Undiagnosed disease. The presentation of new onset anginal pain, particularly with EKG
changes and arrhythmias will require further cardiac workup (echocardiogram, stress
testing, cardiology consult).
TREATMENT
Premedications
• Confirm that regular cardiac medications including nitrates, calcium channel blockers, and
beta-blockers are taken; if not, consider administering PO or an IV dose.
• Anxiolytics as needed
• May be at a higher risk for intraoperative and postoperative cardiac events, especially if
there are pre-existing coronary lesions.
• Explain the risks and benefits of invasive monitors
• Explain the possibility of postoperative admission to stepdown, telemetry, or intensive care
unit.
INTRAOPERATIVE CARE
• Regional, general anesthesia, and deep sedation have all been used. Choice should consider
the surgical procedure, as well as patient comorbidities and preferences.
• Deep sedation may have the benefits of decreased hemodynamic changes.
Monitors
• Additional monitors are used based on patient risk factors (congestive heart failure, previous
myocardial infarction, hypertension, arrhythmias, diabetes mellitus, smoking, etc.) along
with the surgical procedure.
Guided by patient’s medical condition, airway difficulty, and risk for aspiration. Goals should
include a slow controlled induction and avoidance of hyperventilation with bag mask
ventilation.
Maintenance
• Balanced anesthetic combining narcotics with volatile or IV agents. No specific technique
has been shown to be superior.
• Avoid hyperventilation as this may evoke spasm intraoperatively.
• Optimize myocardial oxygen supply and demand.
• Maintain normothermia; hypothermia may be a trigger for vasospasm.
• Intraoperative EKG changes. In patients with known disease, the onset of ST segment
elevation or arrhythmias may indicate coronary spasm. Treatment may include the
following:
• IV administration of nitroglycerin, calcium channel blockers, and magnesium
• Increasing the PaCO2
• Other supportive measures for hypotension, tachycardia, arrhythmias, or congestive heart
failure (if applicable).
• When extubation criteria are met
• Reversal of muscle relaxant can theoretically lead to a Prinzmetal angina attack if ACh is a
known trigger.
POSTOPERATIVE CARE
BED ACUITY
Depends on the surgical procedure, comorbidities, and intraoperative events such as
myocardial ischemia or arrhythmias.
• EKG
• Serial cardiac enzymes if intraoperative ischemia was seen.
• Cardiology consult depends on complications intraoperatively or postoperatively.
COMPLICATIONS
• Arrhythmias
REFERENCES
1. Ajani AE, Yan BP. The mystery of coronary artery spasm. Heart Lung Circ. 2007;16(1):10–
15.
2. Kawano H, Node K. The role of vascular failure in coronary artery spasm. J Cardiol.
2011;57:2–7.
3. Wang SS. Coronary artery vasospasm. Emedicine. 2011:1–16.
4. Massie BM, Amidon TM. Heart. Current Medical Diagnosis & Treatment. 2002:387–398.
ADDITIONAL READING
• ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for
Noncardiac Surgery.
• Raynaud’s syndrome
• Chronic angina
• Smoking
CODES
ICD9
413.1 Prinzmetal angina
ICD10
I20.1 Angina pectoris with documented spasm
CLINICAL PEARLS
• CAS remains a diagnosis of exclusion; therefore intraoperative presentation may be
misdiagnosed initially for ischemia or infarction secondary to hemodynamic imbalance, or
plaque rupture, respectively.
CORONARY STENT
Zdravka Zafirova, MD
BASICS
DESCRIPTION
• Atherosclerotic coronary artery disease (CAD) results in luminal narrowing and thrombosis
leading to coronary perfusion impairment
• Percutaneous coronary intervention (PCI) revascularization is performed to restore arterial
patency and improve myocardial perfusion
• Stent deployment has been shown to improve long-term arterial patency (1)[B], but is
limited by restenosis and thrombosis. And although ischemic symptoms are improved and
the need for repeat intervention is reduced, a decrease in mortality has not been clearly
demonstrated.
• The two currently available stents are:
– Bare metal stents (BMS)
– Drug-eluting stents (DES)
EPIDEMIOLOGY
Prevalence
• Stent restenosis (lifetime)
– BMS: 10–67%
– DES: 0–11%
• Stent thrombosis
– Lifetime: BMS 0.6–3.5%, DES 1.2–3.6%
– Within 1 month (early): BMS 0.1–0.6%, DES 0.5–1%
– 1–12 months (late): BMS 0.1–1.3%, DES 0.1–0.9%
– >12 months (very late): BMS 0–2.1%, DES 0.6–2.8%
Prevalence
• Stent use in PCI: 85–95%
• Although the use of DES have decreased due to concerns for stent thrombosis (2)[B], it is
still used 75% of the time.
Morbidity
• Stent restenosis presents with angina symptoms, acute coronary syndrome (ACS), and
myocardial infarction (MI). DES have a lower rate of restenosis and need for repeat
revascularization
• Stent thrombosis often presents as ACS/MI (50–70%). The overall rate of stent thrombosis is
similar in DES and BMS; however, DES require a longer duration of dual antiplatelet
therapy (DAT)
• Stent fracture
• Native CAD
Mortality
• Similar rate between DES and BMS
• Stent thrombosis carries a 10–45% mortality
• Risk factors for CAD: Atherosclerosis, hypertension, diabetes mellitus (DM), end-stage renal
disease, hypercholesterolemia, smoking, hyperhomocysteinemia, genetic factors
• Risk factors for stent thrombosis
– Patient factors: Premature discontinuation of DAT, DM, low ejection fraction, renal failure,
advanced age.
– Lesion factors: Small vessels, multiple lesions, long or overlapping stents, bifurcations,
suboptimal stent results
• Coronary artery stenting is performed to hold vessel walls open following balloon
angioplasty. Following dilation, the artery wall is prone to weakening and collapse, as well
as restenosis (neointimal hyperplasia); stents were developed to provide a mechanical
framework or scaffold.
• BMS. An expandable metal stent was initially developed and utilized; and although collapse
was decreased, in-stent restenosis was observed in 25% of patients at 6 months.
• DES. Developed in response to the problem of BMS restenosis. Expandable metal stents were
coated with a polymer that allowed time-release of drugs into the arterial wall. Drugs such
as sirolimus, paclitaxel, and everolimus possess antiproliferative and immunosuppressive
properties that impair endothelialization and consequently neointimal hyperplasia
(restenosis). However, in doing so, the denuded vessel walls do not heal and the stent, a
foreign body, remains exposed to the circulation; this can result in clot formation and
thrombosis. To decrease this occurrence, antiplatelet therapy is required for longer periods
than with BMS.
• The risk and benefits of the procoagulant perioperative state versus the risk of bleeding from
antiplatelet agents need to be weighed; may require a discussion with the cardiologist and
surgeon
• Premature interruption of antiplatelet therapy should be avoided, if at all possible. When
necessary, discuss perioperative anticoagulant management with the cardiologist and
surgeon.
• Optimization of myocardial oxygen delivery and control of oxygen consumption
SYMPTOMS
• Angina or anginal equivalents: Chest pain, dyspnea, nausea, and vomiting
– Stable versus unstable (progressive increase in the frequency and duration of the
symptoms, unresolving symptoms, and symptoms at rest)
History
• Stent type: BMS or DES
• Placement date: <1 month, 1–12 months, or >12 months
• Ischemic events pre-stent and post-stent; type, resolution, recurrence.
Signs/Physical Exam
• Tachycardia, arrhythmias
• Hypotension, congestive heart failure, shock
• Pallor, diaphoresis
• Tachypnea, hypoxia
TREATMENT HISTORY
• Antiplatelet therapy: Single, dual (DAT), or triple therapy. Duration (3)[A]:
– BMS require at least 1 month of DAT, followed by aspirin (ASA)
– DES require at least 12 months of uninterrupted DAT, followed by ASA
Medications
• Aspirin
• Thienopyridines: Clopidogrel, ticlopidine, prasugrel. Determine length of discontinuation
• intravenous (IV) glycoprotein (GP) IIb/IIIa inhibitors
• Anticoagulants
• Proton pump inhibitors (PPI) used to prevent or treat gastroesophageal acid and reflux
disorders may attenuate the effects of the antiplatelet agents. This may be an effect of the
individual agent rather than the class of drugs
• Beta-adrenergic antagonists
• hydroxy-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins)
• Antihypertensive medications
• Diuretics
• Antiarrhythmic agents
Labs/Studies
• Recent 12 lead ECG
– Comparison with old one to evaluate for disease progression
– As a baseline study for comparison when evaluating perioperative ECG abnormalities
indicative of acute coronary event
• Cardiac stress test may be indicated as a part of the preoperative evaluation for new or
unresolved symptoms of CAD since the revascularization, or limited exercise tolerance (<4
metabolic equivalents).
• Angiography evaluation of
– New symptoms
– Stent patency
– Abnormal stress test
• Hypertension
• Renal failure
• Bleeding abnormalities due to antiplatelet agents
• Gastrointestinal (GI) abnormalities: Bleeding, peptic ulcer disease
• Elective surgery should be delayed
– >1 month after ACS or stent placement
– If interruption of DAT is necessary for the surgery, it should be delayed until >1 month
for BMS and >12 months for DES
– In patients who have discontinued the minimum antiplatelet therapy duration following
stenting, in order to restart antiplatelet therapy.
CLASSIFICATIONS
• Stent type
– BMS
– DES
First-generation DES stents have a stainless steel construction
Newer generation have thinner, stronger cobalt chromium, and more biocompatible
polymers
TREATMENT
Premedications
• Continue antiplatelet therapy as indicated
– DAT continuation may be appropriate in cases where the risk of bleeding is low
– Reduced dose of antiplatelet agent may be used (e.g., ASA 81 mg)
– Transition to a single agent for 7 days before the procedure, if the risk of bleeding on DAT
is significant
– Parenteral platelet inhibitors: IV IIb/IIIa inhibitor and/or unfractionated heparin infusion
may be used if premature enteral DAT interruption is necessary. Both should be
discontinued the night before surgery.
– Anticoagulants are not an effective substitute for antiplatelet agents in preventing stent
thrombosis.
• H2-blockers should be considered instead of PPI
• Beta-adrenergic antagonists should be continued in the perioperative period; consider
initiation of therapy in appropriate patients.
• Risk of stent thrombosis, especially if premature interruption of antiplatelet therapy is
necessary.
• Risk of bleeding as a result of perioperative antiplatelet therapy.
INTRAOPERATIVE CARE
• General anesthesia versus regional anesthesia: Evaluation of benefits and risks of each
modality
• The bleeding risk of regional anesthesia due to antiplatelet therapy should be considered
and discussed with the patient and the surgeon (4)[C].
Monitors
• Continuous ECG monitoring with ST segment analysis in diagnostic mode
• Invasive hemodynamic monitoring may be considered based on comorbidities and surgical
procedure.
• A slow, controlled induction should be performed to maintain adequate oxygen delivery and
supply during airway manipulation.
• If a rapid sequence induction is being considered, it should be weighed against the patient’s
risk for myocardial ischemia.
Maintenance
• A balanced anesthetic with volatile and/or IV agents. No one technique has shown
superiority in patients with coronary stents or CAD.
• Ischemia and infarction may be suspected from EKG abnormalities (T waves inversions,
premature ventricular contractions, ST depression or elevation). Hypotension and
cardiovascular collapse may result from ACS. Treatment may include the following:
– Discontinuing the surgery and stimulation while stabilizing the patient, if possible.
– Intraoperative echocardiogram
– Increasing myocardial oxygen supply and decreasing demand
– Anticoagulation/antiplatelet agents
– Emergency balloon pump, PCI, or coronary artery bypass
• Support of hemodynamic stability and oxygen delivery
• Pain control
• Attenuation of stress response with adequate pain control, heart rate control, and
antihypertensive medications
FOLLOW-UP
BED ACUITY
Care in a telemetry or intensive care setting may be indicated based on the following:
• Preoperative risk stratification
• Premature antiplatelet therapy discontinuation
• Perioperative events
• Reinstitution of antiplatelet therapy (preoperative regimen) as soon as surgical bleeding risk
is decreased. A bolus dose of antiplatelet agent may be considered.
• Monitoring for coronary ischemia with EKG, cardiac enzymes as indicated.
• Cardiology consult may be indicated
COMPLICATIONS
• Stent thrombosis: Very high mortality rate
• Bleeding: Rarely significant with aspirin only, increases with antiplatelet therapy, and
highest risk with DAT. Severity depends on the surgical procedure (location and extent).
Although posterior eye chamber and neurosurgical procedures demonstrate an increase in
morbidity and mortality, many procedures do not (e.g., CABG, vascular, orthopedic, and
urological). There may be an increase in transfusion rate with continued antiplatelet
therapy.
REFERENCES
1. Kirtane AJ, Gupta A, Iyengar S, et al. Safety and efficacy of drug-eluting and bare metal
stents: Comprehensive meta-analysis of randomized trials and observational studies.
Circulation. 2009;119:3198–3206.
2. Anwaruddin S, Askari AT, Saudye H, et al. Characterization of postoperative risk associated
with prior drug-eluting stent use. JACC Cardiovasc Interv. 2009;2:542–549.
3. Tanzilli G, Greco C, Pelliccia F, et al. Effectiveness of two-year clopidogrel+aspirin in
abolishing the risk of very late thrombosis after drug-eluting stent implantation (from the
TYCOON [two-year ClOpidOgrel need] study). Am J Cardiol. 2009;104:1357–1361.
4. Osta WA, Akbary H, Fuleihan SF. Epidural analgesia in vascular surgery patients actively
taking clopidogrel. Br J Anaesth. 2010;104:429–432.
ADDITIONAL READING
• Grines CL, et al. Prevention of premature discontinuation of dual antiplatelet therapy in
patients with coronary artery stents: A science advisory from the American Heart
Association, American College of Cardiology, Society for Cardiovascular Angiography and
Interventions, American College of Surgeons, and American Dental Association, with
representation from the American College of Physicians J Am Coll Cardiol. 2007;49:1–6.
• Nordmann AJ, et al. Mortality in randomized controlled trials comparing drug-eluting vs.
bare metal stents in coronary artery disease: A meta-analysis. Eur Heart J. 2006;27:2784–
2781.
• Intraoperative ischemia
• Cardiac catheterization
• Unstable angina
CODES
ICD9
414.00 Coronary atherosclerosis of unspecified type of vessel, native or graft
ICD10
I25.10 Athscl heart disease of native coronary artery w/o ang pctrs
CLINICAL PEARLS
• Coronary stents improve the success of revascularization after PCI. However, stent
thrombosis leads to significant morbidity and mortality. Thus, premature interruption of
antiplatelet therapy should be avoided for elective surgical procedures.
CORTISOL
Joe C. Hong, MD
BASICS
DESCRIPTION
• Cortisol is a steroid hormone of the glucocorticoid family that plays a vital role in the
response to stress. In particular, cortisol
– Stimulates gluconeogenesis
– Suppresses inflammation
– Maintains vascular responsiveness to catecholamines
• Cortisol is synthesized and secreted by the adrenal cortex. It is regulated by
adrenocorticotropic hormone (ACTH) produced by the anterior pituitary. ACTH is, in turn,
regulated by corticotropin-releasing hormone (CRH) produced by the hypothalamus.
Cortisol exerts negative feedback control by inhibiting the secretion of CRH and ACTH.
• A 24-hour circadian rhythm causes oscillatory release of CRH, ACTH, and cortisol. For those
who sleep at night, cortisol levels are highest just before waking and lowest in the evening.
• Disease states include Cushing’s syndrome (glucocorticoid excess) and Addison’s disease
(adrenocortical insufficiency).
• Cortisol is a steroid hormone that enters cells and binds to an intracellular cytoplasmic
receptor. This bound complex stimulates DNA transcription resulting in protein production
that mediates the effects of cortisol.
• Cortisol stimulates gluconeogenesis:
– Increases protein catabolism and decreases protein synthesis in the muscle, thereby
providing more amino acids to the liver for gluconeogenesis.
– Decreases insulin sensitivity and decreases glucose utilization in adipose tissue.
– Lipolysis is increased, providing more substrate for gluconeogenesis.
• Cortisol suppresses inflammation:
– Inhibits the production of interleukin-2 and proliferation of T lymphocytes.
– Inhibits release of histamine and serotonin from mast cells and platelets.
– Decreases prostaglandin and leukotriene synthesis by inhibiting the formation of
arachidonic acid.
ANATOMY
• CRH-containing neurons are located in the paraventricular nuclei of the hypothalamus. CRH
is released into the hypothalamic–hypophysial portal blood and delivered to the anterior
pituitary where it stimulates ACTH secretion.
• The anterior lobe of the pituitary synthesizes and secretes ACTH into the bloodstream under
CRH stimulation.
• Cortisol is produced by cells within the zona fasciculata of the adrenal cortex.
• The adrenal gland is composed of the inner medulla that produces catecholamines and the
outer cortex that is divided into three histological zones. Going from outside inwards: The
outer most zona glomerulosa is the source of aldosterone production. Just beneath is the
zona fasciculata, the source of glucocorticoids production. The inner most layer of the
cortex is the zona reticularis; responsible for the production of androgens.
• Cortisol excess states (Cushing’s syndrome):
– Caused by endogenous oversecretion or iatrogenic treatment with glucocorticoids at
supraphysiologic doses.
– Endogenous oversecretion. The majority of instances involve ACTH overproduction (80%).
These disease states include ACTH producing pituitary adenoma and ectopic ACTH
production from tumors such as small cell carcinoma of the lung and pancreatic
carcinoma. ACTH-independent processes such as cortisol secreting adrenal adenoma or
carcinoma make up the remainder of endogenous cortisol oversecretion (20%).
– When the source of endogenous cortisol is caused by overproduction of ACTH by the
pituitary, the condition is known as Cushing’s disease.
– Chronic excess of glucocorticoids results in physical changes. These include central
obesity, moon facies, purple striae, muscle wasting, osteopenia, hirsutism, and
hyperpigmentation. Clinical signs include glucose intolerance hypertension, hypokalemic
alkalosis, and leukocytosis.
– Treatment of endogenous sources of excess glucocorticoid entails surgical resection.
• Cortisol-deficient states:
– Primary adrenocortical insufficiency is caused by the inability of adrenal glands to
produce both glucocorticoids and mineralocorticoids (Addison’s disease).
Most common cause is autoimmune destruction of the adrenal cortex resulting in acute
adrenal crisis. Other causes of adrenocortical insufficiency include metastatic disease to
the adrenal cortex, adrenal hemorrhage, infection of the adrenal gland (tuberculosis,
opportunistic infections with HIV, fungemia), and amyloid infiltration [1].
Characterized by elevated ACTH levels but decreased levels of glucocorticoids and
mineralocorticoids.
Clinical features are related to the adrenocortical hormone deficiency. Hypoglycemia is
caused by cortisol deficiency. Hypotension, postural hypotension, hyperkalemia,
metabolic acidosis, and volume contraction are caused by mineralocorticoid deficiency.
Hyperpigmentation is caused by elevated ACTH secretion. Other signs and symptoms
include weakness, fatigue, lethargy, anorexia, nausea, abdominal pain, prerenal
azotemia, hypercalcemia, convulsions, fever, and syncope.
Treatment: Replacement of glucocorticoids (hydrocortisone, prednisone,
methylprednisolone) and mineralocorticoids (fludrocortisone).
– Secondary adrenocortical insufficiency is caused by decreased ACTH production by the
anterior pituitary gland.
Most common cause of secondary adrenocortical insufficiency is withdrawal of
corticosteroid therapy. Other causes include pituitary tumor, pituitary surgery or
radiation, postpartum hypopituitarism (Sheehan’s syndrome), and sarcoid infiltration of
the pituitary gland.
Chronic corticosteroid therapy suppresses the hypothalamus and anterior pituitary
resulting in decreased production of CRH and ACTH, respectively. Decreased levels of
CRH and ACTH cause atrophy of the zona fasciculata, resulting in glucocorticoid
deficiency. During times of physiologic stress, the patient is unable to acutely increase
cortisol production, resulting in acute secondary adrenocortical insufficiency.
• Cortisol excess states:
– Patients with Cushing’s syndrome must have their diabetes, BP, intravascular volume
status, and electrolytes optimized prior to surgery.
– The body habitus of Cushingoid patients (central obesity, moon facies, buffalo hump) may
present an airway challenge.
– A high cortisol state causes immunosuppression and poor wound healing. Sterile technique
is vital for all procedures and line placements to minimize iatrogenic infections.
– Careful positioning is vital as severe osteopenia increases risk of fractures.
– Patients with adrenal Cushing’s syndrome presenting for adrenalectomy should receive
hydrocortisone at the time of surgery as they are at risk of developing acute
glucocorticoid deficiency postoperatively. Hydrocortisone can then be tapered as the
previously quiescent contralateral adrenal gland resumes corticosteroid production.
• Cortisol-deficient states:
– Patients with adrenocortical insufficiency should continue their mineralocorticoid and
glucocorticoid replacement therapy up until their time of surgery. Clinical features of
overt deficiency include hyperkalemia, hyponatremia, metabolic acidosis, and myocardial
conduction defects.
– Hydrocortisone has both glucocorticoid and mineralocorticoid activity. Therefore, it is an
ideal agent to use for the management of adrenocortical insufficiency.
– Additional perioperative stress dose of glucocorticoids may be necessary as these patients
may not be able to mount an adequate stress response. Traditional recommendation is 200
mg hydrocortisone per 70 kg body weight per day [2]. However, smaller doses of 100 mg
per 70 kg body weight per day have been used with success [3,4].
– The amount of perioperative hydrocortisone supplementation is based on the anticipated
stress of the procedure, relative degree of trauma, and the depth of anesthesia [5].
REFERENCES
1. Dorin RI, Qualls CR, Crapo LM. Diagnosis of adrenal insufficiency. Ann Intern Med.
2003;139(3):194–204.
2. Symreng T, Karlberg BE, Kågedal B, et al. Physiological cortisol substitution of long-term
steroid-treated patients undergoing major surgery. Br J Anaesth. 1981;53(9):949–954.
3. Glowniak JV, Loriaux DL. A double-blind study of perioperative steroid requirements in
secondary adrenal insufficiency. Surgery. 1997;121(2):123–129.
4. Bromberg JS, Alfrey EJ, Barker CF, et al. Adrenal suppression and steroid supplementation
in renal transplant recipients. Transplantation. 1991;51(2):385–390.
5. Lampe GH, Roizen MF. Anesthesia for patients with abnormal function of the adrenal
cortex. Anesthesiol Clin North Am. 1987;5:245.
ADDITIONAL READING
disorders. Int Anesthesiol Clin. 2000;38(4):31–67.
• Udelsman R, Ramp J, Gallucci W, et al. Adaptation during surgical stress: A reevaluation of
the role of glucocorticoids. J Clin Invest. 1986;77(4):1377–1381.
• Aldosterone
• Acute adrenal insufficiency
CLINICAL PEARLS
• Patients with Cushing’s syndrome must have their diabetes, BP, intravascular volume status,
and electrolytes optimized prior to surgery. They are at high risk for poor wound healing
and surgical wound infection.
• The body habitus of Cushingoid patients (central obesity, moon facies, buffalo hump) may
present an airway challenge.
• Patients with adrenal Cushing’s syndrome presenting for adrenalectomy should receive
hydrocortisone at the time of surgery as they are at risk of developing acute glucocorticoid
deficiency postoperatively.
• Patients with adrenocortical insufficiency should continue their mineralocorticoid and
glucocorticoid replacement therapy up until their time of surgery. Clinical features of overt
deficiency include hyperkalemia, hyponatremia, metabolic acidosis, and myocardial
conduction defects.
• Acute withdrawal of exogenous glucocorticoids in the perioperative period may result in
acute adrenocortical insufficiency.
CRANIOSYNOSTOSIS
Ellen Y. Wang, MD
BASICS
DESCRIPTION
General
• Craniosynostosis is an abnormal, premature closure of one or more of the cranial sutures
and can lead to an abnormally shaped head, restricted brain growth, or impaired cognitive
development.
– Nonsyndromic cases typically affect only one suture and are sporadic.
– Syndromic presentations comprise 20% of cases. There are more than 180 syndromes that
can cause this, including Crouzon, Pfeiffer, Apert, and Muenke syndromes.
• Treatment often involves a multidisciplinary team approach with neurosurgery, craniofacial
plastic surgery, oral maxillofacial surgery, ophthalmology, and genetics.
Position
• Supine for metopic and coronal suture release, typically on a cerebellar head rest.
• Prone for sagittal and lambdoid suture release, on a prone headholder, often with the neck
extended in a modified sphinx position.
Incision
Variety of different techniques
• Open cranial vault remodeling (craniectomy or suturectomy) and fronto-orbital
advancement
• Spring-mediated cranioplasty for sagittal synostosis
• Minimally invasive endoscopic reconstruction
• Placement of distraction devices
Approximate Time
• Open surgery: 3–6 hours
• Endoscopic surgery: 1–2 hours
EBL Expected
• Open procedures can range from 20–170% of estimated blood volume (EBV)
• Endoscopic procedures can range from 1–27% of EBV (1)
Hospital Stay
• Open surgery: 3–4 days
• Endoscopic surgery: 1–2 days
Special positioning equipment and padding may be needed if the prone position is
anticipated.
EPIDEMIOLOGY
Prevalence
• Affects 3–5/10,000 live births
• Syndromic cases: Chromosomal abnormalities are often noted. Mutations have been found in
genes involved in the osteogenic process of the skull (most are found on fibroblast growth
factor receptors [FGFRs]).
• Nonsyndromic cases are sporadic, though a familial pattern has been reported as an
autosomal dominant disorder.
• Secondary causes include metabolic disorders (hypothyroidism), fetal teratogen exposure
(phenytoin, valproic acid), and certain forms of mucopolysaccharidosis (Hurler syndrome)
(2).
• Deformational plagiocephaly should not be confused with true craniosynostosis. Since the
advent of sudden infant death syndrome recommendations for supine sleeping positions, the
incidence has increased dramatically.
• Types of suture closure:
– Sagittal suture (∼60%) or scaphocephaly
– Unilateral (anterior plagiocephaly) or bilateral (brachycephaly) coronal suture (25%)
– Metopic suture (15%) or trigonocephaly
– Lambdoid suture (2–3%) or posterior plagiocephaly
Morbidity/Mortality
• Calvarium deformities
• Vision problems with orbital dystocia
• Increased intracranial pressure, papilledema
• Neurocognitive, speech, and behavioral abnormalities
Repair is recommended early in infancy (between 2 and 6 months of life) to prevent the
sequelae associated with restricted brain growth and allow for normal cognitive development.
SYMPTOMS
• There may be mild preoperative deficits in both motor and mental development.
• Look for symptoms of increased intracranial pressure (visual difficulties, nausea/vomiting,
somnolence, or headaches), which may present more commonly in children who are older
or have fusion of multiple sutures (2).
History
• A careful history of prematurity status and course should be taken, as well as any
comorbidities that may present in syndromic cases.
• Obstructive apnea can occur in some syndromic cases (Apert, Crouzon) because of abnormal
airway anatomy (choanal stenosis or atresia, tracheal stenosis or abnormal tracheal
cartilage).
• Associated congenital disease is associated with many syndromes (Apert syndrome).
• Cervical spine fusion (Apert, Crouzon, Pfeiffer), or other bone/cartilage abnormalities
(syndactyly, synostosis of other joints).
Signs/Physical Exam
• A good airway and facial exam is indicated in syndromic cases where a difficult airway is
anticipated (small nasopharynx or fused cervical spine). Note the presence of a large
tongue, shallow orbits, small mandible, and midface hypoplasia (seen in Apert and Crouzon
syndromes), as this can indicate difficult mask ventilation.
• Limb deformities (syndactyly) can pose challenges in venous access.
MEDICATIONS
A basic medication and allergy history should be obtained.
Labs/Studies
• Baseline CBC and coagulation studies
• Plain skull radiographs or ultrasonography for routine diagnosis
• Brain CT scan may be helpful in syndromic or complex cases where physical examination
does not provide a clear diagnosis (3).
• If cervical spine fusion is a concern, cervical spine radiographs should be obtained.
• Type and cross at the minimum. If an open or complicated procedure is expected, one or
more units of packed red blood cells (pRBCs) should be readily available in the operating
room prior to incision.
• If there is coexisting congenital cardiac disease, a preoperative baseline EKG and
echocardiogram may be warranted to evaluate structural anatomy and function.
• Renal abnormalities have been associated with syndromic presentations.
TREATMENT
Premedications
• Consider oral or IV premedication in older children with anxiety, or having a parent present
at induction to ease separation anxiety.
• A history of difficult airway may necessitate an IV placement prior to induction; consider
topical anesthetic creams to decrease pain with IV placement.
Potential for blood transfusion is higher in neonates and open craniectomies
Perioperative antibiotic prophylaxis may be indicated in cases with associated congenital
heart disease.
INTRAOPERATIVE CARE
General anesthesia with an endotracheal tube
Monitors
• Good peripheral IV access (usually 2 large-bore IVs) (1). Consider central venous catheter
placement if peripheral IV access is unsatisfactory
• Consider a radial arterial line
• Consider thoracic/precordial Doppler ultrasound for venous air detection
• Consider a Foley catheter for longer cases
• IV or inhalation induction with sevoflurane
• Oral or nasal endotracheal intubation with controlled ventilation. Consider a muscle
relaxant to facilitate intubation. If a difficult airway is anticipated, ensure all backup
equipment is at hand (LMA, fiberoptic, indirect video laryngoscopy, etc.).
• Inadvertent extubation or bronchial mainstem intubation can occur during positioning,
extension/flexion of the head, and movement between the supine and prone position.
Securing the endotracheal tube (sometimes with silk suture or wire to alveolar ridge) and
confirming the position of the endotracheal tip is extremely important.
• Corneal shields can be used to protect the eyes. If the eyes are proptotic, suturing the eyes
shut may be necessary.
Maintenance
• Balanced technique with volatile anesthetics, oxygen with nitrous oxide or air, IV narcotics,
and a neuromuscular relaxant. Studies have shown equivalent results with isoflurane–
remifentanil and sevoflurane–remifentanil techniques (2,3).
• In patients with elevated intracranial pressure, care should be taken to avoid further
elevations in pressure.
• Typically, the incision site is infiltrated with local anesthetic (combined with epinephrine)
prior to surgery.
• Crystalloid should be administered for replacement of deficit and maintenance
requirements. Colloids (typically albumin 5%) can be used after crystalloid replacements for
decreases in BP.
– Blood loss must be closely monitored and transfusions given when indicated (e.g.,
hemodynamic instability, hemoglobin <6 g/dL). Most of the blood loss occurs during
elevation of the periosteum, with increased risk of bleeding with manipulation of the
dural sinuses; after the osteotomy, there is a slow and steady blood loss. Sagittal suture
craniosynostosis may increase the need for blood transfusions given the close anatomical
position to the suture (1).
• A filter should be used during transfusion of all blood components. pRBCs stored <2–3
weeks should be used in young children to decrease the risk of hyperkalemia. The need for
platelets, fresh frozen plasma, and cryoprecipitates is rare (in small children, ABO-matched
platelets should be used.
– Strategies for decreasing homologous transfusion:
Directed donation, or autologous blood donation in older children
Acute normovolemic hemodilution has not been shown to decrease blood transfusion
requirements.
Perioperative blood salvage may reduce the need for blood transfusion, but has risks of
coagulopathy, hemolysis, and bacterial contamination (2).
Induced hypotension is not recommended
Preoperative use of recombinant human erythropoietin may reduce transfusion
requirements (3).
Combinations of above therapies may decrease the need for transfusions.
• It is critical to closely monitor electrolytes (especially calcium and potassium) if transfusions
are given.
• Venous air embolism (higher incidence in open craniectomies) can occur and should be
treated immediately.
• Plan for extubation at the end of the procedure.
• Consider leaving the endotracheal tube in place if patient has a history of a difficult airway,
or has experienced intraoperative instability.
FOLLOW-UP
BED ACUITY
• Intensive care unit (ICU) monitoring may be indicated for neonates, longer case duration,
large transfusion requirements, respiratory monitoring, and intraoperative hemodynamic
instability.
• For endoscopic cases, a monitored floor familiar with neurosurgical patients is adequate.
• Coagulation studies and hematocrit should be followed closely.
• A postoperative CT scan will often be ordered.
ANALGESIA
• IV narcotics (typically nurse or patient controlled analgesia)
• IV muscle relaxants (such as Valium) are useful for muscle spasms.
COMPLICATIONS
• Infection (rare)
• Blood transfusion related
• Orbital or cortical injury
• Dural sinus tears
• CSF leaks
PROGNOSIS
• The need for reoperation is associated with syndromic and/or multiple-suture
craniosynostosis
• Subsequent procedures include fronto-orbital advancement and calvarial vault
reconstruction.
• Postoperative helmet therapy may be used after endoscopic surgery to promote symmetric
growth.
REFERENCES
1. eier PM, Goobie SM, DiNardo JA, et al. Endoscopic strip craniectomy in early infancy: The
initial five years of anesthesia experience. Anesth Analg. 2011;112(2):407–414.
2. Koh JL, Gries H. Perioperative management of pediatric patients with craniosynostosis.
Anesthesiol Clin. 2007;25(3):465–481, viii.
3. Chim H, Cosain AK. An evidence-based approach to craniosynostosis. Plast Reconstr Surg.
2011;127(2):910–917.
ADDITIONAL READING
• A Practical Approach to Pediatric Anesthesia, Chapter 14. Holzman RS, Mancuso TJ, Polaner
DM. Lippincott Williams & Wilkins, 2008.
CODES
ICD9
756.0 Congenital anomalies of skull and face bones
ICD10
Q75.0 Craniosynostosis
CLINICAL PEARLS
• Craniosynostosis is a complex condition, sometimes involving syndromes with craniofacial
abnormalities and cognitive dysfunction, and often requires a multidisciplinary approach.
• Syndromic cases can have a higher incidence of perioperative respiratory complications,
such as obstructive sleep apnea, difficult airway, and abnormalities of the trachea.
• Early surgical intervention is standard of care.
• The risk of significant blood loss, especially in neonates, requires careful preoperative
planning and intraoperative vigilance. It is often prudent to begin transfusion early, before
hypovolemia occurs.
• The risk of venous air embolism is significant; be prepared to treat cardiovascular collapse
quickly.
CRANIOTOMY FOR CEREBRAL ANEURYSM CLIPPING
BASICS
DESCRIPTION
General
• An open craniotomy is performed to clip an intact, leaking, or ruptured cerebral aneurysm
that is untreatable by endovascular embolization. The first clipping was described in 1937;
since then, there has been continued evolution of shape and size of clips.
• A frontotemporal or pterional craniotomy is performed and the frontal and temporal lobes
are gently retracted. The circle of Willis is exposed and the aneurysm is located. In most
cases, the aneurysm has been imaged preoperatively by cerebral angiography to determine
the location, shape, and size.
• The blood supply to the aneurysm is determined/confirmed under the microscope. Doppler
ultrasound may also be used to determine blood flow around the aneurysm.
• Under microscopic visualization, permanent clips are placed around the neck of the
aneurysm to prevent blood from entering the dome; they are MRI and biocompatible. If
clipping is deemed to be inadequate, temporary clips are placed across the cerebral vessel
while additional clipping and hemostasis is achieved. Temporary clips are large and easy to
place and remove; they are placed proximal to the aneurysm to deprive it of blood flow and
provide a bloodless field. Prolonged temporary clipping increases the risk of ischemia; thus,
clipping time should be closely monitored.
• To confirm the absence of a leak postclipping, one of the following surgeon- and institution-
dependent techniques are performed:
– Angiography. A vascular sheath is placed either preoperatively or intraoperatively
(institution-dependent).
– IV indocyanine green dye (IcG). Can be observed under fluoroscopy while precluding the
need for IV contrast dye and placement of a vascular sheath. Strong data, however, is not
available at this time to obviate angiography.
– IcG and angiography. Decreases the length of angiography and exposure to IV contrast
dye. Requires placement of a vascular sheath.
• Advantages to craniotomy with aneurysm clipping versus endovascular embolization include
definitive aneurysm ablation, lower incidence of rebleeding, decreased cost, and technical
superiority in cases where the aneurysm cannot be coiled endovascularly.
• Disadvantages include increased risk of bleeding, stroke, seizure, myocardial infarction,
aneurysm rupture, vasospasm, and possibly recovery.
Position
• Supine (prone in rare cases of occipital aneurysms)
• Head pinned in a Sugita (or Mayfield) frame
• Shoulder roll placed and the ipsilateral arm can be folded over the body if there is any
tension on the brachial plexus; alternatively, the arm can be tucked.
• If possible, the left arm is left abducted <90° for access to IV, arterial line, and pulse
oximetry.
• Bed turned 90–180°
Incision
Frontotemporal or pterional incision (occipital rare). Temporalis flap, Burr hole, and then
bone flap turned to expose dura.
Approximate Time
• Varies depending on aneurysm size, location, and shape. Technical difficulty can arise from
the aneurysm’s neck shape or blood supply.
• Length can also be prolonged by intraoperative angiography.
EBL Expected
• Unruptured aneurysms: ∼500–1,000 mL.
• Rupture: In excess of 2,000 mL. Sufficient blood products should be typed and crossed, in
the room, and checked in the event that immediate transfusion is needed.
Hospital Stay
• Unruptured aneurysm: 8–10 days
• Ruptured aneurysm: >8–10 days to manage complications.
• Sugita or Mayfield surgical frame
• Surgical microscope
• A variety of MRI and biocompatible temporary and permanent aneurysm clips
• Angiography and accompanying radiological equipment and personnel versus fluoroscopy
for IcG.
• Neuromonitoring equipment and personnel
EPIDEMIOLOGY
Incidence
• Cerebral aneurysms are present in 2–5% of the population.
• The incidence of rupture is 1 in 10,000 patients with aneurysms.
Prevalence
• Risk of rupture increases 1–2% per year, peaking between 40 and 60 years of age.
• Increased in females, smokers, polycystic kidney disease, and hypertensive patients.
Morbidity
• Rupture: 30–35% through one’s lifetime
• All-cause morbidity at 1-year post-repair: 15.7%
• Stroke from surgery: 1–10%.
Mortality
1-year post repair: 1.6%
• The risk of aneurysm rupture and resulting morbidity is significant during the procedure.
• Adequate venous access should be established and blood products made available.
• Anesthetic management revolves around managing intracranial pressure (ICP) and brain
relaxation, minimizing the effects of drugs on neuromonitoring, and potentially inducing
burst suppression.
• Intraoperative neuromonitoring (IONM) can help detect both global and focal ischemia.
• Perioperatively, tight hemodynamic management is paramount to avoid rupture, decrease
bleeding in the event of rupture, or increase perfusion through collateral circulation when
temporary clips are used.
• Postoperative vasospasm needs to be managed aggressively with “triple H" therapy
(hypervolemia, hypertension, and hemodilution) and possible endovascular intervention.
SYMPTOMS
• Headache or neurological changes are often incidental symptoms that lead to diagnosis
• Seizures, stroke, or SAH (“worst headache of my life”).
• SAH can lead to systemic changes including EKG changes, cardiomyopathy, and respiratory
failure.
History
• Commonly an incidental finding on brain imaging for other complaints or trauma.
• 1 in 10,000 patients with aneurysms present with subarachnoid hemorrhage (SAH).
• Standard history with focus on neurologic and cardiovascular history.
Signs/Physical Exam
Full neurological exam
MEDICATIONS
• Nimodipine to prevent vasospasm after SAH
• Other antihypertensives
• Anticonvulsants (phenytoin, levetiracetam)
• Statins (associated with less vasospasm)
• Steroids to treat cerebral edema
• H2 Blockers, proton pumper inhibitors (PPIs) to prevent ulceration from steroid use
• Stool softeners (to prevent straining)
Labs/Studies
• CBC, type and cross, chemistry, and coagulation panel
• Head CT, MRI
• Cerebral angiogram
• Cerebral vascular disease
• Cardiovascular disease in older patients
• Polycystic kidney disease (rare)
TREATMENT
Premedications
Should be used sparingly; small amounts of midazolam (short duration) or opioid may be
administered for preinduction line placement. Avoid other sedatives such as scopolamine,
droperidol, or diazepam that may cloud the postprocedure neurological exam.
• Blood consent
• Possibility of postoperative intubation
Gram positive coverage for skin flora with a third-generation cephalosporin
INTRAOPERATIVE CARE
• General anesthesia with endotracheal tube (ETT)
• Very rarely, an “awake craniotomy” (light MAC with scalp block) for aneurysms in eloquent
parts of the brain
Monitors
• Foley catheter with urometer
• Arterial line (preinduciton for beat-to-beat monitoring (Cushing response, tight
hemodynamic adjustments), and frequent labs (hemoglobin, electrolytes, osmolality)
• Central venous access in patients with SAH, otherwise large-bore (14–18 G) peripheral
access is adequate for rapid resuscitation and transfusion.
• Intraoperative neuromonitoring: Usually EEG and somatosensory-evoked potential (SSEP)
• Bispectral monitoring may not be possible because of pin placement or incision.
• Deep induction with hypnotic, opioid, and paralytic medication to avoid coughing, bucking,
sharp increases in BP, and hypoxemia with laryngoscopy and intubation.
• Avoid ketamine and succinylcholine as they can increase the ICP. If a RSI is warranted (e.g.,
SAH, risk of aspiration), the benefit of quickly securing the airway and controlling
respiratory parameters outweighs the small and transient increase from succinylcholine.
• Antihypertensives and vasopressors with quick onset and short duration should be available
to provide tight hemodynamic control (hypotension can cause ischemia and hypertension
can cause rupture).
Maintenance
• Low-dose inhalational agents, opioids (bolus or infusion), and muscle relaxation can be used
versus total IV anesthesia with propofol (may have better effects on ICP, brain relaxation,
and IONM). Nitrous oxide is generally avoided.
• CO2. The ETCO2 is typically maintained between 25 and 30 mm Hg. If concerned about
dead space (chronic obstructive pulmonary disease, COPD, pneumonectomy) follow PaCO2.
Hypercarbia can lead to increased cerebral blood flow (CBF) and increased ICP. Rapid drops
in CO2 can increase the transmural pressure of the aneurysm and cause rupture. Severe
hypocarbia (<25 mm Hg) can cause ischemia.
• Anticonvulsants should be loaded during the case.
• Corticosteroids (dexamethasone) are given to treat cerebral edema and help prevent PONV.
• ICP. Diuresis with mannitol and the possible addition of a loop diuretic to decrease brain
water and volume. Maintain euvolemia by replacing urine output.
• Fluids. Normal saline is preferred due to its high osmolality; however, it can cause a
metabolic hyperchloremic acidosis.
• IONM. Communicate anesthetic technique and changes to neuromonitoring to avoid
masking or misconstruing changes from the surgical field.
• Tight hemodynamic control. Be prepared to increase BP (with fluids and pressors versus
inotropes) during temporary clipping or occlusion of the internal carotid artery to improve
collateral flow. Be prepared to return BP to normal after clipping. Avoid hypotension to
decrease risk of ischemia.
• Burst suppression with thiopental or propofol may be used during temporary aneurysm
clipping.
• Temperature. Mild intraoperative hypothermia (to 33°C) is controversial. Data has not
proven any benefit in healthy patients with unruptured aneurysms.
• For uncomplicated cases, extubation followed by a neurological exam is important to
identify possible surgical complications. In patients who require postoperative intubation, a
neurological exam should be attempted before reanesthetizing and transporting to the
intensive care unit (ICU). The inability to perform or an abnormality in the neurological
exam requires immediate neuroimaging before transport to the ICU.
• Avoid bucking, coughing, or hypertension
• Patients should remain flat (or reverse Trendelenburg) if an angiography sheath was placed.
POSTOPERATIVE CARE
BED ACUITY
Direct transport to the ICU, preferably a neuro ICU with full monitoring.
ANALGESIA
• Analgesia should be targeted to treat pain while minimizing sedation; utilize low-dose IV or
oral opioids.
• Rectal or IV acetaminophen
• Avoid NSAIDs (postoperative bleeding)
COMPLICATIONS
• Aneurysmal rebleeding: Tight BP control can help prevent rebleeding.
• Stroke and seizure
• Vasospasm should be aggressively treated with “Triple H” therapy (hypertension,
hemodilution, hypervolemia).
PROGNOSIS
In unruptured aneurysm, the prognosis is good. SAH has a much poorer prognosis, especially
if vasospasm occurs.
REFERENCES
1. Molyneux A, Kerr R, Stratton I. International Subarachnoid Aneurysm Trial (ISAT) of
intracranial aneurysms: A randomised comparison of effects of survival, dependency,
seizures, rebleeding, subgroups. Lancet. 2005;366(9488):809–817.
2. lshekhlee A, Mehta S, Edgell RC, et al. Hospital mortality and complications of electively
clipped or coiled unruptured intracranial aneurysms. Stroke. 2010;41:1471–1476.
3. Zipfel GJ, Dacey RG. Update on management of unruptured intracranial aneurysms.
Nuerosurg Focus. 2004;17.
4. Todd MM, Hindman BJ, Clarke WR, et al. Mild intraoperative hypothermia during surgery
for intracranial aneurysm. N Engl J Med. 2005;352(2):135–145.
• Cerebral aneurysm and endovascular embolization
• Subarachnoid hemorrhage
• Transcranial Doppler
• Electromyelogram
CODES
ICD9
437.3 Cerebral aneurysm, nonruptured
ICD10
I67.1 Cerebral aneurysm, nonruptured
CLINICAL PEARLS
• Although open aneurysm clipping is associated with a higher morbidity than the
endovascular approach, endovascular embolization may not be technically possible.
• The risk of rupture is significant and ICP and BP must be controlled before clipping.
• IONM can help detect subclinical focal and global ischemia.
CRANIOTOMY FOR INTRACRANIAL HEMORRHAGE
Keren Ziv, MD
BASICS
DESCRIPTION
General
• Causes of intracranial hemorrhage include cerebrovascular aneurysm or arteriovenous
malformation (AVM) rupture, malignant hypertension, trauma, anticoagulation therapy, and
tumors.
• Intracranial hemorrhage carries a high-risk for morbidity and mortality; therefore, prompt
diagnosis and medical and/or surgical management are cornerstones of therapy.
• Medical management is usually performed for small hemorrhages with minimal deficits, as
clot can be absorbed by the body. It is also performed before and after surgical aneurysm
clipping to gain the best outcome and includes seizure prophylaxis and therapy,
management of intracranial pressure, and prevention of vasospasm. However, despite
ongoing research, major advancements and improvements have not been made in recent
years.
• Surgical management may be performed for aneurysm clipping as the risk of re-bleed can
reach up to 35% within 14 days of the initial bleed (focus of this chapter), AVMs, or large
hemorrhages near the surface of the brain that are accompanied by neurologic
deterioration, brainstem compression, or hydrocephalus.
Position
• Determined by the site of aneurysm (80% occur in the anterior circulation), AVM, or
hematoma, surgeon preference, and patient factors such as intracranial pressure (ICP).
Possibilities include supine, semilateral, lateral, prone, and sitting; variations of these
positions can also be employed.
• Some degree of head elevation is usually employed to aid in venous drainage and brain
relaxation. Air embolism remains a risk, even when head elevation is minimal.
• The sitting position must be chosen very carefully, and is typically only for patients where
either brain relaxation cannot be achieved because of very high ICP, or due to the surgical
access site. The risk of clinically significant venous air embolism is high and steps should be
taken to reduce the risk and ensure early detection (volume loading, precordial Doppler,
and central venous catheter placement at the superior vena cava-right atrium junction to
aspirate air).
• These procedures tend to be long, and therefore, it is imperative to pay very close attention
to proper positioning, heavy padding, and securing of the patient.
Incision
Depends on the location of the lesion and surgeon preference.
Approximate Time
Very variable, from 90 minutes to 16 hours
EBL Expected
• Typically on the order of a few hundred milliliters for aneurysms that do not rupture.
• If the aneurysm ruptures, blood loss will be brisk, and if the aneurysm is not rapidly clipped,
patients can exsanguinate.
• It is advisable to have at least two units of packed red blood cells immediately, and further
blood products and volume expanders easily available.
Operating microscope, possibly 3D navigational equipment, and electrophysiological
monitoring equipment.
EPIDEMIOLOGY
Incidence
• Subarachnoid hemorrhage (SAH): 9 out of 100,000 people annually. By cause:
– Ruptured aneurysms: 85%
– AVMs: 10%
– Cerebral hemorrhage: 10%
– Others (tumors)
• Risk increases with age
Prevalence
About 1–2% of the population has at least one cerebral aneurysm.
Morbidity
• If the early course after aneurysm rupture is survived, 25% of patients will have significant
restrictions in their lifestyle, and only 20% will have no residual symptoms.
• Other problems include long-term cognitive impairment, depression, fatigue, headache,
posttraumatic stress disorder (PTSD), and hypopituitarism.
Mortality
Overall, survival is poor with the death rate after SAH approaching 50%.
• Prevention of rebleeding during induction of anesthesia and other stimulating parts of the
procedure.
• Prevention of vasospasm (triple H therapy: Hypertension, hemodilution, hypervolemia)
• Management of increased ICP.
• Brain “relaxation”
SYMPTOMS
• Increased ICP can present as headache, nausea and vomiting, seizures, or altered sensorium.
• Focal neurologic findings associated with hemorrhage.
History
Most intracranial aneurysms are asymptomatic and remain undetected until the time of
rupture.
Signs/Physical Exam
A thorough neurologic exam needs to be performed to assess the baseline status of the patient
so that it can be compared to the postprocedure exam. In this fashion, subtle changes can be
picked up, and further diagnostics and therapeutics can be pursued in a timely fashion.
MEDICATIONS
• Mannitol
• Furosemide
• 3% saline
• Vasoactive substances such as calcium channel blockers to prevent vasospasm and others to
control BP.
• Steroids for cerebral edema
Labs/Studies
• CBC to assess hemodilution during triple H therapy.
• Chem 7 to assess for cerebral salt wasting (hyponatremia and hypokalemia) due to release of
brain and atrial natriuretic hormone or syndrome of inappropriate antidiuretic hormone
secretion (SIADH).
• EKG: SAH often leads to changes that are consistent with acute ischemia (QT prolongation,
Q waves, cardiac dysrhythmias).
• Echocardiogram only needs to be obtained if cardiac ischemia or failure is suspected.
• Chest radiograph is usually not indicated unless there is a suspicion of neurogenic
pulmonary edema.
• Imaging modalities include CT angiogram, angiogram, MRI/MRA
• Cardiac rhythm disturbances will occur in up to 90% of patients with SAH.
• Ischemic cardiomyopathy may develop in a small percentage of patients due to vasospasm
and high catecholamine state. This needs to be treated in a manner similar to ischemia from
coronary artery disease secondary to atherosclerosis. This ischemia is usually reversible if
treated properly, and patients recover well.
• Neurogenic pulmonary edema (NPE) may develop within minutes to hours after injury. It
manifests as a marked increase in pulmonary interstitial and alveolar fluid, with resultant
dyspnea, tachypnea, tachycardia, basilar rales, copious frothy sputum, possible hemoptysis,
and hypoxemia.
TREATMENT
Premedications
• Patients with altered sensorium or with increased ICP should be cautiously, if at all,
premedicated; small changes in CO2 tension can lead to large changes in ICP and
obtundation.
Potential for prolonged intubation and pharmacologic induced coma.
Cefazolin for skin organisms q4h prophylactically.
INTRAOPERATIVE CARE
Monitors
• Foley catheter
• Arterial line allows for tight BP monitoring and aids in resuscitation should the aneurysm or
AVM re-rupture.
• Central line should be strongly considered given the risk for a venous air embolism, massive
blood loss, and the possible need for vasoactive and barbiturate administration.
• EEG monitoring and evoked potentials are not the standard of care, but should be strongly
considered in cases of giant and wide neck aneurysms, aneurysm in close proximity to other
vessels, high ICP, large SAH, or in those who are otherwise at risk for cerebral ischemia. No
trial has shown an outcome benefit. Findings may be used to further direct therapy and
intervention.
• There is no single recommended induction choice. Goals are as follows:
– Keep the aneurysm’s transmural pressure gradient stable.
– Maintain adequate cerebral perfusion and oxygenation.
– Avoid rapid changes in ICP.
• The risk of aneurysm rupture with induction is about 1% (data on re-rupture is not
available). Good choices for induction are propofol, IV lidocaine, esmolol, and short-acting
opioids such as remifentanil, but other agents may be used with equal efficaciousness.
• Usually, intermediate-acting nondepolarizing muscle relaxants are used. Succinylcholine will
raise the ICP transiently, but to a lesser degree than an unsmooth induction.
Maintenance
• Positioning and head pinning are stimulating events, and may need further doses of
induction agents. Scalp infiltration with local anesthetics is useful in attenuating the stress
response. Long-acting agents are avoided due to the risk of hypotension.
• Brain relaxation. Reducing the content of the cranial vault for surgical exposure is
paramount.
– Mannitol 0.5–1 mg/kg over a period of about 20–30 minutes. Administration may cause
severe hypotension, especially in hypovolemic patients.
– Furosemide
– Cerebrospinal fluid drainage
– Head elevation
– Avoidance of venous outflow obstruction by limiting head rotation (aids in brain
relaxation)
– If brain relaxation is inadequate, switching from volatile agents (usually kept below one
MAC) to a propofol infusion will improve relaxation significantly.
• BP is kept close to normal during the case. However, if the surgeon applies temporary clips
or the aneurysm is secured, BP is elevated to improve collateral flow.
• Cerebral protection. At this time, no cerebral protection study has shown a decrease in the
risk of ischemia.
– Mild hypothermia will reduce cerebral metabolic rate of oxygen (CMRO2), but will not
affect morbidity or mortality. It will, however, aid in brain relaxation, and if the
temperature does not fall below 34.5°C, it has no negative effect on infection rate,
bleeding, and wound healing.
– Barbiturate administration titrated to burst suppression is used in some centers to protect
the brain from ischemia and provide brain relaxation. Again, no outcome evidence exists
to support this practice.
• Nausea should be preempted with multimodal therapy.
• Extubation should be smooth. Postoperative intubation may be considered in patients with
high-grade hemorrhage or if there is any doubt about their ability to protect their airway.
• Hypertension in the early postoperative period is common. Mild hypertension (20%) should
be left untreated as it will aid in collateral flow and is part of the “triple H" therapy to avoid
vasospasm. Hypertension beyond this range will need to be treated with calcium channel or
beta blockers.
• Pain medications should be given cautiously to avoid clouding of the sensorium, and
• Early neurological exam is paramount as to guide whether CT scanning, angiography, or
initiation of “triple H" therapy is warranted.
POSTOPERATIVE CARE
BED ACUITY
All patients will need to be admitted to the ICU for frequent neurological assessment and
tight BP control.
ANALGESIA
Surgical pain is usually easily managed with small doses of long-acting opioids. Their use can
be obviated by a field block with long-acting local anesthetic intraoperatively.
COMPLICATIONS
• Postoperative hemorrhage
• Vasospasm
• Hydrocephalus
PROGNOSIS
Highly variable, and directly correlated to hemorrhage grade.
REFERENCES
1. Gelb AW. Anesthesia and subarachnoid hemorrhage. Revista Mexicana de Anesthesiologia.
2009;32(1):S168–S171.
2. Coghlan L, Hindman B, Bayman E, et al. Independent associations between
electrocardiographic abnormalities and outcomes in patients with subarachnoid
hemorrhage: Findings from the Intraoperative Hypothermia Aneurysm Trial. Stroke.
2009;40:412–418.
3. Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial (ISAT) of
intracranial aneurysms: A randomised trial. Lancet. 2005;366: 809–817.
ADDITIONAL READING
• Pasternak JJ, Lanier WL. Neuroanesthesiology update. J Neurosurg Anesthesiol.
2009;21:73–97.
CODES
ICD9
432.9 Unspecified intracranial hemorrhage
ICD10
I62.9 Nontraumatic intracranial hemorrhage, unspecified
CLINICAL PEARLS
• Good brain relaxation is of paramount importance.
• Be prepared to administer blood, lower the blood pressure, and administer barbiturates
should the aneurysm re-rupture.
• Postoperative care (i.e., institution of “triple H" therapy, avoidance of nausea, and BP
control) are important to good outcomes.
CREATININE CLEARANCE
BASICS
DESCRIPTION
• Creatinine clearance (CrCl) measures the rate at which the kidneys remove creatinine from
the blood. It is expressed as volume of blood plasma that is cleared per unit of time
(milliliters per minute).
• CrCl functions to estimate the glomerular filtration rate (GFR). Thus, it can serve as a tool to
diagnose renal dysfunction or evaluate the progression of renal disease.
• CrCl is traditionally measured by a 24-hour urine collection (2-hour collections may also be
performed)
• Normal values (may vary by laboratory):
– Men: 120 mL/min (range 97–137)
– Women: 95 mL/min (range 88–128)
– Parturients: 150–200 mL/min
• Creatinine is a by-product of creatine phosphate metabolism in skeletal muscle and of
dietary meat. Creatinine is:
– Released into the circulation at a constant rate
– Freely filtered by the glomerulus
– Not metabolized or absorbed by the kidney
– Not affected by a normal diet or normal physical activity
– Secreted into the proximal tubule of the nephron; 10–15%
– Reduced with age due to declining muscle mass.
• CrCl provides the clinician with a method to estimate the GFR.
– GFR is accepted as the most accurate measure of renal function. However, it is costly and
cannot be performed with routine laboratory monitoring (requires IV or subcutaneous
administration of a marker with repeat collections of urine samples every 30–45 minutes).
– Traditional CrCl requires a 24-hour urine collection as well as a serum creatinine blood
draw in order to calculate the value (Cockroft and Gault equation). CrCl should be
adjusted for patient size and incorporate body surface area when comparing to normal
values (1)[B].
– A small amount of creatinine is secreted by the proximal renal tubule; hence, CrCl
measurements overestimate true GFR by 10–15%.
– If the secreted fraction is ignored, then all of the filtered creatinine would be excreted in
the urine. Calculation is as follows: GFR * SCr = UCr * V; where SCr = serum creatinine
clearance, UCr = urine creatinine concentration, V = urine volume. Note, however, that
this makes the assumption that there is no secretion out of the renal tubule.
– Cimetidine administration is a technique that is utilized to eliminate creatinine secretion
by the proximal tubule and provide a more accurate estimation of GFR (2)[B].
• Age
– Creatinine excretion steadily declines by 50% between ages 50 and 90 years due to
decreasing skeletal muscle mass even if renal disease does not exist (3)[B].
– CrCl decreases ∼6.5 mL/min for every 10 years past the age of 20 years.
• Artificially increased CrCl is seen with:
– Strenuous exercise, trauma/burns, excessive protein intake (especially beef), carbon
monoxide poisoning, hypothyroidism, and pregnancy.
• Errors in CrCl
– Calculation errors can result from incomplete or variable urine collections. This may be
reduced by having the patient empty the bladder and discard urine at the start of the test.
Incomplete collections typically underestimate CrCl and thus GFR.
– Most formulas for CrCl assume a steady state. Thus, increasing creatinine levels during the
collection period can also result in errors.
• A 2-hour urine collection may be used to readily estimate CrCl if urine flow is induced by
diuresis (4)[B].
– May be more feasible to perform in certain patient populations (e.g., critically ill patients)
and allows for serial calculations over time to track changes in GFR.
– These collections should be performed at the same time of day to avoid diurnal variation.
ANATOMY
• The kidneys function in volume control, pH and electrolyte balance, hormone secretion, and
excretion of waste products and toxins.
• They are located in the paravertebral gutters behind the peritoneum at the level of the lower
thoracic vertebrae. Renal arteries originate from the aorta at the level of the first lumbar
vertebra and provide blood to the kidneys.
• The kidney is surrounded by a fibrous capsule and composed of an outer cortex and an inner
medulla.
• The nephron is the functional unit of the kidney; there are ∼1 million nephrons per kidney.
It serves as the site where urine is concentrated and transmitted to the ureters. Additionally,
it clears the plasma of metabolic breakdown products including creatinine and urea.
• Nephrons comprise a filtering component with an enclosed capillary network (glomerulus)
that is attached to a complex tubule system where urine is modified (proximal collecting
tubule, loop of Henle, distal collecting tubule). Urine from the tubules drain into the
collecting duct and finally into the ureters. Nephrons are classified into two types based on
if they have a long or short loop of Henle.
• Renal impairment can be seen with renal hypoperfusion, renal outflow obstruction (usually
both kidneys), cancer, shock, life-threatening infections, heart failure, dehydration, acute or
chronic renal failure, end-stage renal disease, cirrhosis, and diuretics.
• Serum creatinine levels can be readily measured as part of a basic metabolic panel.
However, the value does not linearly increase as GFR decreases.
• Renal disease typically exists along a spectrum from decreased renal reserve to renal failure.
Additionally, physical manifestations of renal disease do not typically appear until a large
percent of nephrons are damaged
– GFR usually must fall below 25 mL/min before clinical signs and symptoms appear.
– A minimum CrCl of 10 mL/min is required to sustain life without the aid of dialysis.
• CrCl may become a less accurate predictor of GFR as kidney function declines.
– The body increases the amount of creatinine that is secreted to compensate for increased
serum creatinine. This leads to an overestimation of true GFR.
– Moderate-to-severe renal disease: Renal function may be better estimated by averaging the
CrCl with the urea clearance (Curea). In this patient population, CrCl typically
overestimates the GFR due to creatinine secretion and Curea typically underestimates the
GFR due to urea reabsorption in the nephron.
– Severe renal disease: Bacterial creatininase activity often increases resulting in augmented
CrCl outside the kidney. This results in less filtered serum creatinine and leads to an
overestimation of CrCl.
• Perioperatively, there are several stressors that can affect renal function, particularly in
patients with preexisting disease (hypoxia, hypovolemia, hypotension, nephrotoxic drugs).
Thus, the anesthesia provider should be aware of the extent of renal disease as well as any
therapies the patient may be taking such as antihypertensive agents, electrolyte
replacements, erythropoietin, immunosuppressants (if post-transplant), and dialysis
• Unfortunately, 24-hour CrCl calculations are often impractical in the perioperative setting.
Although they provide a good estimate of GFR, they are time consuming and labor
intensive.
– In lieu, serum creatinine measurements are often utilized, although they have little
predictive value of the GFR.
– Preexisting renal disease thus poses a conundrum. In renal disease, the anesthesia provider
lacks sensitive, specific, and low-cost tools to preoperatively assess and risk stratify
patients at risk for perioperative renal complications.
– Nonetheless, the anesthesia provider has the capability to either preserve or deteriorate
baseline renal function.
• Volume status should be preoperatively assessed in patients with renal disease. Patients that
are volume depleted (e.g., recent dialysis) may demonstrate an exaggerated response to IV
induction agents.
• Concomitant disturbances include electrolyte dysfunction (acidosis, hyperkalemia), insulin
resistance, anemia, uremia, abnormal coagulation, and cardiac dysfunction.
• Medication adjustments
– Succinylcholine. Patients with chronic renal disease do not exhibit an exaggerated
hyperkalemic response; however, if they have an elevated baseline potassium levels, there
is a potential for hyperkalemic-induced arrhythmias.
– Cisatracurium and atracurium are metabolized by Hoffman degradation and do not
depend on renal clearance for metabolism.
– Antibiotics often require dose reduction when the CrCl falls below 50 mL/min.
– Volatile agents. Sevoflurane has a theoretical risk of producing the nephrotoxic Compound
A (not been supported in clinical practice). Desflurane and Isoflurane have not been
shown to worsen renal dysfunction in patients with preexisting disease (5)[A].
• Postoperative CrCl may be a useful predictor of early acute renal failure (ARF); particularly
in trauma patients (6)[B]. ARF carries a high morbidity and mortality rate.
• Underestimation of CrCl may occur with the following medications:
– Barbiturates and cephalosporins may falsely increase serum creatinine.
– H2 blockers and salicylates can decrease tubular secretion of creatinine.
EQUATIONS
• Creatinine clearance (CCr)
– GFR = [UCr × V]/SCr
Derived from GFR × SCr = UCr × V; where GFR is glomerular filtration rate, SCr is
serum creatinine concentration, UCr is urine creatinine concentration, and V is urine
volume.
– GFR = [CCr + Curea]/2
For patients with moderate-to-severe renal disease
– CCr = (140 – age) × IBW/(SCr × 72)▒
CCr is multiplied by 0.85 for females
Cockcroft and Gault equation
IBW = Ideal Body Weight
• [CCr × 1.73]/BSA
– Corrected CrCl adjusted for standard BSA
REFERENCES
1. Pai MP. Estimating the glomerular filtration rate in obese adult patients for drug dosing.
Adv Chronic Kidney Dis. 2010;17:e53–e62.
2. Kabat-Koperska J, Safranow K, Golembiewska E, et al. Creatinine clearance after
cimetidine administration: Is it useful in the monitoring of the function of the transplanted
kidney. Ren Fail. 2007;29:667–672.
3. Fliser D. Assessment of renal function in elderly patients. Curr Opin Nephrol Hypertens.
2008;17:604–608.
4. Sladen RN, Endo E, Harrison T. Two hour vs. twenty-two hour creatinine clearance in
critically ill patients. Anesthesiology. 1987;67:1013–1016.
5. Litz RJ, Hubler M, Lorenz W, et al. Renal responses to desflurane and isoflurane in patients
with renal insufficiency. Anesthesiology. 2002;97:1133–1136.
6. Shin B, Mackenzie C, Helrich M. Creatinine clearance for early detection of posttraumatic
renal dysfunction. Anesthesiology. 1986;64:605–609.
ADDITIONAL READING
• Bazari H. Approach to the patient with renal disease. In: Goldman L, Ausiello D, eds. Cecil
Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 115.
CLINICAL PEARLS
• Following GFR trends can help estimate the progression of renal disease as well as the
effectiveness of treatment, however it is costly and cumbersome. CrCl is a surrogate for
estimating GFR and serial CrCl measurements are a sensitive method for following renal
dysfunction. However, a 24-hour CrCl may also be impractical in the perioperative setting
and a 2-hour CrCl may be performed in certain patients.
• CrCl may slightly overestimate GFR in patients with normal kidneys (10–15%) and severely
overestimate GFR in patients with declining kidney function due to increased Cr secretion
into the nephron.
• Medications that alter CrCl levels include some cephalosporin antibiotics, aminoglycosides,
amphotericin B, cimetidine, captopril, quinine, quinidine, procainamide, phenytoin, vitamin
C, and trimethoprim.
CRICOTHYROIDOTOMY
BASICS
DESCRIPTION
• Cricothyroidotomy is a surgical airway through the cricothyroid membrane (below the vocal
cords) that allows ventilation of the trachea and bypasses the oropharynx and upper airway.
• The airway can be obtained quickly in emergencies and “cannot intubate, cannot ventilate”
situations. It can be performed by a surgeon, anaesthetist, intensivist, or emergency
physician.
• Techniques:
– Surgical
– Seldinger
– Needle (cannula)
• Indications
– Cannot intubate, cannot ventilate
– Airway obstruction: Foreign body, angioedema
– Massive facial or nasal trauma
– Cervical spine instability causing an inability to adequately ventilate
– Fractured larynx (often from a hanging injury)
– Chemical inhalation injury
• Contraindications
– Inability to indentify landmarks
– Underlying abnormality, such as a tumor
– Tracheal transection
– Due to risk of subglottic stenosis, a needle cricothyroidotomy is preferred in pediatric
patients.
• Advantages of cricothyroidotomy over tracheotomy
– Cricothyroid membrane is more superficial and easier to access than tracheal rings
– Cartilage incision is not necessary
– Less vascular
– Can be performed more rapidly; experienced personnel can perform the procedure within
30 seconds
• Disadvantage
– Not a permanent airway and must be converted to a tracheotomy within 24 hours in the
operating room due to the risk of developing subglottic stenosis
ANATOMY
The cricothyroid membrane lies between the thyroid cartilage superiorly and the cricoid
cartilage inferiorly. Identify the thyroid cartilage with the thumb and index finger and then
move the fingers caudally until a space is felt between the thyroid and cricoid cartilages.
FIGURE 1. Anatomy of the cricothyroid membrane.
• Failure to secure a surgical airway in an emergency or “cannot intubate, cannot ventilate”
situation is most likely due to operator inexperience or a delay in the decision to obtain a
surgical airway.
– The use of training with cadavers improves operator confidence (2).
– The use of simulator training shows improvement in operator skills and placement time
after practicing five times (3).
– The number of practice procedures appears to be more important in determining success
than the technique chosen
– However, one study found that the Seldinger technique resulted in a significantly shorter
time to first ventilation and fewer injuries than with the surgical technique (4).
• Immediate complications include the following:
– Bleeding; although less likely than with tracheostomy placement, it can be significant if a
large neck vein is lacerated.
– Insertion into subcutaneous tissue
– Scalpel injury to the posterior trachea and injury to the esophagus
– Injury to the thyroid, vocal cords, and vessels in the event of wrong landmarks
• Jet ventilation via a needle or cannula cricothyroidotomy has the risk of barotrauma,
pneumothorax, subcutaneous emphysema, and hypercarbia.
• Although emergency airway situations and “cannot intubate, cannot ventilate” situations
can arise at anytime, the majority occur during the induction of anesthesia.
• The anesthesia practitioner must have the ability to quickly recognize when an airway
becomes difficult and formulate a plan for securing a method of ventilation.
• When a “cannot intubate, cannot ventilate” situation arises, the American Society of
Anesthesiologists (ASA) Difficult Airway Algorithm should be followed. Upon failure of an
laryngeal mask airway (LMA) or alternative noninvasive technique to secure the airway, a
surgical cricothyroidotomy should be performed (1). Poor outcome is related to length of
time taken to make the decision to convert to surgical airway and time taken to perform the
technique.
• All techniques include the following:
– Positioning the patient with hyperextension of the head, if possible
– A shoulder roll, if possible
– Palpation of the cricoid and thyroid cartilages.
– Prep of the neck with Betadine, if possible
– Local anesthetic if the patient is conscious
• Surgical technique: Use a number 20 scalpel to make a horizontal or vertical incision
through the skin followed by a horizontal incision through the cricoid membrane. Place a
tracheal hook at the incision site, and apply caudal and outward traction to the cricoid
cartilage. Remove the blade. Place a cuffed tracheal tube or tracheostomy tube and inflate.
Confirm ventilation with end-tidal CO2 (ETCO2) and bilateral breath sounds.
FIGURE 2. Surgical cricothyroidotomy. An incision with a scalpel is made in the skin, followed by a horizontal incision
through the cricothyroid membrane. An endotracheal tube or tracheostomy is inserted.
• Seldinger technique (various kits are available): Stabilize the thyroid cartilage and make a
vertical incision in the skin over the cricothyroid membrane. Insert the 19 g catheter with a
5 cc syringe attached and aspirate for air to confirm entry into the trachea. Secure the
catheter with the non-dominant hand and remove the syringe and needle. Advance the
guidewire through the catheter and then remove the catheter. Feed the dilator and airway
catheter over the wire. Remove the dilator and wire simultaneously. Connect the airway
catheter to an AMBU bag or ventilator and confirm ETCO2 and bilateral breath sounds.
FIGURE 3. Seldinger technique and needle cricothyroidotomy utilize a needle attached to a syringe to identify and access
the airway. The catheter is left in place and the needle and syringe are removed.
FIGURE 4. Seldinger technique. Once the airway has been accessed (as in Figure 3), a guidewire is threaded through the
catheter and the catheter is removed. The dilator with the airway catheter is then inserted over the guidewire and the
guidewire and dilator are removed at the same time.
• Needle (cannula) cricothyroidotomy technique: Performed by placing a needle with a

catheter (such as a large-bore IV) through the cricothyroid membrane. Using a syringe
attached to the needle, aspirate air to confirm that the trachea has been entered. Leave the
catheter in place and remove the needle. To ventilate via the catheter, attach a jet nozzle
and use jet ventilation. When initiating jet ventilation, the starting pressure should be set at
25 psi and increased as needed. The maximum pressure should not exceed 50 psi, if
possible, to provide acceptable ventilation. If jet ventilation is unavailable, remove the
plunger from a 3-mL syringe; attach the syringe to the catheter. Insert the connector of a
size 7.0 endotracheal tube into the syringe, then connect an bag or ventilator. This airway
should be converted to a tracheostomy within 45 minutes, as the risk of hypercarbia is
significant.
REFERENCES
1. ombes X, Jabre P, Amathieu R, et al. Cricothyrotomy in emergency context: Assessment of
a cannot intubate cannot ventilate scenario. Ann Fr Anesth Reanim. 2011;30(2):113–116.
[Epub 2011 Feb 1.]
2. atif R, Chhabra N, Ziegler C, et al. Teaching the surgical airway using fresh cadavers and
confirming placement nonsurgically. J Clin Anesth. 2010;22(8):598–602.
3. Wong DT, Prabhu AJ, Coloma M, et al. What is the minimum training required for
successful cricothyroidotomy? A study in mannequins. Anesthesiology. 2003;98(2):349–353.
4. Schaumann N. Evaluation of Seldinger technique emergency criocothyroidomy versus
standard surgical cricothyroidomy in 200 cadavers. Anesthesiology. 2005;102(1):7–11.
ADDITIONAL READING
• Caplan RA, Benumof JL, Berry FA, et al. Practice guidelines for management of the difficult
airway. An updated report by the American Society of Anesthesiologists Task Force on
Management of the Difficult Airway. Anesthesiology. 2003;98:1269–1277.
• Tracheostomy
• Jet ventilation
CLINICAL PEARLS
• Cricothyroidotomy is an invasive technique used to secure the airway when other methods
of ventilation have failed.
• Successful outcome is related to the time taken to make the decision to perform a surgical
airway and the skill of the provider in performing the procedure.
CROHN’S DISEASE
Andrea Parsons, MD
BASICS
DESCRIPTION
• Inflammatory bowel disease that shows inflammation of any portion of the GI tract from the
mouth to the terminal ileum with rectal sparing. The disease is characterized by slowly
progressive spread with alternating periods of remission and exacerbation.
• Patients present for surgical management of problems related to the disease, such as
intestinal obstruction, perirectal abscesses, bleeding, fistulas, perforation, toxic megacolon,
strictures, and cancers, or for management of nonrelated problems.
EPIDEMIOLOGY
Incidence
• US: 3–14 cases per 100,000 persons (1)
• Bimodal distribution with diagnosis peaking in the teens and 20s and then in the 50–70s (1)
Prevalence
• US: 26–200 per 100,000 persons (2)
• Females have a slightly higher prevalence (2)
• More frequent in people who have a first-order relative with the disease (2).
Morbidity
• There is no cure for Crohn’s disease and patients suffer from flare-ups that can cause
significant discomfort and weight loss.
• If medical therapy is not effective, surgical resection of inflamed bowel is the treatment of
choice.
Mortality
Mortality rate is low, but there is an increased rate of small bowel and colorectal cancers.
• The exact cause is unknown. There is some evidence to suggest that normal intestinal flora
can trigger an aggressive and inappropriate immune reaction in patients with a
multifactorial genetic predisposition. However, no specific environment, dietary, or
infectious causes have been identified (3).
• Carries a genetic predisposition as evidenced by a higher prevalence in familial and twin
studies (3).
PATHOPHYSIOLOGY
• Inflammatory responses result in patchy, cobblestone, transmural inflammation of the GI
tract between the mouth and anus. Conversely, ulcerative colitis is continuous, mucosal
inflammation, mostly in the lower intestine and rectum.
– Cytokines lead to differentiation of lymphocytes to T cells (mainly helper T cells type 1),
leading to immune system activation, inflammatory response, and subsequent damage of
the intestinal mucosa
– Macrophages cause granuloma formation
– Cytokine release includes interleukin-1 (IL-1) which causes diarrhea and acts as a pyrogen.
Other cytokines released include IL-6, IL-8, and tumor necrosis factor-α (TNF-α).
• Electrolyte abnormalities and malnutrition occur secondary to diarrhea and pain.
• Anemia occurs due to blood loss (acute or chronic) and due to malabsorption of iron,
vitamin B12, and folate.
• Secondary peritonitis results from abscess formation that can manifest with abdominal pain.
It can be acute or slow to develop, often dull, and poorly localized initially. This can
progress to severe pain and is treated with antibiotics.
• Diagnosis can be made with a biopsy of affected tissue via endoscopy. Imaging with small
bowel follow-through, CT scan, and MRI can aid in diagnosis.
• Assess the severity of disease, recent exacerbations, intravascular fluid status, and
electrolyte abnormalities, as well as treatment and medication history.
• Anesthetic plan should focus on fluid and electrolyte management, assessment of anemia,
and use of steroids.
SYMPTOMS
Exacerbations consist of diarrhea (increased frequency, fluidity, daily volume of stool),
abdominal bloating, distention, discomfort, cramps particularly after meals, acute pain in the
lower right abdomen, hyperactive bowel sounds, infection, blood in stool (or greasy, foul-
smelling, fatty stool), nausea and vomiting, weight loss, dry mouth.
History
• Acute flare versus chronic condition
• History of anti-inflammatory, antidiarrheal, and antidepressant use
• Severity, especially with regard to fluid and electrolyte status
• Current hyperalimentation therapy
• Diabetes and hypertension from chronic steroid use
Signs/Physical Exam
• Signs of dehydration—decreased skin turgor, decreased capillary refill, decreased urinary
output, tachycardia, hypotension, etc.
• Signs of electrolyte abnormalities—ECG changes, muscle weakness, etc.
• Rectocutaneous fistulas
• Malnutrition and vitamin deficiencies
• Painful lower extremity swelling may indicate deep venous thrombosis (increased risk);
shortness of breath or hypoxia should warrant consideration of a pulmonary embolism.
TREATMENT HISTORY
Surgical resection of affected portions of the intestines
MEDICATIONS
• Maintenance therapy typically includes 5-aminosalicylic acid, steroids, and
immunomodulators for refractory disease (azathioprine, methotrexate, infliximab) (4).
• Exacerbations are commonly treated with 5-aminosalicylic acid, glucocorticoids, and
antibiotics (4)
Labs/Studies
• CBC to assess for anemia and hemoconcentration
• Complete metabolic panel (BUN/Cr ratio of 20:1 may indicate dehydration; low bicarbonate
values may indicate acidosis due to dehydration or infection)
• Coagulation studies if liver disease is present
• EKG may be considered for electrolyte abnormalities or patient specific indications
• Type and screen or type and cross.
Extraintestinal manifestations include:
• Oral lesions: Aphthous stomatitis, canker sores found between the gums and lower lip or
along the sides or base of the tongue.
• Arthritis, including ankylosing spondylitis, can result in reduced flexibility and mobility as
well as joint pain. Metabolic bone disease may also be present.
• Skin disorders range from erythema nodosum (tender, red nodules that appear over the
shins and ankles as well as the arms) to pyoderma gangrenosum to perianal lesions
(enterocutaneous fistulas, abscesses, anal fissures).
• Eye disorders: Episcleritis, uveitis, and dry eyes
• Renal complications include kidney stones and hydronephrosis
• Liver: Jaundice, fluid retention, and primary sclerosing cholangitis
• Significant hypovolemia and/or electrolyte disturbances
• Severe anemia requiring blood transfusion
CLASSIFICATIONS
• Based on severity
– Asymptomatic remission
– Mild to moderate
– Moderate to severe
– Severe fulminant
• Based on the region of bowel affected
– Ileocolitis (involvement of the ileum and colon)
– Regional enteritis (such as ileitis or colitis)
TREATMENT
Premedications
• Stress dose steroids should be considered if the patient has been treated for more than 2
weeks within the past 6–12 months to avoid manifestations of adrenal insufficiency.
Steroids with glucocorticoid and mineralocorticoid activity should be administered (e.g.,
hydrocortisone).
INTRAOPERATIVE CARE
• Depends on type of surgery, patient wishes, and surgeon’s preferences.
• Neuraxial placement may be contraindicated if coagulation studies are abnormal.
• Hyperalimentation is usually continued in the intraoperative period. If stopped,
hypoglycemia may result.
Monitors
• Foley catheter in long cases, patients with suspected hypovolemia, or anticipated large fluid
shifts
• Foley catheter may be indicated for long cases, anticipated large fluid shifts, or hypovolemic
patients.
• Consider central venous catheter with central venous pressure for fluid management, as
appropriate.
• In hypovolemic patients consider adequate preoperative fluid hydration prior to induction.
• Etomidate or ketamine can be useful in hypovolemic patients; have vasopressors available.
• In anemic patients, consider having blood available or transfuse prior to induction.
• To avoid additional oral trauma, perform gentle laryngoscopy and intubation.
• If aphthous ulcers are present, may avoid leaving a bite block in the mouth.
Maintenance
• Muscle relaxation can aid surgical exposure and closure of abdominal fascia for bowel
surgery
• Fluid management: Replace deficits with crystalloid and factor in insensible losses. Patients
are at risk for significant third-spacing and bowel edema, especially due to low colloid
oncotic pressures. This can make closure of abdominal incisions more difficult.
• Low albumin levels due to malnutrition: Adjust medication doses appropriately, particularly
with highly protein-bound drugs. Unbound, free drug is pharmacologically active, and is
also available for metabolism. Thus, consider smaller boluses and more frequent dosing.
Additionally, hypoalbuminemia may result in increased total body water and volume of
distribution.
• Consider avoiding nitrous oxide for bowel surgery as it can cause the bowel to expand and
make fascial closure more difficult.
• Chronic steroid use may result in diabetes; intraoperative glucose management may require
insulin administration.
• Intractable intraoperative hypotension may be due to adrenal insufficiency; treat with stress
dose steroids.
• Eye protection to avoid worsening ocular manifestations
• Skin may be thin or easily breached from long-term steroid use; caution with positioning
and tape for IV sites, endotracheal tube (ETT), and eyes.
Reversal of nondepolarizing muscle relaxants can help minimize weakness as patients often
have underlying weakness due to malnutrition and electrolyte disturbances.
POSTOPERATIVE CARE
BED ACUITY
Telemetry if the patient has severe electrolyte derangements.
• Consider epidural or patient-controlled analgesia (PCA) for postoperative pain control for
large bowel resections or exploratory laparotomies.
• Avoid ketorolac and NSAIDs due to metabolic bone disease.
• Consider postoperative CBC
COMPLICATIONS
Hyperalimentation can result in hypo/hyperglycemia, hyperchloremic metabolic acidosis,
fluid overload, electrolyte abnormalities, renal and hepatic dysfunction
REFERENCES
1. Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: Incidence, prevalence,
and environmental influences. Gastroenterology. 2004;126(6):1504–1517.
2. Kappelman MD, Rifas-Shiman SL, Kleinman K, et al. The prevalence and geographic
distribution of Crohn’s disease and ulcerative colitis in the United States. Clin
Gastroenterol Hepatol. 2007;5(12):1424–1429.
3. Abraham C, Cho JH. Inflammatory bowel disease. N Eng J Med. 2009:361(21):2066–2078.
4. Baumgart DC, Sandborn WJ. Inflammatory bowel disease: Clinical aspects and established
and evolving therapies. The Lancet. 2007;369(9573):1641–1657.
5. National Digestive Diseases Information Clearinghouse Slattery E, Keegan D, Hyland J, et
al. Surgery Crohn’s disease, and the biological era: Has there been an impact? J Clin
Gastroenterol Dec 3 2010, E print.
• Ulcerative colitis
CODES
ICD9
• 555.0 Regional enteritis of small intestine
• 555.1 Regional enteritis of large intestine
• 555.9 Regional enteritis of unspecified site
ICD10
• K50.00 Crohn’s disease of small intestine without complications
• K50.10 Crohn’s disease of large intestine without complications
• K50.90 Crohn’s disease, unspecified, without complications
CLINICAL PEARLS
• Crohn’s disease can cause weakness due to electrolyte abnormalities and malnutrition that
can affect anesthetic management and require special perioperative management.
• Patients often present for colectomy, proctolectomy, wound biopsy, incision/drainage,
irrigation, and debridement; urgent surgery for actual or impending perforation.
CRYOPRECIPITATE
Satoru Ogawa, MD
BASICS
DESCRIPTION
• Cryoprecipitate is a blood product derived from plasma and used for supplying clotting
factors to a volume-sensitive patient.
• Transfusion of cryoprecipitate is mainly indicated for the treatment of congenital defects of:
– Factor VIII (FVIII)
– von Willebrand’s factor (vWF)
– Factor XIII (FXIII)
– Fibrinogen
– Fibronectin
• A cross-matching is not required, but ABO compatibility should be considered before
transfusion.
• Normal coagulation is dependent on several components:
– Fibrinogen is converted to fibrin by thrombin. Fibrin is a polymerized protein that is
involved in clot formation.
– FVIII and vWF mediate adhesion of circulating platelets to exposed subendothelium.
– FXIII promotes clot stability by forming covalent bonds between fibrin monomers and by
cross-linking alpha-2 antiplasmin, fibrinogen, fibronectin, collagen, and other proteins to
enhance the mechanical strength of the fibrin clot and protect the clot from proteolytic
degradation.
• Cryoprecipitate preparation
– A unit of fresh frozen plasma (FFP) is thawed at 1–6°C.
– Supernatant is the precipitated, cold-insoluble material that initially thaws.
– It is resuspended in a small volume of plasma (10–15 mL).
• Freezing
– The resuspended fraction is refrozen at −18°C.
– The time should be minimized from attainin the supernatant and freezing.
• Storage
– Up to 12 months
• Contents (about 15 mL per unit)
– Fibrinogen: ∼350 mg
– FVIII: ∼150 units; increased when the donor has higher baseline levels (e.g., postexercise)
– vWF: ∼150 units
ADAMTS13 (a vWF cleaving protease) is minimal in cryoprecipitate.
– FXIII
• Thawing cryoprecipitate
– Requires ∼45–60 minutes
– After thawing, cryoprecipitate should be administered within 4 hours.
• ABO compatibility
– Not required, but should be considered before transfusion. The plasma used to reconstitute
the cryoprecipitate may contain a small amount of RBCs. Incompatible ABO cells will
likely be cleared without undue consequences and sensitization to Rh is unlikely;
however, with larger volumes, it may become problematic.
• Duration of effect
– Fibrinogen: 70–100 hours
– FVIII: 12 hours
– vWF: 10–24 hours
– FXIII: 120–200 hours
• Special handling
– Administer through a 180–260 μm standard blood tubing.
– Consider mixing with 10–15 mL of normal saline to ensure complete removal of all
material from each bag.
• Complications of cryoprecipitate administration:
– Transfusion-related acute lung injury (TRALI) is caused by anti-HLA antibodies present in
donor plasma. The risk appears to be lower with cryoprecipitate compared to FFP.
– Possible worsening of disseminated intravascular coagulation and organ dysfunction by
forming fibrin in microcirculations.
– Viral transmission. The risks of viral transmission, particularly hepatitis C and human
immunodeficiency virus, have been significantly reduced by the nucleic acid testing of
donor blood.
– Acute hemolytic transfusion reaction, nonhemolytic febrile and allergic reactions, or
thrombosis have been reported; however, their occurrence is rare.
– Venous and arterial thromboembolic complications should be cautioned because
cryoprecipitate rapidly increases plasma fibrinogen, FVIII, FXIII, and vWF.
– Hypocalcemia may result from massive transfusion due to citrate overload.
– Platelet microparticles can play an active role in thrombosis, inflammation, and vascular
reactivity.
• Human-derived fibrinogen is a potential alternative; however, adverse events include
thrombotic complications and anaphylactic reactions.
• Cryoprecipitate rapidly increases plasma levels of fibrinogen, FVIII, FXIII, and vWF, which
collectively exert hemostatic activity. Indications include the following (1):
– Congenital fibrinogen deficiency, von Willebrand’s disease, congenital FXIII deficiency for
prevention (perioperative and peripartum), as well as treatment of bleeding. When
possible, however, hereditary deficiencies of FVIII, FXIII, and vWF should be managed
with virally inactivated human-derived products or recombinant products.
– Massive transfusion with microvascular bleeding and fibrinogen <80–100 mg/dL. If
fibrinogen measurement cannot be performed in a timely manner, clinical decision-
making may warrant administration of cryoprecipitate (2).
– Hemorrhage after cardiac surgery if fibrinogen level is below 150 mg/dL.
– Hemorrhage secondary to thrombolytic therapy
– Management of bleeding due to snake venom
– Iatrogenic premature rupture of amniotic membranes
– Amniotic fluid embolism
– Uremia; prevention and treatment of bleeding
– Fibronectin deficiency after major surgery, trauma, burns, and sepsis. Deficiency impairs
the reticuloendothelial system from clearing particulate debris in the circulation resulting
in the accumulation of fibrin microaggregates, collagenous debris, and immune
complexes.
– Topical use as in fibrin glue (virally inactivated human-derived fibrin sealant products are
preferred)
• Cryoprecipitate has the benefit of causing less hemodilution and thrombocytopenia after
infusion compared to FFP.
See Table
• Large amounts of shed blood processed in the cell salvage system can deplete plasma
fractions including fibrinogen.
• Fibrinogen measurements by the Clauss method may be falsely elevated after large amounts
of hydroxyethylstarch infusion.
• Thromboelastography/metry can be used to guide fibrinogen replacement (3).
EQUATIONS
For fibrinogen replacement therapy, one unit of cryoprecipitate per 10 kg body weight
increases plasma fibrinogen by ∼50 mg/dL in the absence of continued consumption or
massive bleeding. To increase it to 100 mg/dL, the required number of cryoprecipitate is 0.2
x weight (kg).
REFERENCES
1. ’Shaughnessy DF, Atterbury C, Bolton Maggs P, et al. Guidelines for the use of fresh-frozen
plasma, cryoprecipitate, and cryosupernatant. Br J Haematol. 2004;126:11–28.
2. Hiippala ST, Myllylä GJ, Vahtera EM. Hemostatic factors and replacement of major blood
loss with plasma-poor red cell concentrates. Anesth Analg. 1995;81:360–365.
3. Tanaka KA, Ogawa S, Bolliger D. A primer for clinical use of rotational
thromboelastometry. Point of Care. 2012;11:77–84.
• Fibrinogen
• Fresh frozen plasma (FFP)
• Transfusion-related lung injury (TRALI)
• Blood transfusion infection
CLINICAL PEARLS
• Fibrinogen replacement with cryoprecipitate is preferred to FFP because of a lower volume
of transfusion, and lower incidence of TRALI.
• Compared to purified human fibrinogen, cryoprecipitate provides clinically relevant
amounts of FXIII.
• Assuming normal fibrinogen level at baseline, a critical level (1 g/L) of fibrinogen is reached
after a loss of about 1.4 times the blood volume.
• For hereditary deficiency of FVIII, FXIII, or vWF, plasma-derived or recombinant factor
concentrate is available and is preferred to cryoprecipitate for improved safety.
CRYSTALLOIDS
Trent Emerick, MD
James Cain, MD
BASICS
DESCRIPTION
• Crystalloids are solutions of water, electrolytes, and other nonprotein solutes. They are
administered for volume replacement and expansion, electrolyte replacement, as a
medication carrier, and for dilution of blood products during transfusion to decrease
viscosity.
• Benefits include: Inexpensive, easy to store, long shelf–life, readily available, few adverse
actions, available in a variety of formulations, do not require special compatibility testing,
and there are no religious objections to their use.
• Crystalloids may be classified as hypertonic, isotonic, or hypotonic with respect to plasma
osmolarity; some may also be described as “balanced” or “physiological” solutions with
regard to their chloride concentration relative to plasma; unbalanced fluids have a
proportionally high chloride concentration.
• Average 70 kg man has 42 L of total body water (TBW). The intracellular volume has 28 L
(67% of TBW); the interstitial volume has 10.5 L (25% of TBW); and the intravascular
volume has 3.5 L (8% of TBW).
• Electrolyte solutions distribute through these spaces; ∼1/3rd to 1/4th will remain in the
intravascular space following isotonic administration.
• Normal saline (0.9% NaCl); “unbalanced” solution
– Sodium 154 mEq/L; greater than plasma
– Chloride 154 mEq/L; significantly greater than plasma
– Osmolarity 308 mEq/L; slightly greater than serum osmolarity (∼285 mOsm/L).
• Lactated Ringer’s; “balanced” solution. pH 6.5
– Sodium 130 mEq/L; less than plasma
– Chloride 109 mEq/L; slightly greater than plasma
– Potassium 4 mEq/L; similar to plasma
– Calcium 3 mEq/L; similar to plasma
– Lactate 28 mEq/L; hepatically metabolized to glycogen that is then oxidatively
metabolized to CO2 and H2O. The CO2 accepts a hydrogen ion (H+) to yield bicarbonate.
Thus, lactate functions as an alternative source of bicarbonate. However, because the
conversion takes ∼1–2 hours, depending on the integrity of cellular oxidative processes, it
is a less effective source of bicarbonate in lactic acidosis, shock, or decreased perfusion
states.
– Osmolarity: 275 mOsm/L; slightly less than plasma, hence hypotonic
• Normosol; “balanced.” pH 7.4
– Sodium 140 mEq/L; similar to plasma
– Chloride 98 mEq/L; similar to plasma
– Potassium 5 mEq/L; slightly greater than plasma
– Magnesium 3 mEq/L; Mg++ is the second most plentiful cation of intracellular fluid and
plays an important role as a cofactor for enzymatic reactions and in neurochemical
transmission and muscular excitability.
– Acetate 27 mEq/L; CH3COO− is metabolized in the liver (even in severe disease) to
become a source of H+ acceptors. Thus, it is an alternate source of bicarbonate.
– Gluconate 23 mEq/L; a theoretical alternate metabolic source of bicarbonate ion.
However, a significant antiacidotic action has not been established. Thus, the gluconate
anion serves primarily to complete the cation–anion balance of the solution.
– Osmolarity 295 mOsm/L; greater than plasma
• Plasmalyte; “balanced” solution
– Sodium 140 mEq/L; similar to plasma
– Chloride 98 mEq/L; similar to plasma
– Potassium 5 mEq/L; slightly greater than plasma
– Magnesium 3 mEq/L
– Acetate 27 mEq/L; serves as a bicarbonate alternative or precursor
– Gluconate 23 mEq/L; a theoretical alternative to bicarbonate
– Osmolarity 294 mOsm/L; slightly greater than plasma
• Hypertonic saline 3%; pH 4.5–7
– Sodium 513 mEq/L
– Chloride 513 mEq/L
– Osmolarity 1,027 mOsm/L; the hypertonicity creates an osmotic gradient for fluid to shift
from the intracellular to interstitial and intravascular space, resulting in an increase in
preload. It can also cause vasodilation from direct vascular smooth muscle relaxation with
resultant improvement in capillary blood flow. Furthermore, hypertonicity can decrease
endothelial cell volume (intracellular to extracellular flow) that increases capillary
diameter and decreases vascular resistance.
• Dextrose 5% in water; D5W. pH 4.5
– Dextrose 50 g/L; promotes glycogen deposition and decreases or prevents ketosis if
sufficient doses are provided.
– Osmolarity “inactive;” glucose is metabolized as an energy source and there is no sodium.
Thus, the net effect is equivalent to giving pure water that is distributed throughout TBW
with each compartment receiving fluid in proportion to TBW. A large percentage moves
intracellularly.
ANATOMY
• Plasma electrolytes pass freely between the intravascular space and interstitial fluid. Plasma
proteins are restricted to the intravascular space. Because of its abundance, sodium is the
most important osmolar force in the interstitial space. Potassium and intracellular proteins
are the most important oncotic forces in the intracellular space.
• The renin-angiotensin system affects cardiac output, BP, and fluid status. It is activated by
decreased BP in the renal artery, decreased plasma sodium levels at the macula densa,
and/or the surgical stress response.
• Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are proteins released by
the cardiac atria and ventricles, respectively, when the chamber walls are distended due to
increased volume and pressure. These peptides increase the glomerular filtration rate (GFR),
sodium excretion, and water excretion. BNP is also utilized as a marker for congestive heart
failure.
• Sympathetic nervous system fibers exit the spinal cord at the T1–L2 level. Neuraxial
blockade induced sympathectomy occurs when T1–L2 fibers are blocked causing peripheral
dilation and hypotension. Fluid is commonly administered for this perturbation.
• A neuraxial block affecting T1–T4 fibers affects the cardioaccelerator fibers and blunts the
tachycardic response to hypotension. Fluid is commonly administered for this perturbation.
• Normal saline
– Nongap hyperchloremic metabolic acidosis; previously believed to be secondary to
“dilutional acidosis.” NaCl dissolves into NaOH and HCl in plasma. The 154 mEq/L of
chloride found in normal saline is much greater than that of plasma (100 mEq/L). This
results in more hydrochloric acid as compared to sodium hydroxide and causes acidosis
(1)[C]. NaCl + H2O ←→→ HCl + NaOH. Additionally, normal saline lacks a buffering
salt such as lactate or acetate and bicarbonate is eliminated renally to maintain electrical
neutrality.
• Lactated Ringer’s
– In acidotic and anoxic states, lactate metabolism is affected.
– Hyperkalemia can be worsened
– Cannot be administered with blood products; calcium in solution can clot blood products.
– Respiratory acidosis from carbon dioxide production can occur.
– Mild hyponatremia
– May be associated with panic attacks secondary to the complexing of calcium, despite the
absence of serum levels or symptoms of hypocalcemia.
• Normosol and Plasmalyte
– Hyperkalemia can be worsened
– Cautious use with metabolic or respiratory alkalosis; the bicarbonate alternatives, acetate
and gluconate, can exacerbate
– Severe hepatic insufficiency may preclude the conversion of acetate and gluconate.
– Dilutional hyponatremia
• D5W can cause hyperglycemia and hypotonicity. Hypotonicity can affect intracellular
volume and cause cell lysis.
• Hypertonic saline
– Central myelinolysis can result from the rapid increase in sodium. May be avoided by
limiting sodium increases to a maximum rate of 0.5 mEq/L/hour, not to exceed 10–12
mEq/L in 24 hours.
– Renal insufficiency and failure are seen with a higher incidence than with other
crystalloids.
– Hemorrhage secondary to excessive fluid resuscitation
– Decreases in afterload can result; transient hypotension can be seen after boluses are
administered.
– Dilution of plasma constituents (coagulation factors) can occur with rapid intravascular
volume expansion.
– Hypokalemia or hyperchloremic acidosis
– Rebound increases in ICP after boluses or when continuous infusions are stopped.
– Phlebitis or tissue necrosis can result from hypertonicity; central lines are preferable.
• Anesthesia blunts the normal sympathetic tone and physiologic response to hypovolemia.
• Transurethral resection of the prostate (TURP) syndrome refers to hypotonic hypervolemic
hyponatremia due to absorption of the free water surgical field irrigant during a TURP
procedure. This can lead to sodium levels <125 mEq/L and symptoms of hyponatremia
(neurologic symptoms, including seizures, confusion, lethargy) (2)[A].
• Overly aggressive fluid replacement can lead to the development of pulmonary edema and
impaired oxygen/carbon dioxide exchange, particularly in patients with compromised
cardiac performance such as neonates and the elderly.
• Crystalloid versus colloid resuscitation: Crystalloids are significantly less expensive.
Resuscitation requiring volume replacement does not show a benefit of colloids over
crystalloids (3)[A].
• SAFE study: Prospective randomized controlled trial comparing colloids versus crystalloids
for fluid resuscitation in critical care patients: No significant difference is found in clinical
outcome between colloid and crystalloid groups (4)[A].
• Normal saline. Hyperchloremic acidosis has been shown to decrease mucosal perfusion,
profoundly affect eicosanoid release in renal tissue that leads to vasoconstriction and
decreased GFR, inactivate membrane calcium channels, and inhibit norepinephrine release
from sympathetic nerve fibers resulting in redistribution of cardiac output away from
internal organs. Attempts to correct this abnormality may actually be the main adverse
effect. Acidosis is often seen as a reflection of poor organ perfusion or poor myocardial
function. A negative base excess may prompt more saline boluses containing fluids that
exacerbate acidosis, the use of blood products, escalation of inotropic support, and initiation
of ventilator support. Furthermore, when coupled with acidosis from a different source (e.g.,
lactic acidosis from tissue hypoperfusion) this can further complicate the management of
patient care.
• Hypertonic saline. May be useful in cerebral edema, burn injuries, or trauma; outcome
studies are currently underway.
– Cerebral edema. Increased osmolarity can draw fluid from brain cells into the
intravascular space; this results in decreased cerebral water content, edema formation,
and ICP. Increased intravascular volume may lead to an autoregulatory decrease in
intracerebral blood volume (assuming autoregulation remains intact). Studies have
demonstrated improved survival in traumatic brain injury.
– Burn injuries. The physiochemical interaction with glycocalyx may result in a less “leaky”
vascular endothelium. Studies have shown that severe burns have a decreased incidence
of abdominal compartment syndrome, possibly from decreased capillary leak (less bowel
wall and intra-abdominal fluid accumulation)
– Trauma. Can increase BP with small volume resuscitation and may increase survival. This
is attributed to the avoidance of hemodilution seen with excess amounts of isotonic fluids,
hypothermia, acidosis, coagulopathy, and sustained hyperosmolar state.
EQUATIONS
• Plasma osmolarity (mOsm/L) = ([Na+] × 2) + (BUN/2.8) + (glucose/18) where BUN and
glucose are mg/dL (normal plasma osmolarity ∼285 mg/dL)
• Maintenance fluids can be administered using the 4-2-1 rule: 4 mL/kg/hr for first 10 kg, 2
mL/kg/hr for next 10 kg, and 1 mL/kg/hr for each kg above 20 kg.
• Fluid deficit calculations. Initial fluid deficit due to NPO status: Number of hours NPO ×
maintenance rate, administer ½ during the first hour of procedure, 1/4 during the second
hour, and 1/4 during the third hour. Third spacing/evaporative surgical field losses should
be corrected at 0–10 mL/kg/hr depending on the degree of tissue exposure (e.g., 2–4
mL/kg/hr for open cholecystectomy and 4–8 mL/kg/hr for bowel resection). Replace blood
loss with crystalloid fluid in a 1:4 ratio until transfusion of blood products is indicated.
• Free water deficit (useful with hypernatremia) = 0.6 × (weight in kg) × ([serum
sodium/140]–1). Can replace deficit over 2–3 days with free water enterally, or with
isotonic/hypotonic solutions intravenously.
REFERENCES
1. Kellum JA. Saline-induced hyperchloremic metabolic acidosis. Crit Care Med.
2002;30(1):259–261.
2. Gravenstein D. Review article: Transurethral resection of the prostate (TURP) syndrome: A
review of the pathophysiology and management. Anesth Analg. 1997;84(2):438–446.
3. Hartog C, et al. Review article: The efficacy and safety of colloid resuscitation in the
critically Ill. Anesth Analg. 2011;112:156–164.
4. SAFE study: A comparison of albumin and saline for fluid resuscitation in the intensive care
unit. N Engl J Med. 2004;350:2247–2256.
ADDITIONAL READING
• Chappell D, et al. A rational approach to perioperative fluid management. Anesthesiology.
2008;109:723–740.
• McGee S, Abernethy WB 3rd, Simel DL. The rational clinical examination. Is this patient
hypovolemic? JAMA. 1999;281(11):1022–1029.
• Shafiee MA, Bohn D, Hoorn EJ, et al. How to select optimal maintenance intravenous fluid
therapy. QJM. 2003;96(8):601–610.
• Colloids
• Plasma osmolarity
• TURP syndrome
CLINICAL PEARLS
• Lactated Ringer’s solution should not be used as diluents for packed red blood cells because
the calcium in this fluid can bind to the citrated anticoagulant in the packed cells, inactivate
the anticoagulant, and promote clot formation in the donor cells.
• Lactated Ringer’s solution and Plasmalyte contain potassium and should not be used in
patients with hyperkalemia or in patients at risk of hyperkalemia such as in renal failure.
CUSHING’S REFLEX
Steve Wang, MD
BASICS
DESCRIPTION
• Rapid increases in intracranial pressure (ICP) can lead to a central nervous compensatory
response which results in an increase in sympathetic tone and hypertension, with a reflexive
bradycardia and irregular respirations.
• The brain utilizes ∼20% of the total body oxygen consumption. Oxygen is required for the
maintenance of depolarization and repolarization activity necessary for executive function,
autonomic processes, and reflexes; as well as for cell homeostasis.
– Cerebral blood flow (CBF) is ∼45–55 mL/100 g/minute.
– Cerebral metabolic rate is ∼3–3.5 mL/100 g/minute and describes the amount of oxygen
utilized.
– No oxygen or glucose storage is present and a continual, adequate supply is necessary to
provide adequate function.
– Cerebral autoregulation serves to maintain a constant flow of blood (and constant supply
of oxygen and glucose) within a range of mean arterial pressures.
ANATOMY
The constituents of the cranium include the following:
• Brain tissue
• Cerebrospinal fluid (CSF)
• Blood
• The cranium is a rigid structure that contains a fixed volume of brain tissue, blood, and CSF.
Initially, an increase in the volume in one of the constituents is compensated by a decrease
in another; this serves to avoid elevations in ICP. This compensatory response is limited,
however; beyond a certain point, small changes in volume can result in significant increases
in pressure.
• Increases in cranial volume can result from
– Brain tissue: Tumor, edema (ischemic stroke, cerebral contusion), trauma (epidural
hematoma, subdural hematoma, cerebral contusion), pseudomotor cerebri
– CSF: Hydrocephalus
– Blood: Hypoxia, hypercarbia, obstruction of venous return from head position, Valsalva
maneuvers or increased intrathoracic pressures (coughing, gagging, excessive PEEP),
seizures, severe hypertension, hypotension (vasodilation to maintain cerebral blood flow
can increase cerebral blood volume)
• Abrupt or excessive increases in intracranial volume can cause increased ICP with resultant
decreases in the cerebral perfusion pressure (CPP). CPP = MAP–ICP. A decrease in the CPP
can impair oxygenation and delivery of substrate.
– A CPP <15 mm Hg always results in a Cushing’s reflex.
– A CPP between 15 and 30 mm Hg typically results in its occurrence.
– A CPP between 30 and 45 mm Hg almost never results in its occurrence.
• Reflex bradycardia. Increased BP stimulates the carotid sinus, a baroreceptor within the
carotid arteries, resulting in a reflexive bradycardia.
• Other
– Pressure exerted on the medulla of the brainstem may cause irregular respirations.
– Cardiac output initially increases in its attempt to restore cerebral perfusion pressure.
• The manifestation of these signs suggests the presence of cerebral ischemia from increased
ICP and impending brain herniation, which can be fatal.
• Immediate medical/surgical attention is warranted to re-establish cerebral blood flow.
– Intubation with hyperventilation to a PaCO2 of 30–35 mm Hg. Decreases in PaCO2
alkalinize the CSF and cause cerebral vasoconstriction. Although the effect is limited (11–
20 hours), it is one of the fastest techniques to reduce ICP. Avoid excessive
hyperventilation (PaCO2 <25 mm Hg), as it can contribute to cerebral ischemia.
– Elevation of the head of the bed facilitates cerebral venous drainage to the right atrium
– Propofol decreases CBF and CMR
– Mannitol 0.25–1.0 g/kg can decrease the ICP within 1–5 minutes (peak effect 20–60
minutes, duration up to 6 hours). It is a hyperosmolar agent that draws water from
neurons across the blood brain barrier into the intravascular space. The effect is a
reduction in intracranial volume, and hence ICP.
– Hypertonic saline, similarly, creates an osmotic gradient for intracerebral fluid to shift
intravascularly. Additionally, it may be used in hypotensive and hypovolemic patients to
expand intravascular volume.
– CSF drainage is a quick and reliable method to lower the ICP. A ventriculostomy has the
advantage of being therapeutic and diagnostic.
– Craniotomy to remove the inciting cause. Medical management should be aggressively
continued en route to the operating room.
• Cushing’s reflex is a compensatory response to offset impaired cerebral perfusion pressure.
Cushing’s triad consists of
– Hypertension. Systolic BP is primarily increased and widens the pulse pressure.
– Bradycardia. A “late” reflex. Often, tachycardia may first be observed from the initial
sympathetic response (2).
– Irregular respirations. Under general anesthesia or with an intubated and mechanically
ventilated patient, this may not manifest or be obvious.
• The use of total intravenous anesthesia (TIVA) may make the detection of a relative
bradycardia more difficult to detect.
EQUATIONS
CPP = MAP – ICP, where CPP is cerebral perfusion pressure, MAP is mean arterial pressure,
and ICP is intracranial pressure.
REFERENCES
1. yling J. Managing head injuries. Emerg Med Serv. 2002;8:42.
2. Kalmar AF, Van Aken J, Caemaert J, et al. Value of Cushing reflex as warning sign for
brain ischemia during neuroendoscopy. Br J Anaesth. 2005;94(6):791–799.
3. Molnar C, Nemes C, Szabo S, et al. Harvey Cushing, a pioneer of neuroanesthesia. J Anesth.
2008;22(4):483–486.
4. Hwang Wan W, Ti Ang B. The Cushing response: A case for its role as a physiological
reflex. J Clin Neurosci. 2008;15(3):223–228.
ADDITIONAL READING
• Kosieradzki M, Rowinski W. Ischemia/reperfusion injury in kidney transplantation:
Mechanisms and prevention. Transplant Proc. 2008;40(10):3279–3288.
CLINICAL PEARLS
• Marked increases in intracranial volume may lead to an increase in ICP; this can
compromise cerebral blood flow and cause cerebral ischemia.
• The Cushing’s reflex is the activation of sympathetic tone elicited by the increase in ICP in
an effort to restore cerebral perfusion. Thus, it is also an indicator of severe intracranial
ischemia and suggests impending brain herniation. Identification of the Cushing’s reflex by
its signs warrants immediate medical/surgical intervention; death can ensue within minutes.
• Studies have suggested, however, that hypertension and tachycardia can offer an earlier and
more reliable warning sign of increased ICP (2).
• With sustained moderate increases in ICP, the decreased CPP leads to the development of
plateau waves on ICP monitors. When the Cushing’s reflex is activated, it abolishes the
plateau waves by increasing CPP.
CUSHING’S SYNDROME
BASICS
DESCRIPTION
• Cushing’s disease refers specifically to hypercortisolism caused by adrenocorticotropic
hormone (ACTH)-secreting pituitary tumors, usually microadenomas
• Cushing’s syndrome, however, is the constellation of symptoms resulting from high levels of
circulating cortisol in the body; it refers to hypercortisolism from all causes. The syndrome
was first described in 1912 by Dr. Harvey Cushing.
• Patients with Cushing’s syndrome commonly present to the operating room for corrective
surgery to remove pituitary tumors, lung tumors, adrenal tumors or adrenalectomies, or
may present for surgical procedures unrelated to the syndrome.
EPIDEMIOLOGY
Incidence
• In the US, it is estimated that 10–15 per million people per year will develop Cushing’s
syndrome.
• Another study (2) estimated the incidence of cushing’s disease as only 2.4 per million and
noted that there was an increase between 1975 and 1992.
Prevalence
• 39.1 per million inhabitants.
• Gender: More common in females than males (15:1)
• Age: commonly between 25 and 40 years
Morbidity
• Cushing’s syndrome predisposes to high rates of cardiovascular disease and hypertension,
even after a surgical “cure.”
• Other complications include osteopenia, impaired reproductive and sexual function,
diabetes, depression, and skeletal muscle wasting.
Mortality
• There is a four-fold higher mortality rate than age- or gender-matched cohorts (2).
• Once an adrenal adenoma is removed, the cure rate is 100%; however, most patients with
adrenal carcinoma die within 2 years of diagnosis.
• Chronic exogenous corticosteroid therapy
• ACTH oversecretion from tumor-related syndromes is responsible for 80–85% of cases. They
most commonly result from pituitary adenomas (Conn’s syndrome) but can also be seen
with oat cell lung cancers or other ACTH or corticotrophin-releasing hormone (CRH)
producing tumors.
• ACTH-independent tumors are responsible for 15–20% of cases and may be from unilateral
or bilateral adrenal adenoma or carcinoma.
PATHOPHYSIOLOGY
• CRH release is triggered by stressors such as fever, surgery, burns, exercise, psychological
stress, and hypotension. CRH, stimulates ACTH release from the pituitary gland into the
bloodstream; in turn, ACTH stimulates cortisol release by the adrenal glands.
• Cortisol has a normal diurnal variation, highest from 5 to 9 am and lowest from 6 pm to
midnight.
• Cortisol affects gluconeogenesis as well as fat and protein metabolism; suppresses the
immune system; increases myocardial contractility and output; and enhances the
catecholamine pressor effect.
• Abnormally elevated cortisol levels can cause (1)
– BP elevation from deoxycorticosterone and increased vascular sensitivity to circulating
vasopressors.
– Vascular disease; prolonged hypertension may lead to vascular functional abnormalities.
– Increased gastric acid secretion via increased pepsin levels.
– Decreased collagen synthesis
– Osteoporosis; inhibits osteoblast function and intestinal calcium absorption.
– Hyperglycemia; increases glycogen synthase that increases hepatic glucose output and also
decreases insulin sensitivity.
– Hypokalemia can result from potassium wasting secondary to the triggering of a
mineralocorticoid response in the kidneys.
– Water retention from an increase in mineralocorticoids.
– Muscle weakness; induces catabolic changes in muscle and decreases muscle protein
synthesis as well as type II muscle fibers.
– Hypercoagulability may be partially due to alterations of von Willebrand factor and
hyperresponsiveness of platelets (3).
– Immune suppression: may cause leukocytopenia and can inhibit the
immune/inflammatory response to injury.
• Assess for concomitant diseases including diabetes mellitus and cardiac or vascular disease
(4).
• Difficulty with ventilation or intubation may be encountered; perform a careful airway exam
(4).
• In patients with Cushing’s syndrome from exogenous steroid use, evaluate the underlying
disease for anesthetic implications (e.g., cervical spine instability in patients with
rheumatoid arthritis, electrolyte imbalances and dehydration in Crohn’s and ulcerative
colitis, etc).
• Perioperative thrombus risk is increased due to hypercoagulability.
SYMPTOMS
• Frequent infections due to a relatively immunocompromised state (high levels of cortisol
and elevated blood sugar)
• Edema due to sodium and water retention
• Rapid onset of weight gain
History
• If secondary to chronic steroid use, determine the indication and status of the comorbidities
(e.g., systemic lupus, etc)
• Chronic or repeated steroids may be used in the treatment of some chronic pain conditions.
Signs/Physical Exam
• Facial adiposity (moon facies), darkened skin with purple striae, acne, cervicodorsal fat
deposits (buffalo hump), hirsutism, edema
• Elevated blood glucose
• Muscle weakness
• Hypertension
TREATMENT HISTORY
“Stress dose” steroids may be necessary in patients undergoing surgery and who have been on
chronic steroid therapy.
MEDICATIONS
• Patients with Cushing’s syndrome are often on medications to inhibit adrenal steroid
production (4).
• Ketoconazole: Midazolam levels and effects may be increased; fentanyl levels may be
increased and result in delayed emergence or other adverse effects; and lidocaine systemic
levels may be increased.
• Metyrapone: Not as frequently used in the US but is quite common elsewhere. May cause
edema and neurologic side effects.
• Mitotane: The effects of benzodiazepines, opioids, and inhaled anesthetics may be
potentiated; can result in increased CNS depression or other side effects.
• Bromocriptine: Can inhibit ACTH release. When combined with phenylephrine or other
sympathomimetics may cause hypertension, ventricular tachyarrhythmias, or seizures.
Labs/Studies
• Blood glucose
• Basic Metabolic Profile to evaluate for hypokalemia
• EKG
• If lung cancer is the underlying etiology of Cushing’s, a chest x-ray/CT should be reviewed
to evaluate thoracic and airway anatomy.
• Diagnosing Cushing’s syndrome in pregnancy is difficult because of the natural changes in
the hypothalamic-pituitary-adrenal axis that occur with pregnancy.
• Pregnancy also can commonly result in weight gain, edema, possibly hypertension, or
elevation of blood glucose.
• Vascular and cardiac disease
• Hypertension
• Hypercoagulability
• Uncontrolled hyperglycemia
• Abnormal EKG that may require further cardiac workup
• Hypertensive crisis
• Severe hypokalemia
TREATMENT
Premedications
• Benzodiazepines and opioids may be potentiated by home medications.
• Perioperative antacids/H2 blockers should be considered.
• DVT prophylaxis should be considered.
• If risk factor for a difficult airway are present, a thorough discussion of airway management
options and risks, including an awake, fiberoptic intubation, and possible emergent
tracheostomy should take place
• Patients with significant muscle weakness should be informed of the risk of prolonged
postoperative intubation/ventilation.
INTRAOPERATIVE CARE
• General or regional anesthetic techniques are both considered
• General endotracheal anesthesia is required for hypophysectomy or adrenalectomy surgeries
• Since many patients will be on anticoagulants for DVT prophylaxis, neuraxial anesthesia
may be contraindicated.
Monitors
• Neuromuscular twitch monitoring if muscle relaxants are used.
• Additional intraoperative monitors are chosen based on the patient’s cardiovascular and
other comorbidities as well as the expected extent or type of surgery being performed.
• If there are no signs of a potentially difficult airway, a standard of rapid sequence induction
and intubation are appropriate.
• If a difficult airway is suspected, consider an awake fiberoptic intubation, indirect video
laryngoscopy, or other method as an initial attempt.
Maintenance
• Great care must be taken when positioning patients with osteoporosis as fractures may
occur.
• Doses of muscle relaxants should be decreased in patients with muscle weakness.
• Even if muscle relaxants are not used, mechanical ventilation may be recommended due to
the possibility of muscle weakness and inadequate ventilation.
• Ensure adequate respiratory muscle strength prior to extubation by assessing tidal volumes
and/or NIF
• Delayed emergence, hypotension, and confusion may be signs of steroid deficiency or
Addisonian crisis after removal of an ACTH-secreting tumor.
• Delayed emergence may also be caused by potentiation of opioids or benzodiazepines due to
the patient’s home medications.
POSTOPERATIVE CARE
BED ACUITY
Telemetry or intensive care unit (ICU) for adrenal gland removal may be considered
depending on blood loss, intraoperative events, or other comorbidities.
• Close monitoring of BP and blood glucose are recommended.
• If surgery is for removal of a pituitary adenoma, postoperative steroid replacement must be
given for 3–14 months after surgery or until endogenous steroid synthesis normalizes.
• Endocrinology consult may be warranted for evaluation and treatment postoperatively.
COMPLICATIONS
• Hypercortisolism causes hypercoagulability and DVT risk is higher in patients with
Cushing’s syndrome (4).
• Diabetes insipidus is a possible complication of pituitary resection.
• New neurological deficits or pituitary hormonal insufficiency are possible.
• Postoperative mortality from pituitary surgery may reach 2% (4).
REFERENCES
1. Arnaldi A, et al. Diagnosis and complications of Cushing’s syndrome: A consensus
statement. J Clin Endocrinol Metab. 2003;88(12):5593–5602.
2. Etxabe J, Vasquez JA. Morbidity and mortality in Cushing’s disease: An epidemiological
approach. J Clin Endocrinol. 1994;40:479–484.
3. Casonato A, et al. Abnormalities of von Willebrand factor are also part of the
prothrombotic state of Cushing’s syndrome. Blood Coag Fibrinolysis. 1999;10:145–151.
4. Utz A, et al. Pituitary surgery and postoperative management in Cushing’s disease.
Endocrinol Metab Clin N Am. 2005;34:459–478.
ADDITIONAL READING
• Melmed S. ed. Williams Textbook of Endocrinology, 12th edition. Philadelphia: Elsevier Inc.
2011. Chapter 15.
• Hypokalemia
• Cortisol
• Hypertension
CODES
ICD9
255.0 Cushing’s syndrome
ICD10
E24.9 Cushing’s syndrome, unspecified
CLINICAL PEARLS
• Hypercortisolism can lead to multiple comorbid conditions with increased anesthetic risk
(e.g., vascular disease, coronary disease, diabetes).
• Be vigilant for signs of hypoadrenalism and steroid withdrawal in the immediate
postoperative period after adrenalectomy or partial hypophysectomy
• When performing adrenal carcinoma resection, ensure there is no pneumothorax prior to
closure of the wound. This is a common complication, approaching 20% incidence.
CYANIDE POISONING
BASICS
DESCRIPTION
• Cyanide is a highly volatile liquid that has, in the past, been utilized as a chemical warfare
agent. Today, it presents most commonly from fire smoke or nitroprusside administration.
• Cyanide is a mitochondrial toxin that inhibits the activity of mitochondrial cytochrome
oxidase, an enzyme necessary for normal cell respiration. As a result, it prevents cells from
extracting and using oxygen from arterial blood.
• Clinical manifestations and laboratory findings stem from an inability to utilize oxygen
despite its presence or availability: “Starvation among plenty.”
• Toxicity ranges from extremely rapid, with death occurring within minutes, to hours
depending on the amount, route of exposure, and the length of time a person is exposed.
EPIDEMIOLOGY
Incidence
Estimates vary widely due to concurrent carbon monoxide poisoning.
Morbidity/Mortality
No clear data
• Smoke inhalation from fire is the most common cause of cyanide poisoning in developed
countries. Hydrogen cyanide is produced from combustion of carbon-based and nitrogen-
based materials; high concentrations are produced with plastic, polymer, synthetic fiber,
wool, and silk substrates. Toxic and/or lethal concentrations are found in the blood in most
fire victims.
• Sodium nitroprusside (SNP) use; although newer drugs with safer profiles have reduced its
use today, the ability to easily titrate to desired effect (quick onset and offset) make it an
attractive option in certain cases. The risk of cyanide toxicity from SNP is increased with
hypoalbuminemia, cardiopulmonary bypass procedures, and moderate-to-high doses.
• Industrial exposure through metal extraction in mining, photography, electroplating in
jewelry, plastics, and rubber manufacturing increases cyanide exposure.
• Suicide or homicide attempts
• Food like bitter almonds, peaches, pears, apples, and apricots are also responsible for
cyanide poisoning.
• Cyanide toxicity hinders aerobic respiration by inhibiting the final enzyme in the electron
transport chain (ETC), known as cytochrome c oxidase.
• Normally, the ETC couples a reaction between an electron donor (NADH) and an electron
acceptor (oxygen). The ETC is located in the mitochondrial inner membrane, and as the
electron passes down the chain it generates a proton gradient and potential energy across
the mitochondrial membrane. The potential energy is harnessed when the protons flow back
across the membrane via adenosine triphosphate (ATP) synthase (down their gradient): ADP
+ H+ →ATP.
• Normally, oxygen serves as the terminal electron acceptor at cytochrome c oxidase. In this
manner, aerobic respiration is capable of producing 36 ATP from a single glucose molecule.
• Cyanide molecules inhibit cytochrome c oxidase from reducing oxygen; it binds more tightly
than oxygen to the ferric ion (Fe3+) binding spot. In doing so, it hinders the ETC, and hence
oxidative phosphorylation.
• Cells resort to anaerobic respiration (without oxygen); it is less efficient and produces only 2
ATP molecules in addition to lactic acid.
• “Starvation among plenty.” Despite an ample oxygen supply, cells become hypoxic because
they are incapable of utilizing the oxygen.
• Additionally, cyanide also nonspecifically inhibits antioxidants (catalase, glutathione
reductase, superoxide dismutase); this results in the accumulation of toxic oxygen-free
radicals. Furthermore, it causes the release of glutamate and inhibits the enzyme glutamic
acid decarboxylase (GAD), the enzyme responsible for the formation of GABA (thus reduces
the seizure threshold).
• SNP binds to the Fe3+ moiety in oxyhemoglobin to yield methemoglobin and SNP- . SNP- is
a reduced and unstable molecule that spontaneously breaks down into 1 nitric oxide
(therapeutic) and 5 cyanide (toxic by-product) molecules. This slow release of cyanide
typically allows the body time to detoxify before it interferes with cellular respiration.
Detoxificationcan occurs in two manners:
– Methemoglobin (normally comprises 2% of all hemoglobin) binds to cyanide to yield
cyanomethemoglobin (a non-toxic, non-oxygen carrying hemoglobin)
– Thiosulfate binds to cyanide to yield thiocyanate via the rhodanese enzyme in the liver
and kidneys. Thiosulfate levels can become exhausted with high blood concentrations of
cyanide, high SNP dose, or low thiosulfate levels (e.g., malnutrition, postoperative states).
Thus, it is the “rate-limiting" step for the development of cyanide toxicity.
• Absorption. Cyanide is rapidly absorbed through the respiratory tract and mucus
membranes. It can be absorbed through the GI tract and skin. Protein binding: 60%; Vd 1.5
L/kg.
• When utilizing SNP, initial rates should not exceed 0.3 μg/kg/min, and maximum rates of
10 μg/kg/min should not be maintained for more than 10 minutes. Additionally, avoid total
doses >500 μg/kg when using a continuous infusion >2 μg/kg/min (cyanide is produced
faster than endogenous mechanisms can handle).
• Cyanide toxicity may be more likely if a patient has hepatic dysfunction; thus consider
reducing above-mentioned dosages. Thiocyanate toxicity may be more likely if there is renal
dysfunction.
DIAGNOSIS
• Patients can present with nonspecific signs and symptoms; furthermore there is no quick
blood cyanide test to confirm toxicity.
• Hypoxia, elevated lactic acid levels, and metabolic acidosis are considered to be the
hallmarks of cyanide poisoning.
• Perioperatively, anesthesia providers should maintain a high index of suspicion,
presumptive diagnosis, and rule out cyanide toxicity in patients exposed to fire smoke,
especially when the mouth and nares are tinged with soot (in addition to carbon monoxide
poisoning). Additionally, patients on nitrovasodilators may also present with clinical
symptoms and should be ruled out if appropriate
• Central nervous system: Headache, confusion, dizziness, flushing, vertigo, seizures, and
coma. At non-fatal levels, patients report the smell of almonds and feeling apprehensive.
Survivors of cyanide toxicity may develop Parkinsonism due to damage to the basal ganglia.
• Cardiac: Initial tachycardia and hypertension (sympathetic response to metabolic acidosis),
followed by bradycardia and hypotension, AV block, and cardiovascular collapse.
• Respiratory: An early sign is hyperventilation, which can increase the absorbed dose. This is
followed by bradypnea, pulmonary edema, absence of cyanosis (due to increased mixed
venous oxygen saturation), apnea, and respiratory arrest
• GI: Vomiting, abdominal pain
• Renal and hepatic failure
• Dermatologic: Flushing and cherry red color of skin are late findings.
• Chronic cyanide exposure can result in headache, Leber’s neuropathy, and tobacco
amblyopia. Bright red retinal veins may be noticed due to elevated venous oxygen
concentration
Labs/Studies
• Blood cyanide concentration. Laboratory measurement provides definitive diagnosis.
Because results are not immediate or “on-the-spot,” they cannot aid in initial management.
However, samples should be sent as soon as possible due to cyanide’s rapid metabolism and
instability in blood samples. Toxicity threshold ranges from 0.5 to 1 mg/L, and the lethal
threshold ranges from 2.5 to 3 mg/L
• Arterial blood gas reveals a severe metabolic acidosis (low pH and low sodium bicarbonate)
due to anaerobic metabolism with lactic acid production
– PaO2 is high (represents cell’s inability to extract and utilize arterial oxygen, despite cell
hypoxia).
– Alveolar–arterial (A–a) gradient <10 mm Hg. The A–a gradient is reduced due to the
highly oxygenated venous blood that results in higher arterial oxygen levels.
• Lactate is increased in arterial and venous samples due to anaerobic respiration and can be
additionally increased from other causes such as seizures, apnea, or administered
catecholamines.
• Anion gap: [Na +] – ([Cl−] + [HCO3−]) >15; gap is affected by changes in unmeasured
ions, in this case lactic acid. Bicarbonate buffers and binds to lactic acid, thus decreasing its
concentration.
• Mixed venous oxygen saturation. Venous blood has an abnormally high oxygen saturation
that reflects tissue and cell inability to utilize oxygen (despite hypoxia).
Monitors
• Pulse oximetry: Normal, despite cellular hypoxia
• EKG: Tachycardia followed by bradycardia, AV block
• Noninvasive BP: Hypertension followed by hypotension.
• Arterial line: Placement allows for frequent arterial blood gas measurements to follow
therapy.
• Tricyclic antidepressant poisoning
• Isoniazid overdose
• Organophosphate poisoning
• Salicylate poisoning
TREATMENT
• Cyanide poisoning is rapidly lethal; therefore, prompt recognition and early initiation of
treatment are necessary to save live.
• Decontamination. Prehospital care involves removing the victim from the source of cyanide
to an area of fresh air and decontaminating the victim (removal of contaminated clothing,
rinsing of skin if dermal exposure, gastric lavage and activated charcoal if ingested). If
administering a nitrovasodilator (SNP), infusion should be immediately discontinued.
• Supportive care. Administration of 100% oxygen can hasten respiratory excretion of cyanide
and reactivate mitochondrial enzymes. Furthermore, carbon monoxide poisoning also
requires high inspired oxygen and intubation (particularly with smoke inhalation injury due
to the potential for airway swelling).
• Benzodiazepines for seizure control and sodium bicarbonate can be administered to treat
metabolic acidosis (pH <7.1).
• Antidote treatment. The cyanide antidote kit (CAK) is the only currently available kit in the
US. It is comprised of two forms of nitrites and sodium thiosulfate. Nitrite displaces oxygen
(Amyl nitrite and Sodium nitrite) from hemoglobin to form methemoglobin that attracts
cyanide to form cyanomethemoglobin. Sodium thiosulfate is the natural substrate for
enzyme rhodanese and promotes conversion of cyanide to thiocyanate, an excretable and
less toxic compound. Antidote kits have several side effects and are controversial; nitrite
doses can result in dangerous levels of methemoglobinemia (reduces ability of blood to
transport oxygen to the cells, blue skin and mucus membranes, vomiting, shock, and coma).
Treatment is with 1% methylene blue 1–2 mg/kg.
• Alternatively, sodium nitrate 300 mg IV over 2–4 minutes; sodium thiosulfate 12.5 g IV
initial bolus and repeat 6.25 g IV in 30 minutes; or hydroxycobalmin.
REFERENCES
1. Desai S, Su M. Cyanide Poisoning: UpToDate Literature review 18.2: May 2010.
2. Barillo D. Diagnosis and treatment of cyanide toxicity. Journal of Burn Care and Research.
2009 January/February:148–152.
3. Baud FJ, Cyanide: Critical issues in diagnosis and treatment, human and experimental
toxicology. (2007)26;191–201.
ADDITIONAL READING
• Koshchel MJ. Management of cyanide poisoned patient. J Emerg Nurs. 2006;32:S19–126.
• Baker D. Chemical and Biological Warfare agents: The role of the Anesthesiologist; Miller’s
Anesthesia, 7th ed. (Chapter 74), 2010. pp. 2345–2347.
• Mixed venous oxygen
CODES
ICD9
989.0 Toxic effect of hydrocyanic acid and cyanides
ICD10
• T65.0X1A Toxic effect of cyanides, accidental (unintentional), init
• T65.0X2A Toxic effect of cyanides, intentional self-harm, init encntr
• T65.0X3A Toxic effect of cyanides, assault, initial encounter
CLINICAL PEARLS
• Anesthesia providers may encounter cyanide poisoning in the perioperative setting when
patients present from fire smoke inhalation (in addition to carbon monoxide poisoning) or
when utilizing nitrovasodilators (particularly SNP).
• Cyanide binds to cytochrome c oxidase in the ETC, thereby preventing oxygen from
accepting the donor electron. By hindering oxidative phosphorylation, it precludes aerobic
metabolism, and the body resorts to anaerobic respiration with lactic acid production
despite there being normal oxygen availability.
CYSTIC FIBROSIS
Matthew Delph, MD
Neal Campbell, MD
BASICS
DESCRIPTION
• Cystic fibrosis (CF) is a progressive, autosomal recessive disease caused by impaired chloride
ion transport with multiple organ system involvement.
• The major source of morbidity and mortality is attributed to progressive obstructive
pulmonary disease precipitated by chronic inflammation, infection, and destruction of
airways.
EPIDEMIOLOGY
Incidence
• Caucasian births: 1:2,500 (1)
• Hispanic births: 1:13,500 (1)
• African American births: 1:15,100 (1)
• New cases per year: 1,000 (2)
Prevalence
• Nearly 30,000 CF patients in the US (2)
• Prevalence rapidly increasing due to increased survival rates and median age
• 45% of patients are over the age of 18 (2)
Morbidity
• At least once yearly hospitalization: 35%
• Most frequent cause of morbidity is acute exacerbation of pulmonary disease
Mortality
• Median survival is 38 years (2).
• Respiratory disease accounts for 80–90% of morbidity and mortality (2)
• Autosomal recessive disorder
• More common in Caucasians; it is the most common lethal inherited disease in Caucasians
• Presence of meconium ileus, tobacco use, and female gender are associated with a more
rapidly progressing disease course
PATHOPHYSIOLOGY
• Mutation of the Cystic Fibrosis Transmembrane Regulator (CFTR) gene on Chromosome 7
can result in CF. Defects result in abnormal chloride channel proteins, and impaired cAMP-
regulated chloride transport across epithelial cells. Thousands of different mutations exist;
however, 75% of cases are due to deletion of phenylalanine (Δ 508) (2).
• Mutations lead to decreased chloride secretion and increased absorption of cations, such as
sodium, and water back into the cell. Although there are multiple theories, there is no
consensus on the pathophysiology of clinical symptoms.
• Mutations result in abnormally thick and sticky mucus that can build up in the exocrine
glands of the lungs, pancreas, hepatic, and GI tract. See section “Concomitant Organ
Dysfunction.”
• Preoperatively, assess and treat concomitant organ system dysfunction. The pulmonary
system requires careful preoperative evaluation; optimization may involve the use of
bronchodilators, incentive spirometry, and postural drainage.
• Intraoperatively, limit airway manipulation, humidify the airway, adequately hydrate, and
adjust ventilator settings in order to increase alveolar recruitment. Avoid atelectasis and
other parameters that may exacerbate obstructive lung disease.
• Postoperatively, ensure adequate reversal of neuromuscular blocking drugs (NMBDs) and
avoid prolonged post-op intubation if possible, as it increases morbidity and mortality.
• Regional or neuraxial techniques should be considered to provide pain relief while limiting
opioid use due to their depressive effect on the respiratory system.
SYMPTOMS
• Presence of cough
• Quality and quantity of mucous
• Dyspnea, paroxysmal nocturnal dyspnea (PND), orthopnea
History
• Age at diagnosis
• Progression and severity of disease, affected organ systems, pulmonary functional status
• Date and severity of last exacerbation or hospitalization
• History of smoking
• History of obstructive sleep apnea
Signs/Physical Exam
• Airway exam, neck, TMJ mobility
• Work of breathing, use of accessory muscles
• Wheezing, crackles, decreased breath sounds
• Signs of chronic hypoxia (digital clubbing)
• Hepatojugular reflex, peripheral edema
• Stigmata of liver disease
TREATMENT HISTORY
• Oxygen therapy
• CPAP/BIPAP use
• Chest physiotherapy
• Lung transplantation
MEDICATIONS
• Steroids
• B-agonists and other bronchodilators
• Recombinant DNAse (cleaves mucous)
• Theophylline
• Antibiotics
• Insulin or oral hypoglycemic
• Pancreatic enzyme replacement
Labs/Studies
• The 1996 Cystic Fibrosis Foundation developed criteria for diagnosis:
– Presence of 1 or more clinical features, family history of CF in a sibling, or positive
newborn screening test and abnormal sweat chloride test, nasal potential difference, or
identification of a known CF mutation (3)[C].
– The sweat-chloride test is the gold standard; values >60 mEq/L are considered positive.
• Preoperative studies
– CBC/chemistry panel
– Coagulation studies: PT, PTT, INR
– LFTs may reveal posthepatic obstruction due to increased bile viscosity.
– Baseline ABG
– Chest x-ray (CXR): Hyperinflation, pneumothorax, peribronchial thickening
– CT chest: Bronchiectasis, apical blebs
– Pulmonary function tests (PFTs): Obstructive pattern with a decrease in FEV1 and peak
expiratory flow, and increase in residual volume (RV).
• Airway manifestations include an increased incidence of nasal polyps and chronic sinusitis.
Nasal mucosa hypertrophy and hyperplasia may also be present.
• Pulmonary disease manifests as airway obstruction, bacterial colonization, atelectasis, and
hypoxia. It results from an increase in goblet cells and mucus production. PFTs demonstrate
an obstructive pattern with decreased FEV1, vital capacity, and peak flows as well as
increased RV.
– Although there are multiple hypotheses, there is no consensus on why bacterial
colonization occurs, most commonly with organisms Pseudomonas aeruginosa, Haemophilus
influenza, and Staphylococcus aureus.
– Chronic disease leads to pulmonary hypertension and cor pulmonale; patients often
require lung transplantation.
• Pancreatic disease manifests as exocrine and endocrine dysfunction secondary to impaired
bicarbonate secretion. The retention of digestive enzymes can cause autodigestion with an
increased risk for pancreatitis.
– Pancreatic exocrine dysfunction describes protein and fat malabsorption, failure to thrive,
deficiency of fat soluble vitamins (A, D, E, K)
– Pancreatic endocrine dysfunction describes pancreatic beta-cell destruction and can often
lead to diabetes mellitus (DM). Approximately 30% of patients develop DM by age 30 (2).
• Hepatobiliary disease manifests as cholelithiasis and cholecystitis from pancreatic duct
stenosis as well as cirrhosis, and hepatocellular carcinoma. Cirrhosis is the second most
common cause of death and is present in 10% of patients; abnormal LFTs are seen in 33% of
patients; fatty infiltration is present in 70% of patients.
• GI tract disease presents as meconium ileus; thickened feces can result in distal intestinal
obstruction syndrome. There is a high incidence of GERD.
• Musculoskeletal abnormalities present as low bone mineral density, kyphosis, scoliosis, and
rib fractures. This results from a combination of decreased vitamin D absorption, lack of
exercise, chronic steroid therapy, and low androgen levels.
• Coagulation abnormalities can manifest from pancreatic dysfunction (impaired absorption of
vitamin K) and hepatic disease.
• (In)Fertility. The majority of males are infertile due to the absence of a vas deferens.
Females have thick cervical mucus that often prevents pregnancy.
• Increased incidence of preterm labor.
• Gravid patients are more susceptible to right heart failure.
• Acute pulmonary exacerbation
• LFTs greater than 1.5 times normal should be investigated (2)[C].
• Coagulopathies should be corrected
CLASSIFICATIONS
See ICD9 section
TREATMENT
PRE-HOSPITAL
Premedications
• Bronchodilators should be considered preoperatively when signs of bronchoconstriction or
wheezing are present (2)[C].
• Mucolytics (DNAses) can be used to improve airway clearance.
• Anticholinergics may further dry mucous and secretions; consider avoiding.
• Acid reducers (H2 blockers) should be considered in patients with poorly controlled GERD
(4)[C].
The potential for postoperative respiratory failure and the need for ventilator support
INTRAOPERATIVE CARE
Consider regional or neuraxial anesthesia to limit airway manipulation or as an adjunct for
postoperative pain control (4)[C].
Monitors
• Consider arterial line for frequent ABGs or blood glucose levels in diabetics
• TEE in patients with right heart failure
• Sedation should be considered whenever possible to avoid airway manipulation and
• For general anesthesia, IV or inhalational induction may be used. Patients may exhibit a
prolonged inhalation induction secondary to increases in RV. If an inhalation induction is
chosen, consider sevoflurane (favorable blood:gas solubility compared to isoflurane and less
irritating to the airways than desflurane). Ketamine can increase secretions and should be
avoided (4).
• Laryngeal mask airways have the potential benefit of reduced airway reactivity; drawbacks
include the inability to protect against GERD or airway secretions, provide significant
positive pressure ventilation, or ventilate and oxygenate in the event of laryngospasm.
• Avoid nasotracheal intubation (and nasal airways) due to nasal mucosa hyperplasia.
• Large single lumen tubes are preferred to allow for lavage or bronchoscopy.
• Neuromuscular blockade may lead to airway obstruction.
• A RSI may be considered in patients with uncontrolled GERD.
Maintenance
• A balanced technique with volatile or total IV anesthesia. Volatile agents have the potential
benefit of providing bronchodilation.
• Humidifying inhaled gases can reduce thickening of secretions.
• Frequent intraoperative suctioning should be considered.
• Treat bronchospasm with bronchodilators, deepening of the anesthetic (volatile agent),
epinephrine subcutaneous or IV, terbutaline, or theophylline as appropriate.
• Avoid nitrous oxide due to an increased risk of pneumothorax (4)[C]
• Opioids should be limited due to respiratory depression. Attempt to treat postoperative pain
with NSAIDS and/or regional/neuraxial blocks (2)[C].
• Ensure adequate reversal of NMBDs
• Endotracheal suctioning, alveolar recruitment measures should be performed; consider chest
physiotherapy (2)[C].
• Position the patient with the head of the bed elevated 30–40° for extubation (4)[C].
• Early extubation improves morbidity and mortality (2)[C].
POSTOPERATIVE CARE
BED ACUITY
• Patients with mild disease and less complex procedures may be discharged home after being
monitored in the PACU (2)[C].
• Patients with more severe pulmonary disease or those undergoing more invasive procedures
should be monitored either in an intensive care unit (ICU) or monitored bed (4)[C].
• Chest physiotherapy, CXR
• Consider pulmonary consultation if postoperative mechanical ventilation is required.
COMPLICATIONS
• Respiratory depression, airway obstruction, atelectasis, pneumonia, pneumothorax
• Postoperative jaundice
REFERENCES
1. Cystic Fibrosis Clinical Validity. Sept 10 2007.
http://www.lungusa.org/assets/documents/ALA_LDD08_CF_FINAL.PDF. Accessed on Jan
26, 2011.
2. Huffmyer JL. Perioperative management of the adult with cystic fibrosis. Anesth Analg.
2009;109(6):1949–1961.
3. Farrell PM. Guidelines for diagnosis of cystic fibrosis in newborns through older adults:
Cystic fibrosis foundation consensus report. J Pediatr. 2009;153(2):S4–S14.
4. Della Rocca G. Anaesthesia in patients with cystic fibrosis. Curr Opin Anaesthesiol.
2002;15(1):95–101.
ADDITIONAL READING
• Davis PB. Cystic fibrosis since 1938. Am J Respir Crit Care Med. 2005;173:475–482.
• Ciliary function
• Chloride
• Cor pulmonale
CODES
ICD9
• 277.00 Cystic fibrosis without mention of meconium ileus
• 277.01 Cystic fibrosis with meconium ileus
• 277.02 Cystic fibrosis with pulmonary manifestations
ICD10
• E84.0 Cystic fibrosis with pulmonary manifestations
• E84.9 Cystic fibrosis, unspecified
• E84.11 Meconium ileus in cystic fibrosis
CLINICAL PEARLS
• Optimize preoperative pulmonary function; intraoperative and postoperative management
should aim at clearing secretions and managing as an “obstructive pulmonary disease”
patient. Extubation is desired but must be balanced against risks.
• Assess and treat CF-associated comorbidities.
CYSTOSCOPY
Jonathan Anson, MD
BASICS
DESCRIPTION
General
• A cystoscopy is performed to visualize and examine the inner surface of the urethra and
bladder; it is an endoscopic procedure.
• The cystoscope is either flexible or rigid and is inserted into the urethra. The distal end has
either a lens or fiberoptic apparatus to allow visualization via a proximal eyepiece or
monitor, respectively.
– To enhance visualization, sterile fluid is used to distend and stretch the bladder.
– The cystoscope has extra channels that allow for instruments to be inserted in order to
perform biopsies, stent placement, dilation, laser procedures, stone removal, or
intravesical administration of medications (e.g., Bacillus-Calmette-Guérin (BCG): A live,
attenuated strain of Mycobacterium bovis as adjuvant treatment for nonmuscle invasive
bladder cancer).
• Modifications/enhancements of this endoscopic procedure include transurethral resection of
bladder tumor (TURBT) and transurethral resection of the prostate (TURP). A resectoscope
is utilized to remove the tissue.
• Indications include frequent urinary tract infections (UTIs), hematuria, unusual cells seen in
urine samples, chronic pelvic pain, cystitis, dysuria, blockage from the prostate, stones, or
abnormal growth/tumor/polyps.
• A ureteroscope is a longer, thinner instrument that can be used to visualize and examine the
ureters and upper urinary tract structures.
Position
• Lithotomy
• Often requires the Trendelenburg position
Incision
Natural orifice procedure via the urethra
Approximate Time
5 minutes to 1 hour
EBL Expected
Minimal
Hospital Stay
Pathology dependent. Many procedures are performed on an outpatient basis.
• Cystoscope
• Ureteroscope
• Resectoscope
EPIDEMIOLOGY
Incidence
Approximately 67,000 new cases of bladder cancer per year.
Prevalence
Bladder cancer is three times more common in males than females; more common in patients
>55 years old; and twice as common in Caucasians as African Americans.
Morbidity
• Pain
• Urinary tract infection
• Urinary tract obstruction
• Bladder, urethral, or urethra perforation or injury
• The lithotomy and Trendelenburg positioning can result in decreased functional residual
capacity (FRC) and decreased pulmonary compliance.
• Akinesis should be maintained during the procedure to reduce the risk of bladder or ureteral
perforation. Leg movement should be prevented at the end of the procedure and until the
patient is out of the lithotomy position to avoid hip injury.
• Patients are often elderly and with multiple comorbidities. Geriatric considerations and
adjustment of drug dosages are often necessary.
• Autonomic hyperreflexia can occur in patients with spinal cord injury; thus, neuraxial or
general anesthesia is needed to prevent this occurrence with bladder distension.
• If laser therapy is used, protective goggles for the patient and operating room personnel
should be utilized.
SYMPTOMS
• Often asymptomatic
• May present with hematuria
• Abdominal pain, flank pain
• Urinary frequency, urgency, or dysuria
• Anuria if there is urinary tract obstruction
History
• Hematuria
• Calculi
• Bladder tumor/cancer
• UTI
• Urinary tract obstruction
• Hydronephrosis
Signs/Physical Exam
• Tachycardia or fever may suggest an infectious process
• Cardiopulmonary exam
MEDICATIONS
• Alpha blockers for benign prostatic hypertrophy (BPH) can compound hypotensive effects of
anesthetics
• 5-alpha-reductase inhibitors for BPH
• Antimuscarinics for overactive bladder
• Drugs for erectile dysfunction are nitric oxide derivatives and can compound hypotensive
effects of anesthetics
• Anticoagulants and blood thinner for coexisting conditions may contraindicate neuraxial
techniques.
Labs/Studies
• Metabolic panel if acute kidney injury is suspected
• CBC and coagulation factors if hematuria
• Urinalysis and urine culture, if UTI
• EKG and chest x-ray as per standard criteria
• Renal ultrasound for urinary tract obstruction and hydronephrosis
• Abdominal plain film or CT scan may show calculi
• Acute kidney injury, especially in the face of urinary tract obstruction (postrenal failure)
• Chronic kidney disease
• Patients with prosthetic heart valves or atrial fibrillation may develop hematuria from
heparin or warfarin.
• Urosepsis in patients with UTI or pyelonephritis.
• The incidence of calculi is the same in pregnancy as the general population. When it does
occur, it is seen more commonly in the 2nd and 3rd trimester. Stones typically pass
spontaneously but cystoscopy with stent placement may be necessary if the patient is septic
or has a urinary tract obstruction. The complication rate of ureteroscopic stone removal is
no different in pregnant patients than in nonpregnant patients (1)[A].
• A neuraxial or general technique can be utilized. Spinal and epidural blocks can decrease
the amount of medication administered and should be considered in patients who are early
in pregnancy or have a potentially difficult airway.
• Goals should be to avoid teratogenic drugs, maintain oxygenation and baseline
hemodynamics, and provide left uterine displacement if possible.
• Consult an obstetrician for guidance on preoperative, intraoperative, and postoperative fetal
monitoring.
TREATMENT
Premedications
• Anxiolysis as appropriate; use cautiously in elderly patients.
• Opioids as appropriate
Patients undergoing monitored anesthesia care or a regional technique plus MAC should still
be consented for general anesthesia as a backup.
• First line: Fluoroquinolone within 1 hour of the procedure
• Second line: Trimethoprim–sulfamethoxazole, or gentamicin with ampicillin
• Escherichia coli is most common organism
INTRAOPERATIVE CARE
• Local anesthesia is often used for flexible diagnostic cystoscopy.
• Monitored anesthesia care should be considered for diagnostic flexible cystoscopy in
patients unable to tolerate local anesthesia.
• Neuraxial anesthesia with a T10 level is adequate for most urologic procedures. However, it
does not reliably block the obturator nerve. An awake patient is the best monitor for mental
status changes in TURP syndrome.
• Regional anesthesia. An obturator nerve block may be considered in conjunction with
neuraxial techniques if inferolateral bladder wall resection is anticipated. It prevents patient
movement if the nerve is stimulated and decreases the risk of bladder perforation (2)[A].
• General anesthesia is commonly used.
Monitors
• Invasive monitoring is dictated by the patient’s comorbidities
• General anesthesia with a laryngeal mask airway (LMA) or endotracheal tube (ETT).
• LMA can be used if the patient is NPO, not at risk for aspiration, and has an “adequate" FRC.
Supraglottic devices may decrease the incidence of airway reactivity in patients with asthma
or chronic obstructive pulmonary disease (COPD). Muscle relaxation for the procedure may
still be utilized.
• ETT should be used if the patient is not NPO, possesses risk factors for aspiration, or if the
lithotomy and Trendelenburg positions may hinder spontaneous ventilation (e.g., truncal
obesity, decreased pulmonary compliance).
• In patients with renal failure or hyperkalemia, succinylcholine may be contraindicated. If a
rapid sequence induction is indicated, consider rocuronium (drawback = duration may be
prolonged) or cisatracurium (drawback = longer time to onset).
Maintenance
• Balanced anesthetic with volatile or IV medications.
• Surgical irrigating fluids may be absorbed in some cases. TURP procedures pose the highest
risk due to open prostatic venous sinuses; thus irrigating time should be kept as short as
possible.
• Hemodynamics should be maintained close to baseline values, particularly in patients with
end-organ damage.
• Hypothermia may occur due to cold irrigating fluids. Normothermia can be maintained with
increased ambient room temperature, upper body forced air warming blanket, or warm IV
fluids.
• Narcotics. In patients who are spontaneously breathing with an LMA, titrate to respiratory
rate.
• Duration of action of nondepolarizing muscle relaxants may be prolonged if gentamicin is
given or the patient is hypothermic.
• Radiation safety precautions should be implemented if fluoroscopy is used.
• Laser protective goggles should be implemented for the patient and OR staff if laser therapy
is utilized.
• Antiemetic prior to emergence
• Ensure complete akinesis until legs are out of lithotomy.
• Awake extubation after reversal of muscle relaxation and when routine respiratory
parameters are met.
POSTOPERATIVE CARE
BED ACUITY
• PACU for immediate postoperative care
• Nontelemetry floor bed is appropriate for most inpatients.
• Telemetry unit if the patient has a history of arrhythmia or severe cardiovascular disease.
• Intensive care unit (ICU) admission for TURP syndrome.
ANALGESIA
• Some patients feel more comfortable postoperatively (e.g., after stone removal)
• IV opioids with transition to PO opioids
COMPLICATIONS
• Monitor urine output as clots may form in the urinary catheter.
• Abdominal pain with referred shoulder pain warrants workup for bladder perforation.
• UTI
• Stent migration
• TURP syndrome
• Ureteral perforation
• Autonomic hyperreflexia
• Hematuria/clots in Foley catheter
• Acute kidney injury
• Sepsis and cystitis from BCG; considerably higher incidence in patients >70 years old,
especially with repeated doses (3)[B].
PROGNOSIS
Urinary obstruction may lead to irreversible kidney injury. Reversibility is dependent on
duration and severity of obstruction.
REFERENCES
1. Khorrami MH, Javid A, Saryazdi H, et al. Transvesical blockade of the obturator nerve to
prevent adductor contraction in transurethral bladder surgery. J Endourol.
2010;24(10):1651–1654.
2. Semins MJ, Trock BJ, Matlaga BR. The safety or ureteroscopy during pregnancy: A
systematic review and meta-analysis. J Urol. 2009;181:139–143.
3. Heiner JG, Terris MK. Effect of advanced age on the development of complications from
intravesical bacillus Calmette-Guérin therapy. Urol Oncol. 2008;(26)2:137–140.
ADDITIONAL READING
• http://www.auanet.org (American Urological Association). See clinical guidelines tab.
• Acute renal failure
• Postrenal failure
• TURP syndrome
CLINICAL PEARLS
• Patients are often elderly and have numerous comorbidities, requiring careful preoperative
evaluation.
• Obturator nerve block is an easy, effective means to avoid obturator stimulation during a
TURBT.
• Duration of action of nondepolarizing muscle relaxants may be extended with
administration of gentamicin.
• There are no studies showing improved renal outcome with general versus neuraxial
anesthesia.
• Neuraxial anesthesia allows early recognition of mental status change in TURP syndrome.
D-DIMER
Mark R. Bombulie, BS
BASICS
DESCRIPTION
• D-dimer is an antigen that is produced from plasmin-mediated degradation of fibrin-rich
thrombi.
• D-dimer assays are a useful tool for the:
– Exclusion of deep venous thrombosis (DVT) and pulmonary embolism (PE)
– Diagnosis of disseminated intravascular coagulation (DIC) (1)
• The D-dimer measurement is an adjunct test and should never be used in isolation for
diagnosis or exclusion (2).
• In the final steps of the coagulation pathway, thrombin cleaves fibrinogen to produce fibrin
monomers. These fibrin monomers polymerize with one another forming protofibrils, thus
allowing factor XIII to bind.
• Thrombin also serves to activate factor XIII bound to fibrin polymers (forming factor XIIIa).
• Factor XIIIa catalyzes the formation of covalent bonds between the D-domains (the segment
of the fibrin protein containing the D-dimer antigen sequence) in adjacent protofibrils of
polymerized fibrin.
• During fibrinolysis, activated plasmin degrades the cross-linked fibrin, which releases fibrin
degradation products and exposes the D-dimer antigen, which is typically not present in the
body except when the coagulation system has been activated.
• The D-dimer assay
– The required sample is venous blood in a light blue tube (the same tube used for PT/PTT).
The tube must be completely filled.
– Quantitative values are performed in the laboratory with plasma and have a sensitivity of
95% and specificity of 50%. Quantitative tests rely on either enzyme-linked
immunosorbent assays (ELISA) or enzyme-linked fluorescent assays (ELFA) to detect the
amount of D-dimer present.
– Qualitative values can be obtained at the bedside with whole blood and have lower
sensitivities (85%) but slightly higher specificities (70%) than quantitative values. Whole
blood is mixed with a reagent (a D-dimer monoclonal antibody that is joined to a
monoclonal antibody capable of binding to the surface of a red blood cell). When D-dimer
is present above a threshold value, agglutination occurs (the conjoined antibodies cause
D-dimer and RBCs to clump together). This technique has the advantage of yielding
results quickly without advanced laboratory equipment, but it is unable to detect low
levels of D-dimer (3).
– Increased values suggest increased thrombus formation or breakdown in the body.
• DVTs can embolize and travel through the right heart and into the pulmonary vasculature,
causing a mechanical obstruction to blood flow (pulmonary embolism) and a secondary
immune-inflammatory response. Risk factors include:
– Previous history
– Hereditary causes:
Antithrombin III deficiency
Protein C and S deficiencies
Factor V Leiden
Prothrombin gene mutations
– Acquired causes:
Reduced mobility
Cancer
Pregnancy/postpartum
Nephrotic syndrome
Trauma
Spinal cord injury
– Medications:
Hormone replacement therapy
Oral contraceptives
Chemotherapy
Antipsychotics
– Surgical factors:
Major surgery
Hip or leg fracture
Hip or knee replacement
General anesthesia compared to epidural/spinal anesthesia (4)
• Dead space: Pulmonary emboli result in an increase in alveolar dead space with an
associated right-to-left shunt and V/Q mismatch. Blood shunted away from the blocked
pulmonary arteries can cause edema, loss of surfactant, and alveolar hemorrhage in the
overly perfused lung segments (5). Acute blockage can cause right heart strain or acute cor
pulmonale.
• DIC causes include infection, malignancy, obstetric disorders, shock, liver disease,
extracorporeal circulation, intravascular hemolysis; it is the end result of several disease
processes and has a high mortality rate. DIC is characterized by continuous thrombin
generation and fibrin formation in the microvasculature which ultimately deplete
coagulation factors and their inhibitors, leading to bleeding and/or thrombotic state. The
subsequent breakdown of formed fibrin leads to the elevated D-dimer seen in this condition.
– Perioperative PE has an incidence of 1.6% in patients undergoing general surgery. The
incidence in patients undergoing orthopedic procedures, especially hip procedures, has
been reported as high as 30%.
– ELISA D-dimer assays have a sensitivity of 95% and specificity of 50% and are therefore
helpful in ruling out perioperative PE in patients with low clinical suspicion. In patients
with high clinical suspicion, ordering a D-dimer does not change management and should
not delay treatment.
– Values >500 ng/mL are considered positive.
– False positives may be seen in other conditions unrelated to PE, including infection,
cancer, trauma, cardiac disease, rheumatoid arthritis, hyperbilirubinemia, hepatic disease,
in the elderly, the surgical procedure itself, hemolysis, or other inflammatory states.
• Disseminated intravascular coagulation
– In pregnant women with microangiopathic hemolytic anemia, elevated liver enzymes, and
low platelets (HELLP) syndrome, 15–38% can progress to DIC.
– DIC can be diagnosed intraoperatively with thrombocytopenia, elevated PT, aPTT, and D-
dimer (6).
– D-dimer levels >200 ng/mL are considered elevated. Levels correlate with the severity of
the disease and can be monitored to assess the effectiveness of therapy.
REFERENCES
1. Thachil A, Fitzmaurice DA, Toh CH. Appropriate use of d-dimer in hospital patients. Am J
Med. 2010;123:17–19.
2. Frost SD, Brotman DJ, Michota FA. Rational use of D-dimer measurement to exclude acute
venous thromboembolic disease. Mayo Clin Proc. 2003;78:1385–1391.
3. Adam SS, Key NS, Greenburg CS. D-dimer antigen: Current concepts and future prospects.
Blood. 2008;113:2878–2887.
4. Martlew VJ. Peri-operative management of patients with coagulation disorders. Br J
Anaesth. 2000;85(3):446–455.
5. Desciak MC, Martin DE. Perioperative pulmonary embolism: Diagnosis and anesthetic
management. J Clin Anesth. 2011;23:153–165.
6. Garg R, Nath MP, Bhalla AP, et al. Disseminated intravascular coagulation complicating
HELLP syndrome: Perioperative management. BMJ Case Rep. 2009.
CLINICAL PEARLS
• A positive D-dimer may indicate an increased level of fibrin degradation products that can
result from increased thrombus formation or breakdown in the body. It cannot identify the
location or the cause.
• D-dimer assay can be used to rule out PE in patients with low clinical suspicion.
• D-dimer levels can be followed to monitor the effectiveness of treatment in patients with
DIC.
• D-dimer assay should never be used in isolation.
DEAD SPACE
Siamak Rahman, MD
BASICS
DESCRIPTION
• Dead space (VD) describes the lung areas that are ventilated but not perfused.
Perioperatively it includes:
– Physiologic dead space: Anatomic and alveolar
– Apparatus dead space: Most concerning for neonates
• Increases in the dead space to alveolar ventilation (VD:VA) ratio result in the retention of
carbon dioxide. Thus, any cause of increased VD would require increases in ventilatory
support/parameters in order to maintain normocarbia.
• Physiologic dead space (VDtotal) does not participate in carbon dioxide or oxygen exchange.
It is composed of 2 different components of lung volume:
– Anatomic (VDanatomic): Upper airway structures that do not contribute to gas exchange;
includes air in the nose, pharynx, larynx, trachea, and larger airways. This volume does
not reach the alveolar level, will not participate in gas exchange, and is thus “wasted.” It
is ∼1/3rd of the tidal volume, or 2 mL/kg.
– Alveolar (VDalveolar): Ventilated alveoli receiving minimal blood flow; includes zone 1 and
nondependent lung areas.
– VDtotal = VDanatomic + VDalveolar
• Apparatus, mechanical, or equipment dead space: Perioperatively, the anesthetic delivery
system and monitors can add dead space; it can become significant with pediatric patients.
As the volume increases, less fresh gas moves into the patient’s alveoli to participate in gas
exchange. This also applies to intubated and ventilated patients in the ICU.
– Endotracheal tube or laryngeal mask airway; dead space volume exists in the portion that
extends beyond the patient’s incisors (can be decreased by cutting the ETT). Of note,
however, intubation results in ∼1/2 of the anatomical dead space being bypassed
(volume of dead space in nasopharynx and mouth).
– Airway adaptors: Straight and elbow can add ∼2 mL of dead space
– End-tidal CO2 monitors can add ∼8 mL of dead space. The closer the ETCO2 monitor is
positioned to the ETT, the less is the amount of dead space.
– Extenders such as corrugated devices
– Face masks
– Humidification management exchangers (HME)
– Y piece: Adults ∼8 mL; pediatric ∼4 mL
– Malfunctioning one-way valves
– Bain circuit with a cracked or broken center portion
– Exhausted soda lime: Unique in that it normally clears CO2 within the circuit; thus, when
it is exhausted, it no longer participates in “ventilation.”
• Bohr equation was presented in the beginning of the 20th century. The dead space fraction
could be determined by measuring the arterial CO2 (PaCO2) via blood gas measurements
and the mean expired CO2 (PeCO2). The end-tidal CO2 (ETCO2) is often substituted for the
mean expired CO2 (1).
• Fowler’s method—a test for measuring the dead space via nitrogen washout during one or
multiple breaths. The patient takes a breath of 100% oxygen and exhales through a one-way
valve measuring nitrogen content and volume. It is not commonly used or available
perioperatively.
• Breathing efficiency—defined as the volume of fresh gas reaching the alveoli (alveolar tidal
volume) divided by the total volume of the gas inhaled per breath (total tidal volume). In
normal healthy adults who are breathing spontaneously at rest, it is normally between 60%
and 70% (this means that ∼30–40% of inhaled fresh gas does not reach the alveoli).
• Alveolar dead space can be increased in pathological states. Non-perfused, but ventilated,
alveoli are defined as lung units with a V/Q ratio of infinity. They include:
– Pulmonary embolus
– Low cardiac output
– Increased alveolar pressure from mechanical ventilation or positive end expiratory
pressure (PEEP)
– Chronic obstructive pulmonary disease
• “Shunt dead space” is an erroneous description of right-to-left lung shunt that brings the
higher CO2 concentration in venous blood to the arterial side, thereby producing an arterial-
to-end-tidal CO2 difference. However, the influence of shunt on dead space is fairly small
when shunt values are low; they become significant when the shunt has reached 50%.
• Hypercarbia can potentially have profound effects:
– Directly increases cerebral blood flow and intracranial pressure
– Increases pulmonary arterial pressure
• Sympathetic activation can result in tachycardia, hypertension, or arrhythmias.
• Assessing and measuring VD/VA or dead space will give insight into the matching of
ventilation and perfusion and is useful in:
– Evaluating mortality risk in acute respiratory distress syndrome; increases in VD/VA
correlate with the severity of lung injury.
– Indicating lung recruitment versus overdistention when PEEP is added or increased to
improve oxygenation
– Predicting successful extubation in pediatric and adult patients
– Diagnosing and assessing the severity of pulmonary embolism. The alveolar dead space
can increase to excessive amounts (80–90% of the tidal volume in recurrent pulmonary
embolism).
– Providing valuable information on the ventilatory support of the critically ill by providing
information regarding changes in volume of alveolar dead space (2)
• Breathing pattern: Rapid, shallow breathing, as may be seen from abdominal or thoracic
incisional pain, can result in small tidal volumes, and an increased fraction of dead space
ventilation (may reach >50%). Continuous epidural anesthesia in the postoperative period
may decrease this (as well as atelectasis); the benefits may be pronounced in pulmonary
cripples with low reserves.
• Pulmonary embolism: Fat, venous, air, or clot embolic phenomenon may result
intraoperatively with sudden pulmonary vascular occlusion. The resultant V/Q mismatch
can produce a sudden increase in alveolar dead space and decreased ETCO2 readings
(PaCO2 will increase).
• Neonates and infants: Apparatus dead space is more concerning in this patient population. A
5 kg neonate has a dead space of ∼10 mL. The addition of apparatus can add several
milliliters causing the VD/VA ratio to increase significantly.
• Tracheostomy: Reduces dead space ventilation and improves the efficiency of ventilation.
Studies have shown that tracheostomy can reduce VD by 70 mL and reduce the work of
breathing by over 30% (3)[C].
• Compensatory breathing techniques: During respiratory distress in the spontaneously
ventilating, non-intubated patient, an instinctive unidirectional breathing pattern may
develop to avoid rebreathing air in the nose with a high CO2. This consists of inhaling via
the nose, and exhaling through the mouth.
EQUATIONS
• VDtotal = VDanatomic + VDalveolar
• Bohr equation was presented in the beginning of the 20th century:
– Where PeCO2 is the partial pressure of CO2 in mixed expired gas and is equal to the mean
expired CO2 or end-tidal CO2
– PaCO2 is equal to arterial CO2.
GRAPHS/FIGURES
FIGURE 1. Total dead space is equal to the anatomic dead space plus the alveolar dead space.
REFERENCES
1. Blanch L, Romero PV, Lucangelo U. Volumetric capnography in the mechanically
ventilated patient. Minerva Anestesiol. 2006;72(6):577–585.
2. Hedenstierna G, Sandhagen B. Assessing dead space: A meaningful variable? Minerva
Anestesiol. 2006;72(6):521–528.
3. Chadda K, Louis B, Benaissa L, et al. Physiological effects of decannulation in
tracheostomized patients. Intens Care Med. 2002;28:1761–1767.
• ETCO2
• Fat embolism
• Tracheostomy
CLINICAL PEARLS
• Patients with normal lung function have narrow gradients between their ETCO2 and arterial
CO2 concentration (PaCO2) of 0–5 mm Hg. Air in the physiologic dead space accounts for
this normal gradient. In diseased lungs, the gradient will increase due to ventilation–
perfusion mismatch.
• The increase in physiologic dead space and worsening of ventilation–perfusion matching
that occurs with venous air embolism produce a sudden fall in ETCO2, which, although
sensitive, is a nonspecific sign of venous air emboli and also occurs with other type of
emboli, massive blood loss, circulatory arrest, or disconnection from the anesthesia circuit.
DEEP EXTUBATION (ANESTHETIZED EXTUBATION)
Katy E. French-Bloom, MD
BASICS
DESCRIPTION
Deep extubation describes removal of the endotracheal tube (ETT) from the trachea while the
patient is still anesthetized, or deeply anesthetized (1). It requires that the:
• Muscle relaxation is fully reversed.
• Patient is maintaining an acceptable respiratory rate and tidal volume for their size.
• Patient does not respond to pharyngeal suctioning.
• Provider must remain vigilant in their attention to airway maintenance until the patient is
fully awake.
• Removal of the ETT occurs during a positive pressure breath.
ALERT
This is a controversial technique. It is not considered mandatory in most postoperative
settings. When conducting a deep extubation, be aware you are giving up a secure airway (1).
Can be advantageous in patients with certain comorbidities, including hypertension and
chronic obstructive pulmonary disease (2)
Can be advantageous for certain pediatric procedures. Remember that the cricoid cartilage is
the narrowest part of the pediatric airway. Use cautiously in cases where laryngeal edema is
common. Children can be symptomatic as their small airway size is more severely
compromised by edema (3).
pregnancy considerations
Contraindicated in this patient population as they are always considered full stomach and at a
high risk for pulmonary aspiration (4)
• There are 4 stages of anesthetic depth:
– Stage 1 (Analgesia): Characterized by slow, regular breathing with diaphragm and
intercostal muscles, and the presence of lid reflex
– Stage 2 (Delirium): Characterized by irregular and unpredictable ventilation, reflex
dilation of the pupils, and intact lid reflex. The risk of clinically important reflex activity
such as vomiting, laryngospasm, or arrhythmias increases
– Stage 3 (Surgical anesthesia): This stage has 4 planes:
Plane 1: Slight somatic relaxation, regular periodic breathing, active ocular muscles
Plane 2: Breathing changes, inhalation becomes briefer than exhalation, eyes become
immobile
Plane 3: Abdominal muscles relax, diaphragmatic breathing becomes very prominent,
eyelid reflex is absent
Plane 4: Intercostal muscles become completely pararlyzed, rib cage movement
paradoxical, breathing irregular, pupils dilate.
– Stage 4 (Respiratory paralysis): Muscles are flaccid, eyes wide and dilated
ANATOMY
• Pharynx: The pharyngeal airway extends from the posterior aspect of the nose down to the
cricoid cartilage.
• Larynx: Lies at the level of the cervical vertebrae 3–6; it is an organ of phonation and acts as
a valve to protect the lower airways from contents of alimentary tract.
• Epiglottis: A fibrous cartilage that is a part of the larynx. It has a mucous membrane
covering that reflects as the glossoepiglottic fold onto the pharyngeal surface of the tongue.
The epiglottis projects into the pharynx and overhangs the laryngeal inlet. It is not
absolutely necessary for sealing off the airway during swallowing.
• Advantages of deep extubation (1,2,5,6):
– Decreases stress response to extubation; less fluctuation in blood pressure/hypertension
and heart rate/tachycardia
– Decreases coughing and bucking on the ETT
– Less incidence of desaturation
– Less laryngotracheal trauma
– Less breath-holding, bronchospasm
• Disadvantages/complications of deep extubation (4):
– Laryngospasm and/or bronchospasm can occur if the patient is extubated in between the
awake and anesthetized states (Stage 2).
– Loss of a secure airway
– Aspiration
– Negative pressure pulmonary edema
– May require nasal/oral airway or laryngeal mask airway (LMA) after removal of ETT
• Indications for deep extubation:
– Specific surgeries including (6):
Unclipped intracranial aneurysms
Open globe eye surgery
Intracranial aneurysm clipping (5)
Tympanoplasty surgery
Thyroid/parathyroid surgery
Tonsillectomy/adenoidectomy (7,8)
Removal of laryngeal papillomatosis (9)
– Patients with specific comorbidities:
Hypertension (2)
Tachydysrhythmias
Reactive airway disease (4)
• Contraindications to deep extubation (1):
– Difficult mask ventilation
– Difficult intubation
– Increased risk of aspiration/full stomach
– Surgery that may cause airway edema
– Obesity
– Diagnosis of obstructive sleep apnea (relative)
– Neuromuscular disorders such as primary muscle diseases, demyelinating diseases,
myasthenic syndromes, ion channel myotonias
• Prior to a deep extubation (same for adult and pediatric patients)
– Muscle relaxants must be fully reversed.
– An adequate anesthetic depth must be maintained; eyes in midline, indicating at least a
Stage 3 depth of anesthesia.
– Patient should be breathing 100% oxygen.
– Patient must be maintaining an acceptable respiratory rate and depth.
– The posterior pharynx of the patient must be thoroughly suctioned; there should be no
reaction by the patient to this.
– Placement of a well-lubricated nasal trumpet may be considered in patients at risk for
obstruction (e.g., large tongue).
– The ETT is removed after a positive pressure breath has been given with the anesthesia
reservoir bag to allow expulsion or secretions out of the glottis.
• Immediately following deep extubation:
– Oxygen should be administered to the patient in the form of a facemask for adults, and
either a facemask or blow-by oxygen for pediatric patients.
– Laryngospasm can occur especially when extubation is performed during Stage 2.
Laryngospasm is the prolonged, intense glottis closure in response to direct glottis or
supraglottic stimulation from inhaled agents, secretions, or foreign bodies. Patients
usually produce sounds that range from high-pitched and squeaky to complete absence.
Treatment of laryngospasm consists of recognizing this condition and then treating it
appropriately; partial laryngospasm may be managed with 100% oxygen administration,
CPAP, and jaw thrust whereas complete laryngospasm (or unremitting partial
laryngospasm) requires propofol or muscle relaxation (most commonly succinylcholine).
– Obstruction from the tongue or redundant tissue may be relieved with repositioning of the
head, jaw thrust, insertion of an oral airway or nasal trumpet, or positive pressure
ventilation with a facemask.
• Recovery room care following deep extubation:
– The “no-touch” technique for pediatric and adult patients involves not touching or
manipulating the airway until the patient is fully awake.
– Patients must be fully monitored for the duration of their stay in PACU.
REFERENCES
1. Daley MD, Norman PH, Coveler LA. Tracheal extubation of adult surgical patients while
deeply anesthetized: A survey of U.S. anesthesiologists. J Clin Anesth. 1999;11(6):441–444.
2. Ma HN, Li HL, Che W. Effect of exchange of tracheal tube for laryngeal mask airway (LMA)
on intratracheal extubation stress response under deep anesthesia level after surgery in
elderly patients with hypertension. Zhonghua Wai Ke Za Zhi. 2010;48(23):1811–1814.
3. Valley RD, Freid EB, Bailey AG, et al. Tracheal extubation of deeply anesthetized pediatric
patients: A comparison of desflurane and sevoflurane. Anesth Analg. 2003;96(5):1320–
1324.
4. Koga K, Asai T, Vaughan RS, et al. Respiratory complications associated with tracheal
extubation. Anesthesia. 1998;53(6):540–544.
5. Suzuki A, Ogawa H. A new technique of extubation using laryngeal mask in the
neurosurgical anesthesia. Masui. 1997;46(7):994–996.
6. Smith I, Taylor E, White PF. Comparison of tracheal extubation in patients deeply
anesthetized with desflurane or isoflurane. Anesth Analg. 1994;79(4):642–645.
7. Valley RD, Ramza JT, Calhoun P, et al. Tracheal extubation of deeply anesthetized
pediatric patients: A comparison of isoflurane and sevoflurane. Anesth Analg.
1999;88(4):742–745.
8. Higuchi H, Ura T, Taoda M, et al. Minimum alveolar concentration of sevoflurane for
tracheal extubation in children. Acta Anaesthesiol Scand. 1997;41(7):911–913.
9. Forestner JE, McGraw SA, Norman PF. Laryngeal papillomatosis: Anesthetic management.
South Med J. 1979;72(9):1107–1112.
• Laryngospasm
• Superior laryngeal nerve
• Aspiration
CLINICAL PEARLS
• Deep extubation is a technique that can be used in certain circumstances when minimal
hemodynamic change is advantageous, or where avoidance of coughing and bucking would
be beneficial.
• The major drawback is that the anesthetist is relinquishing a known secured airway for an
unsecured one.
• Deep extubation does have uses, but serious negative complications can result if not vigilant
about the technique.
DEFIBRILLATION
Jochen Steppan, MD
Nanhi Mitter, MD
BASICS
DESCRIPTION
• Defibrillation is the application of electricity during cardiac arrest either to the chest wall or
directly to the heart muscle to restore a coordinated cardiac rhythm and a spontaneous
circulation.
• The first scientific work on defibrillation was published by a team of researchers at the
Johns Hopkins University in 1933. Funding was provided from an electrical company as a
result of an increase in the rate of sudden death among utility workers who were rewiring
American homes with electricity. This work was followed by the development of closed
chest cardiac massage by the same team and publication in 1960.
• Adequate current flow through the heart is required for successful defibrillation: I = V/R,
where I = current, V = voltage, and R = resistance. Therefore, for the same voltage (V)
applied, the current (I) delivered to the patient varies depending on the transthoracic
impedance (R).
• Transthoracic impedance (70–80 Ohm) is influenced by:
– Electrode surface area: Electrodes should be 8–12 cm in diameter for adults. Large
electrode pads result in smaller transthoracic impedance.
– Pressure on the electrodes: As per the American Heart Association guidelines, a force of 8
kg applied to paddles results in an optimal reduction of transthoracic impedance.
– Body habitus and tissue properties of the rib cage, muscle, subcutaneous fat and skin
contribute to transthoracic impedance. In order to further reduce transthoracic
impedance, a conductive material such as gel pads or electrode paste should be used.
• There is no direct relationship between the energy applied (Energy = Power × Time) and
current flow.
• Theories about mechanisms of defibrillation:
– Critical mass theory (original): The delivery of current to a critical mass of myocardium
can stun and make the muscle unexcitable. The uncoordinated waveforms of excitation
that perpetuate ventricular fibrillation would then be extinguished and a normal cardiac
excitation will resume. Tissue in close proximity to the shocking electrodes produces
virtual electrodes that either hyperpolarize or depolarize the surrounding cardiac tissue.
– Vulnerability theory (newer): Defibrillation is mediated by depolarizing fully excitable
cells and also by depolarizing cells in the relative refractory period by a stimulus that
exceeds the upper limit of vulnerability.
• Defibrillator waveforms:
– Monophasic defibrillators deliver current in one direction (one polarity).
– Biphasic defibrillators deliver current in 2 directions. The current flows in one direction
during the first phase of the waveform and in the opposite direction during the second
phase. Therefore, lower energy levels can be used during defibrillation for equivalent or
higher success rates.
– No specific waveform has shown to be consistently associated with a greater incidence of
return of spontaneous circulation or higher survival to hospital discharge.
– All newer defibrillators deliver biphasic shocks, but monophasic shocks are still acceptable
and currently in clinical use.
ANATOMY
• Physiological cardiac excitation is initiated in the sinus node. It travels through atrial tissue
to the AV node and is then conducted through the bundle of His to the bundle branches
over the Purkinje fibers and finally to the myocardium.
• Ventricular fibrillation (Vfib) is a state of disorganized electrical activity that leads to
uncoordinated contraction of the myocardium, making its ejection ineffective.
Cardiac arrest is a leading cause of death in many parts of the world.
• In the US and Canada, approximately 350,000 people suffer a cardiac arrest per year and
require resuscitation (half of the cases occur in-hospital).
• The incidence of in-hospital cardiac arrests is estimated at 3–6/1,000 admissions.
• For every minute that elapses between collapse and defibrillation, the chance of survival
from ventricular fibrillation diminishes by 7–10% every minute if no CPR is provided and
by 3–4% with CPR.
• Defibrillation is the only effective treatment of Vfib and should be performed within 10
minutes after sudden onset cardiac arrest (<3 minutes in hospital) to achieve a good
neurologic outcome.
• External (transthoracic) defibrillation:
– Initial energy level: For biphasic defibrillators, follow the recommendations by the
manufacturer. If those are not readily available, it is reasonable to start with 150–200 J
when using a biphasic defibrillator to treat Vfib/pulseless ventricular tachycardia (Vtach),
and it is optional to increase up to 360 J for subsequent shocks or to continue with the
initial amount of energy. The recommendation for monophasic defibrillators is to use 360
J for the initial and all subsequent shocks.
– Unsynchronized shock describes the delivery of a shock that is not synchronized with the
QRS wave. As there is no organized electrical activity during Vfib or pulseless Vtach, this
is the treatment of choice for those entities and an integral part in the treatment of sudden
cardiac arrest.
– Pads or paddles:
To decrease transthoracic impedance one should use gel pads or electrode paste
(American guidelines only), shave the chest if it does not delay chest compressions or
shock delivery, and press the paddles firmly to the chest (8 kg of force).
Can be placed in the following positions: Antero-lateral (default location), antero-
posterior, anterior-left infrascapular, or anterior-right infrascapular position. There are
no studies in patients with Vfib or pulseless Vtach directly comparing the effects of
electrode positioning to success of defibrillation. Therefore, practical considerations
usually dictate electrode placement to optimize current flow through the patient’s heart.
In adults, antero-lateral placement is favored, while in children the antero-posterior
placement is often used in order for the pads not to overlap.
In patients with an implantable cardioverter defibrillator (ICD), pads should be placed at
least 8 cm away from the device in an anterior-posterior or anterior-lateral position.
Do not place pads or paddles directly over transdermal medication patches because the
patch may block the delivery of energy and may cause burns to the skin.
– Pediatric:
Energy levels should start at 2 J/kg and can be escalated up to 10 J/kg (not to escalate
the adult maximum dose).
In children aged 1–8 years, pediatric electrodes should be used.
Pads or paddles should be applied with 5 kg of force and can be in the following
positions: Antero-apical, antero-posterior, or apex-posterior position.
• Temporary transvenous defibrillation can be considered as an alternative in patients
undergoing electrophysiological procedures.
• ICDs are usually implanted underneath the pectoral muscle below the left clavicle and
defibrillate with 40 J of energy via an internal pacing wire embedded in the right ventricle
(up to 8 times per detected Vfib/Vtach).
EQUATIONS
• I = V/R, where I = current, V = voltage, R = resistance
• Energy = power × time
GRAPHS/FIGURES
• 2010 ACLS Cardiac Arrest Algorithm for Vfib or pulseless Vtach arrest:
– Activate Emergency Response System
– Start CPR, administer oxygen, attach monitor/defibrillator
– Confirm Vfib or pulseless Vtach and defibrillate
– Continue CPR for 2 minutes and establish intravenous/intraosseous access
– Check rhythm: If shockable, defibrillate; otherwise proceed with ACLS pathway for
asystole/PEA, or postcardiac arrest care
– Continue CPR for 2 minutes, administer epinephrine every 3–5 minutes, consider
advanced airway and capnography
– Check rhythm: If shockable defibrillate; otherwise proceed with ACLS pathway for
asystole/PEA, or postcardiac arrest care
– Continue CPR for 2 minutes, give amiodarone and treat reversible causes
– Repeat check rhythm.
• For witnessed cardiac arrest, 1 shock followed immediately by CPR is favored over 3 stacked
shocks. The European guidelines allow consideration of 3 stacked shocks in the early
postoperative period following cardiac surgery, in the catheterization lab, or when the
patient is already connected to a defibrillator and the cardiac arrest is witnessed.
REFERENCES
1. Jacobs I, Sunde K, Deakin CD, et al. Part 6: Defibrillation. 2010 International Consensus on
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with
Treatment Recommendations. Circulation. 2010;122(16 Suppl 2):S325–S337.
2. Link MS, Atkins DL, Passman RS, et al. Part 6: Electrical therapies: Automated external
defibrillators, defibrillation, cardioversion, and pacing. 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010;122(18 Suppl 3):S706–S719.
3. Haskell SE, Atkins DL. Defibrillation in children. J Emerg Trauma Shock. 2010;3(3):261–
266.
4. Deakin CD, Nolan JP, Sunde K, et al. European Resuscitation Council Guidelines for
Resuscitation 2010. Section 3: Electrical therapies: Automated external defibrillators,
defibrillation, cardioversion and pacing. Resuscitation. 2010;81(10):1293–1304.
5. Dosdall DJ, Fast VG, Ideker RE. Mechanisms of defibrillation. Annu Rev Biomed Eng.
2010;12:233–258.
6. Hooker DR, Kouwenhoven WB, Langworthy O. The effect of alternating electric currents on
the heart. Am J Physiol. 1933;103:444–454.
7. Travers AH, Rea TD, Bobrow BJ, et al. Part 4: CPR overview. 2010 American Heart
Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular
Care. Circulation. 2010;122(18 Suppl 3):S676–S684.
ADDITIONAL READING
• Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life support.
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S729–S767.
CLINICAL PEARLS
• During external defibrilation, avoid an oxygen-rich environment as this might lead to an
increased risk of fire (remove insufflations of oxygen over the field of defibrillation as well
as face masks or nasal cannulas; however, keep endotracheal tubes connected to the
ventilator).
• Automated external defibrillators (AEDs) are easy-to-use, computerized devices that use
voice and visual prompts to aid lay rescuers and healthcare professionals to safely
defibrillate Vfib and pulseless Vtach. AEDs automatically analyze a surface ECG signal and
recommend the delivery of a shock, if indicated. The use of AEDs in combination with CPR
in public locations (airports, casinos, sports facilities) has doubled the number of survivors
in those public areas.
DEMENTIA
Kamilia S. Funder, MD
Jacob Steinmetz, MD, PhD
BASICS
DESCRIPTION
• Dementia describes a progressive loss of intellectual functions such as memory, learning,
problem solving, and abstract thinking, resulting in occupational and social decline.
Consciousness remains unaffected.
• It can be classified into different subtypes:
– Alzheimer’s disease dementia (AD); accounts for 50% of all cases
– Vascular dementia
– Lewy body dementia
– Parkinson’s dementia
– Frontotemporal dementia
EPIDEMIOLOGY
Incidence
4.6 million new cases worldwide each year and doubling every 20 years (1)
Prevalence
• 29 million people suffer from dementia globally.
• Affects 4% of people above 60 years of age
• Doubles with every 5-year increase in age
• More prevalent in developing countries
Morbidity
• Impaired social and occupational functioning
• Higher risk of depression
Mortality
• Accounts for 3.4% of all deaths in high-income countries
• Limited treatment and poor prognosis
• Highly associated with advancing age
• Degenerative neuropathological changes such as cerebral atrophy and plaques (2)
• Cerebrovascular disease (CVD)
• Female gender
PATHOPHYSIOLOGY
• The pathogenesis is not fully uncovered; it is likely the result of complex interactions
between genes, lifestyle factors, and other environmental influences.
• Mutations in genes that control the production of proteins like amyloid precursor protein
(APP), presenilin 1+2, and apolipoprotein E (apoE), may play a role.
• Evidence suggests that triggers, such as protein aggregation (e.g., Lewy bodies),
accumulation of β-amyloid plaques, infection, inflammation, and hypothermia, may play a
role.
• Assess cognitive function and optimize the perioperative setting accordingly in order to
minimize external stress
• Optimize physical health status
• Restrict drug usage to avoid drug interactions and polypharmacy; carefully titrate all
medications
• Patience is crucial
SYMPTOMS
• Problems with concentration, language, and ability to recognize objects/family members (2)
• Memory loss, especially short-term memory
• Later: Irritability, agitation, apathy
History
• Type and severity of dementia; recent worsening
• Family history
• Concurrent diseases, including atherosclerosis, and diabetes
• Smoking and alcohol use
• Current activity level
• Social relations and adequacy of home care
• Cognitive capacity
Signs/Physical Exam
• Identify any signs of stroke and perform a neurologic examination
• Difficulty comprehending detailed information
• Exclusion of any treatable, reversible condition such as depression, delirium, intoxication,
and normal pressure hydrocephalus
TREATMENT HISTORY
None
MEDICATIONS
• Antidepressants
• Anti-Parkinson drugs. Reports suggest that Selegiline (MAO-B inhibitor) in combination with
meperidine/pethidine may cause agitation and muscle rigidity (3). Before the use of
decarboxylase inhibitors, peripheral conversion of L-DOPA to dopamine may have caused
orthostatic hypotension because of peripheral vasodilatation (4).
• Anxiolytics
• Acetylcholinesterase inhibitors may decrease the duration of muscle relaxants.
• Herbal supplements
Labs/Studies
• Minimal Mental State Examination (MMSE) to assess cognitive skills
• Laboratory tests: CBC, electrolyte status, blood glucose test, only rarely consider thyroid and
thyroid-stimulating hormone levels, Urineanalysis including toxicology screen
• Neurologic deficits
• Possible altered pain perception and drug sensitivity (2)
• Suboptimal physical health and unstable psychiatric patients
• Failure to obtain informed consent from patient or representative (e.g., family member)
CLASSIFICATIONS
Severity of dementia can be classified according to the MMSE. Maximum score is 30:
• Score ≥25 indicates no cognitive impairment.
• Score between 21 and 24 indicates mild dementia.
• Score from 10 to 20 indicates moderate dementia.
• Score <10 corresponds to severe dementia.
TREATMENT
Premedications
• Preoperative analgesics should be administered similar to other frail patients.
• If an anxiolytic is indicated, utilize short-acting benzodiazepines.
• Neuroleptics are best avoided because of a potential increased risk of extrapyramidal side
effects. Demented patients may be particularly sensitive (5).
• If antipsychotics are warranted, risperidone and clozapine are generally better tolerated
than haloperidol (2).
• Require great patience
• Correction of sensory deficit (e.g., hearing aid and glasses) to facilitate the patient’s
perception
• Assessment of the ability to make informed consent by ensuring that the patient is able to
retain and process the information given. Help from family members is often needed.
INTRAOPERATIVE CARE
• No significant advantage of regional anesthesia compared to general anesthesia, but may
improve recovery and minimize opioid use (2).
• Inhalational anesthetics might be easier to adjust individually, using end-tidal concentration,
compared to intravenous anesthesia (2).
• Intravenous anesthetics should, in general, be titrated and given in smaller doses to elderly
demented patients secondary to altered pharmacodynamics and pharmacokinetics.
– Decreased renal and hepatic clearance due to decreased organ mass and blood flow in the
elderly
– Decreased volume and rate of distribution; dependent on protein binding, cardiac output,
and blood volume which are altered in the elderly
– Increased drug sensitivity (2)
• Risk of opioid-induced muscle rigidity
• Risk of hyperkalemia following succinylcholine, especially in patients with neuromuscular
disorders (e.g., Parkinson’s dementia)
Monitors
• Consider arterial blood pressure monitoring
• Foley catheter to monitor urine output and thereby hemodynamic status (or to avoid the
mess that may be made from incontinence)
• Bispectral index (BIS) monitoring may assist the administration of hypnotics, by measuring
the depth of anesthesia. Baseline BIS might be lower in demented patients (2).
• Reduce induction medication doses and administer slowly to avoid excessive hemodynamic
depression and prolonged recovery
• Vasopressor agents should be easily available.
• Be aware of previous history of difficult intubation. Limited head and neck movement may
impede tracheal intubation; prepare to have an alternative airway management plan.
• Neuromuscular blocking agents (NMBAs) should be used with caution because of risk of
drug interactions, especially combined with acetylcholinesterase inhibitors used for treating
AD (2).
Maintenance
• Volatile anesthetics: Use end-tidal concentrations to maintain adequate dose. MAC can be
reduced by 30–50% in patients above 80 years of age (2).
• Intravenous anesthetics should be infused at lower rates in order to maintain a lower plasma
concentration.
• Avoid bolus injections. Because of altered pharmacokinetics and pharmacodynamics, the
administration of anesthetics and pain-relieving treatments should be carefully titrated to
minimize the risk of adverse drug effects or excessive responses.
• Avoid perioperative hypothermia. Elderly patients are more prone to hypothermia as a
result of reduced metabolism, and animal studies suggest that hypothermia might be an
independent risk factor for Alzheimer’s disease (2).
• Avoid antiemetics with anti-dopaminergic properties
• Dose reduction of anesthetics and analgesics will help promote an uneventful recovery.
• Shorter-acting drugs may be beneficial.
POSTOPERATIVE CARE
BED ACUITY
• Continue close monitoring
• Encourage quick mobilization by sufficient pain control. Consider using The Mobilization-
Observation-Behavior-Intensity-Dementia (MOBID) pain scale.
• Ensure calm surroundings to aid the patients sleep and minimize stress
• Early discharge can help facilitate a patient’s return to well-known surroundings.
• Resume daily medication
COMPLICATIONS
• Hemodynamic depression
• Hypothermia
• Delirium
• Postoperative cognitive dysfunction (POCD)
• Unrecognized pain
• Reduced compliance
REFERENCES
1. Ferri CP,Prince M, Brayne C, et al. Global prevalence of dementia: A Delphi consensus
study. Lancet. 2005;366:2112–2117.
2. Funder KS, Steinmetz J, Rasmussen LS. Anesthesia for the patient with dementia. J
Alzheimer Dis. 2010;22(Suppl 3):129–134.
3. Zornberg GL, Bodkin JA, Cohen BM. Severe adverse interaction between pethidine and
selegiline. Lancet. 1991;337:246.
4. icholson G, Pereira AC, Hall GM. Parkinson’s disease and anaesthesia. Br J Anaesth.
2002;89:904–916.
5. Pijnenburg YA, Sampson EL, Harvey RJ, et al. Vulnerability to neuroleptic side effects in
frontotemporal lobar degeneration. Int J Geriatr Psychiatry. 2003;18:67–72.
6. World Health Organization (WHO). www.who.int/en/
• Hypothermia
CODES
ICD9
• 294.10 Dementia in conditions classified elsewhere without behavioral disturbance
• 294.20 Dementia, unspecified, without behavioral disturbance
• 331.0 Alzheimer’s disease
ICD10
• F01.50 Vascular dementia without behavioral disturbance
• F03.90 Unspecified dementia without behavioral disturbance
• G30.9 Alzheimer’s disease, unspecified
CLINICAL PEARLS
• Patience is essential. Obtain help and information from family membe
• Careful drug titration; onset is delayed.
• Huge variability in physical status of the elderly, but co-morbidity is common.
DENTAL DAMAGE
David W. Lui, DMD, MD
BASICS
DESCRIPTION
• Amongst the most common claim against anaesthetist. Damage can occur from
laryngoscopy, hard suction catheters, and the insertion, removal, or biting on emergence of
the airway device or oral airway.
• The incidence increases in patients with pre-existing dental disease, difficult and emergent
intubations, or the skill of the laryngoscopist.
• Types of damage include avulsions (complete removal), damage to crowns and bridges,
dislocation, and fractures.
EPIDEMIOLOGY
Incidence
• Damage is difficult to assess due to inconsistent reporting or recognition; ranges from 0.02%
to 12.1% (1).
• Dental injury requiring dental intervention is estimated to occur in 1:4,500 anesthetics (1).
• Damage in the setting of:
– Difficult intubation: 20% of all cases
– >2 laryngoscopy attempts: 1–4%
– Trainees/level of training: Surprisingly incidence amongst residents is lower than
“experienced” hands (1,2,3)
• Damage during:
– Intubation: 50–75%
– Extubation or recovery room: 9–20% (2)
• Maxillary incisors (#8, #9) are most commonly injured.
• Types of damage:
– Enamel fractures and partial dislocation: 55.2%
– Avulsion: 9%
– Crown fracture: 7.7% (3)
Prevalence
Age 45–65 years: Approximately 2/3rd of all claims
Morbidity
Aspiration of the tooth or fragments, particularly if it goes unnoticed or unrecognized
• Laryngoscopy in the setting of:
– Difficult intubations; small mouth opening, prominent upper teeth, poor neck mobility,
large neck, and small thyromental distance
– Emergency intubations
– Pre-existing dental condition; caries, periodontitis
– Restorations, prosthetics; synthetic materials may not be as “hard” as natural enamel
(1,2,3).
• Traumatic insertion, removal, or biting of the airway device or oral airway
• Hard suction catheters
• There are 16 maxillary teeth and 16 mandibular teeth. The Universal Numbering System
provides a method to identify teeth: Maxillary teeth are #1–16 and mandibular teeth are
#17–32.
• The tooth is composed of a crown (enamel and dentin) and the root (cementum and pulp):
– Enamel is the exposed portion of the tooth. It is composed of mineralized substances and
is the hardest substance in the human body.
– Dentin lies directly underneath and is softer than enamel. However, it functions to provide
a foundation or framework.
– Cementum is a specialized bony substance covering the root of a tooth. It functions in
providing a substance to which the periodontal ligaments can attach to.
– Pulp is the innermost portion. It contains nerves and blood vessels and connects to the
gums.
• The periodontium is composed of the periodontal ligaments, gingiva, and alveolar bone.
• Laryngoscopy: Blades attached to a handle are utilized to displace the tongue and epiglottis
in order to insert the endotracheal tube. They are composed of metal and are inflexible and
noncompliant. Optimal patient positioning and laryngoscopy technique aim to align the
oropharynx, hypopharynx, and larynx in order to attain direct visualization of the glottis
opening.
– In the event that this alignment is not, or cannot, be achieved, the laryngoscopist may be
more likely to “crank” the wrist and utilize the maxillary teeth (maxillary central incisors
#8, #9) as a fulcrum.
– In addition to the vulnerable location during laryngoscopy, teeth #8 and #9 are single
rooted and have a small cross-sectional area.
– These 2 incisors are estimated to be involved in >90% of reported instances of dental
damage.
• Airway devices: Endotracheal tubes, laryngeal mask airways, bite blocks, and oral airways
can cause damage during insertion, removal, or biting during emergence.
• Pre-existing dental conditions increase the risk of dental injury.
– Cavities or caries consist of a bacterial process that causes rotting of the root.
– Periodontal disease consists of gingival inflammation, alveolar bone loss, and tartar build-
up.
• Restorations and prosthetics increase the risk of dental injury:
– Bridges: Replacement of one or more missing teeth. A pontic is fused between 2 porcelain
crowns to fill in the space left by the missing teeth.
– Bonding: Restoration of decaying teeth or cosmetically improving teeth (discoloration,
abnormal shapes, small gaps). A composite resin filling is applied to the anterior face of
the tooth, followed by a bonding material that can be shaped or colored to achieve the
desired result.
– Veneers: Improvement cosmetically of discolored, worn, chipped, or misaligned teeth
– Crowns: Coverage of the visible surface of a decayed or worn-down tooth in order to
reduce further wearing down
• Pulmonary aspiration of foreign body: Detection requires identification of the event. Any
missing tooth should be assumed to have been aspirated until proven otherwise. A chest
radiograph can identify the presence and location.
• Preoperative evaluation and assessment of the airway should include the dentition:
– Loose teeth
– Chips
– Fractures
– Restoration or prosthetics (crowns, bridges, veneers, bonding)
– Periodontal disease
• Documentation preoperatively: If pre-existing dental disease is present, the patient should be
informed and findings should be confirmed with the patient. Documentation should include
a careful description of the preoperative evaluation record.
• Consent: Anesthesia consent should include a verbal discussion, followed by a written
consent that is signed by the patient or their designated caretaker/power of attorney
regarding the possibility of dental injury. More time or attention should be given to those
with pre-existing dental disease or anticipated difficult intubation.
• Alternative airway management:
– Anticipated difficult intubation: May be prudent to preemptively utilize special airway
management tools such as fiberoptic bronchoscopy, indirect laryngoscopy tools
(GlideScope, etc.), laryngeal mask airway guided intubation, etc. If laryngoscopy is to be
attempted, consider special angulated blades (McCoy, Belscope), plastic blades, or blades
with soft heels.
– Unexpected difficult airways: Consider alternative devices early to avoid repeated
laryngoscopy attempts and fulcruming the laryngoscope.
• Standard and routine laryngoscopy: Should avoid teeth with gentle insertion and
advancement. Proper patient positioning (head, neck, shoulder rolls, ramps), pre-
oxygenation (“buys time” before desaturation), and avoidance of “cranking” the wrist
should always be performed.
• Tooth guards: Routine use is controversial. They may impair visualization, insertion of the
endotracheal tube, or increase apneic time. One study demonstrated that insertion increased
intubation time by 7 seconds (statistically significant) (4).
• Insertion and removal of airway devices and bite blocks should always be done gently.
Laryngeal mask airways have a thicker diameter and are less compliant than endotracheal
tubes. Avoid forceful pulling and removal of items while the patient is biting (downward
movement).
• Soft bite blocks constructed from gauze may reduce damage from biting of the endotracheal
tube. Consider utilizing when motor evoked potentials are being performed.
• Dental consultation and treatment prior to surgery for dentition “at risk” for avulsion or
further damage may prevent or reduce the incidence of damage. If this is not feasible, one
technique that has been suggested is the wrapping of suture around the gingival margins
several times and taping the other end to the cheek.
• Studies have suggested that despite careful attention to poor dentition, the risk of dental
lesions cannot be completely eliminated.
DIAGNOSIS
• Visual inspection after routine intubation with documentation in the anesthetic record may
reduce ambiguity postoperatively.
• Visual inspection following a difficult or traumatic intubation, suctioning, insertion or
removal of other airway devices is always suggested (1).
• Missing teeth should be assumed to have been aspirated until proven otherwise. A chest
radiograph can easily rule out this possibility.
Pre-existing chips, fractures, missing teeth (a careful preoperative evaluation will remove any
doubts or confusion)
TREATMENT
• Dental consultation
• Avulsed and retrieved. Transport medium of choice is Hanks Balanced Salt Solution,
followed by cool milk, saliva, and cool saline. In the operating room, cool saline may be the
most easily available.
• Avulsions may require repositioning and splinting with non-rigid fixation (wire) for 7–10
days.
• Tooth fractures can range from composite bonding, to root canal therapy (with coronal
restoration), to dental extraction, depending on the size/depth/location of the fracture.
• Alveolar fractures require segmental arch bar placement.
• Consider antibiotics and Peridex oral rinse in the event of any dental or intraoral injury. If
the damage extends extraorally, check for tetanus status and vaccinate if indicated.
FOLLOW-UP
• A discussion with the patient and family should inform them of the situation as well as the
immediate efforts that will be taken to remedy the situation (dental consultation).
• Dental consultation may be coordinated while an inpatient if appropriate.
• Reimbursement may be considered as per department, group, or hospital policy.
CLOSED CLAIMS DATA
• Reported to the National Practitioner Data Bank
• Estimated to be as high as 1/3rd of all claims against anesthesiologis (3)
REFERENCES
1. Yasny JS. Perioperative dental considerations for the anesthesiologist. Anesth Analg.
2009;108(5):1564–1573.
2. Rosa Maria G, Paolo F, Stefania B, et al. Traumatic dental injuries during anaesthesia. Part
1: Clinical evaluation. Dental Trauma. 2010;26(6):459–465.
3. Warner ME, Benenfeld SM, Warner MA, et al. Perianesthetic dental injuries. Anesthesiology.
1990;90:1302–1305.
4. Brosnan C, Radford P. The effect of a toothguard on the difficult of intubation. Anaesthesia.
1997;52:1011–1012.
ADDITIONAL READING
• Gasier RR, Castro AD. The level of anesthesia resident training does not affect the risk of
dental injury. Anesth Analg. 1998;87:255–257.
• Givol N, Gershtansky Y, Halamish-Shani T, et al. Perianesthetic dental injuries: Analysis of
incidence reports. J Clin Anesth. 2004;16:173–176.
• Newland MC, Ellis SJ, Peters KR, et al. Dental injury associated with anesthesia: A report of
161,687 anesthetics given over 14 years. J Clin Anaesth. 2007;19:339–345.
CODES
ICD9
• 525.11 Loss of teeth due to trauma
• 525.63 Fractured dental restorative material without loss of material
• 525.64 Fractured dental restorative material with loss of material
ICD10
• S03.2XXA Dislocation of tooth, initial encounter
• S02.5XXA Fracture of tooth (traumatic), init for clos fx
• S02.5XXB Fracture of tooth (traumatic), init encntr for open fracture
CLINICAL PEARLS
• A preoperative exam of dentition should be performed on every patient receiving an
anesthetic. Additionally, in the event of pre-existing disease, it should be confirmed with the
patient and appropriately documented in the preoperative evaluation.
• Routine examination following airway management may reduce the ambiguity of pre-
existing or postoperative incidents that can be misconstrued or mislabeled as intraoperative
dental damage. In patients in whom injury may have occurred (difficult intubation,
traumatic insertion or removal of airway devices or oral airway, biting down on the suction
catheter) it is prudent to do so.
• Identification of dental damage should be discussed with the patient, and appropriate
follow-up should be determined and coordinated.
DEPRESSION
Dmitri Souzdalnitski, MD, PhD
Samuel Samuel, MD
BASICS
DESCRIPTION
• Major depressive disorder (also known as “depression”) can be diagnosed on the basis of one
or more major depressive episodes. The symptoms cause significant distress as well as
impairment in social, occupational, and/or other important areas of functioning.
• Symptoms persist for longer than 2 months and are characterized by distinct functional
impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic
symptoms, or psychomotor retardation.
• The diagnostic criteria for a depressive episode requires that 5 (or more) of the following
symptoms have been present during a 2-week period and represent a change from previous
function (1)[A] and that at least one of the symptoms has to be either a depressed mood or
(2) loss of interest or pleasure:
– Depressed mood
– Noticeably diminished interest or pleasure
– Significant weight loss (when not dieting) or weight gain, or decrease/increase in appetite
– Insomnia or hypersomnia
– Psychomotor agitation or retardation
– Fatigue or loss of energy
– Feelings of worthlessness or excessive/inappropriate guilt
– Diminished ability to think or concentrate, indecisiveness
– Frequent thoughts of death or suicide
EPIDEMIOLOGY
Incidence
2.0–4.5 per 1,000 persons per year (2)[B]
Prevalence
• Lifetime prevalence rates for significant depressive symptoms are 11–21% and 3–7% for
major depressive disorder.
• Rates in women and men are highest in the 25–44 year-old age group.
• Major depressive disorder is about 2–3 times as common in adolescent and adult females as
in adolescent and adult males.
• In children, boys and girls are affected equally.
Morbidity
Rather than producing its own morbidity, depression commonly influences the morbidity
resulting from other medical conditions. For example, it complicates the management of
patients with chronic back pain. 9% of these patients take anti-anxiety medications, and 25%
take antidepressants (3)[B].
Mortality
• One in 7 patients with major depressive disorder eventually dies by suicide.
• Major depression accounts for about half of suicides, which are the 8th leading cause of
death in the US.
• Various genetic, biological, or psychosocial models have been implicated in the etiology of
depression. However, the exact cause of major depressive disorder is not known.
• The traditional thinking that depression follows a triggering event, such as emotional
trauma, has been observed in fewer than 20% of patients. The following risk factors have
also been observed:
– Alcohol or drug abuse
– Loneliness
– Inadequate social support
– Remote significant emotional trauma
– Recent negative life events
– Financial problems
– Unemployment or underemployment
– History of depression in the family
– Medical problems, chronic pain
– Early childhood trauma or abuse
– Marital or relationship problems
– Terminally or severely ill children
– Insecure
PATHOPHYSIOLOGY
• The exact mechanism of development of major depressive disorder is unknown. Commonly
discussed mechanisms are:
– Biological: Genetically mediated neurotransmitter misbalance of norepinephrine,
serotonin, dopamine, acetylcholine, gamma-aminobutyric acid, melatonin, glycine,
histamine, etc.
– Neuroendocrine and hormonal mechanisms: Corticotropin-releasing hormone, endorphins,
enkephalins, vasopressin, cholecystokinin, substance P, thyroid and adrenal hormones,
and others
– Psychoanalytic, psychodynamic, and behavioral mechanisms
• Literature recommends that anesthetist be more sensitive to the psychological concerns in
depressed patients who are undergoing surgery.
• Antidepressants are important elements in the treatment of depression and should be
continued in the perioperative period with certain exceptions (discussed in the
“Medications” section).
SYMPTOMS
• Commonly reported symptoms are:
– Depressed mood
– Feelings of helplessness and hopelessness
– Anhedonia
– Irritability or restlessness
– Change in appetite
• Weight changes
• Unexplained aches and pains
• Change in sleep
• Change in body activity
• Loss of interest in daily activities
• Loss of energy
• Feelings of worthlessness
• Excessive or inappropriate guilt
• Indecisiveness or decreased concentration
• Suicidal ideation
History
• Clues to potential depression also include the general appearance and manners of
communication of the patient.
• Review relevant medical records, including history of suicide, emotional trauma, domestic
violence, abuse, etc.
• Family history may be helpful as well. For example there is a high risk for clinical
depression in families with history of depression (7%) or alcoholism (8%).
Signs/Physical Exam
• Physical exam findings may demonstrate poor eye contact, malnutrition, disheveled
appearance, or other evidence of poor personal hygiene.
• A further exam may reveal certain personality changes. They might be worried, introverted,
stress sensitive, obsessive, unassertive, very dependent.
TREATMENT HISTORY
• Outpatient counseling
• Psychiatric admissions
• Electroconvulsive therapy
MEDICATIONS
• Selective serotonin reuptake inhibitors (SSRIs)
• Serotonin/norepinephrine reuptake inhibitors (SNRIs)
• Tricyclic antidepressants (TCAs)
• Monoamine oxidase inhibitors (MAOIs)
• Lithium
• Antipsychotics
Labs/Studies
Not applicable to the anesthetist
It is not uncommon to have concurrent chronic pain problems. If this is the case, the
perioperative pain management should be carefully planned and discussed with the patient in
details.
Typically, cases are not delayed because of depression.
CLASSIFICATIONS
• Major depression (one or more episodes)
• Melancholic subtype
• Atypical depression
• Seasonal affective disorder
TREATMENT
Premedications
Benzodiazepines to decrease preoperative anxiety
No special concerns for informed consent
INTRAOPERATIVE CARE
General or regional, or MAC anesthesia for routine cases
Monitors
• Serum cholinesterase activity may decrease in patients treated with phenelzine; thus, the
dose of succinylcholine may need to be reduced.
• Ketamine should be avoided in patients taking MAOIs since it may exaggerate the
sympathetic stimulation.
Maintenance
• Any volatile anesthetic with or without nitrous oxide is acceptable for maintenance of
general anesthesia.
• The MAC may be higher in patients with depression because of the medications they are on
(MAOIs, SSRIs, SNRIs, TCAs).
• The epinephrine used for spinal anesthesia should be limited in patients taking MAOIs
because of the potential of an exaggerated sympathetic response.
No special considerations in extubation or emergence in patients with depression
POSTOPERATIVE CARE
BED ACUITY
No special considerations
• Brief psychological screening. Also, if needed, a comprehensive assessment and assistance
from mental health professionals to improve the depressed patient’s and his/her family’s
experience during the acute postoperative period.
• The analgesic potency has been demonstrated for some of the antidepressant medications.
TCAs, duloxetine, milnacipran, and several others are approved for the treatment of chronic
neuropathic or myofascial pain. These medications, therefore, may contribute to the overall
effects of postoperative pain management.
• SSRIs and SNRIs should be continued at preoperative dosages.
• TCAS should be continued at their regular dose in the perioperative period.
– Adverse effects are common, and patients should be re-evaluated if there is evidence of
sedation and delirium, or other anticholinergic effects, particularly in elderly patients.
– Cardiovascular risks at regular doses are extremely low.
COMPLICATIONS
• Meperidine should be avoided in combination with SSRIs (paroxetine, fluoxetine, sertraline,
citalopram, and others), MAOIs, and certain other antidepressant medications (phenelzine,
selegiline, tranylcypromine) since these combinations may produce somatic, autonomic, and
neuropsychiatric derangements (including hyperreflexia, myoclonus, ataxia, fever,
shivering, diaphoresis, diarrhea, anxiety, salivation, confusion and others, termed “serotonin
syndrome”).
• Less than 1% of all patients treated with antipsychotic drugs may develop a neuroleptic
malignant syndrome (presenting as hyperthermia, hypertonicity of the skeletal muscles,
fluctuating levels of consciousness and autonomic nervous system instability), and it is
therefore advisable that patients taking antipsychotics should be very closely monitored in
the perioperative period.
REFERENCES
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders,
4th ed., text revision. Washington, DC: American Psychiatric Association, 2000.
2. Kruijshaar ME, Barendregt J, Vos T, et al. Lifetime prevalence estimates of major
depression: An indirect estimation method and a quantification of recall bias. Eur J
Epidemiol. 2005;20(1):103–111.
3. Walid MS, Robinson JS, 3rd, Robinson ER, et al. Comparison of outpatient and inpatient
spine surgery patients with regards to obesity, comorbidities and readmission for infection.
J Clin Neurosci. 2010;17(12):1497–1498.
ADDITIONAL READING
• Ebert TJ, Schid PG. Inhaled anesthetics. In: Barash PG, et al., eds. Clinical anesthesia, 6th
ed. Philadelphia: Lippincott Williams & Wilkins, 2009:424.
• Hines RL, Marschall KE. Psychiatric disease/substance abuse/drug overdose. In: Hines RL,
Marschall KE, eds. Stoelting’s anesthesia and co-existing disease, 5th ed. Philadelphia:
Churchill Livingstone, 2008:533–538.
• Electroconvulsive therapy
• Complex regional pain syndrome type I
• Complex regional pain syndrome type II
CODES
ICD9
• 296.20 Major depressive affective disorder, single episode, unspecified
• 296.30 Major depressive affective disorder, recurrent episode, unspecified
• 311 Depressive disorder, not elsewhere classified
ICD10
• F32.9 Major depressive disorder, single episode, unspecified
• F33.9 Major depressive disorder, recurrent, unspecified
CLINICAL PEARLS
• Earlier recommendations suggested discontinuation of MAOIs 14 days prior to elective
operations, to permit the restoration of normal enzyme activity. The current literature
suggests that anesthesia can be safely administered to patients being treated with MAOIs.
However, excessive sympathetic stimulation or use of sympathomimetic drugs should be
limited.
• Patients with a history of bipolar disorder may be on lithium. It is important to be aware of
signs of acute lithium intoxication: Vomiting, profuse diarrhea, tremor, confusion,
hyperreflexia, ataxia, coma, convulsions, and seizures. The toxicity can be triggered by
drugs that reduce lithium excretion or increase reabsorption, such as NSAIDs, ACE
inhibitors, thiazide diuretics, and metronidazole. Cardiac toxicity can be presented as sinus
dysfunction, T-wave flattening, ventricular arrhythmia, and myocarditis. Lithium
potentiates depolarizing and non-depolarizing neuromuscular blocking drugs causing
potentially dangerous reactions with ECT.
DIABETES INSIPIDUS
Keren Ziv, MD
BASICS
DESCRIPTION
• Diabetes insipidus (DI) describes a disease process defined by polyuria and polydipsia
resulting from either:
– Decreased or absent secretion of antidiuretic hormone (ADH)
– Resistance to the action of ADH at the level of the kidneys
• There are multiple etiologies:
– Neurogenic
– Nephrogenic
– Dipsogenic
– Gestational
EPIDEMIOLOGY
Incidence
• Occurs during the postoperative course in ∼30% of pituitary surgeries, although the course
is usually transient
• Overall incidence is difficult to obtain due to the various etiologies of DI.
Prevalence
• 1 in 25,000
• Equal prevalence in males and females
Morbidity
• Severe dehydration resulting in hypernatremia
• Fever and cardiovascular collapse can occur in patients with coexisting illnesses, the elderly,
or children.
Mortality
Rare, especially in adults without coexisting illness. However, may occur if treatment is
delayed in children or the elderly in which the disease progresses to complete cardiovascular
collapse.
• Neurogenic: Decreased production of ADH by the hypothalamus in the brain. Risk factors
include:
– Trauma
– Tumor in the region of the pituitary or hypothalamus
– Surgery in the region of the pituitary or hypothalamus
• Nephrogenic: Decreased sensitivity to ADH by the kidneys. The most common cause in
children is hereditary; 90% are associated with mutations in the AVPR2 gene that encodes
for a dysfunctional vasopressin receptor (V2R). In adults, acquired nephrogenic DI is usually
secondary to medications such as lithium, foscarnet, cidofovir, amphotericin B,
demeclocycline, as well as a result of chronic hypercalcemia and hyperkalemia.
• Dipsogenic: Defect in the thirst trigger (located in the hypothalamus) which causes
increased thirst and fluid intake that subsequently suppresses vasopressin secretion and
increases urine output.
• Gestational: During pregnancy, all women produce vasopressinase by the placenta, which
breaks down ADH. When excess vasopressinase is produced, gestational DI will occur. This
etiology is the most common and can be treated by desmopressin.
– In a small subset of patients, the thirst mechanism is disrupted, causing DI; it is not
improved with desmopressin.
– DI is also associated with other diseases of pregnancy, such as preeclampsia and HELLP
syndrome. In these disease processes, hepatic vasopressinase is activated, and the only
treatment is delivery of the fetus.
PATHOPHYSIOLOGY
• Hypothalamus: Produces ADH in the supraoptic and paraventricular nuclei. ADH is then
transported to the posterior lobe of the pituitary gland where it is stored for later use. It is
released when the body senses that electrolyte and/or fluid status are unbalanced.
• Kidney: The primary target for ADH and water retention; the hormone acts on the collecting
ducts and distal convoluted tubules (DCT) to allow more water to be reabsorbed into the
systemic circulation and therefore create a more concentrated urine.
• Thirst sensation: Also regulated by the hypothalamus when it senses decreases in serum
osmolarity.
• In DI, either ADH secretion is deficient or the renal response to ADH is abnormal. This
results in the following pathology:
– Increased urine output; water remains in the urine (polyuria)
– Decreased body water (dehydration)
– Increased serum [Na+]
– Increased serum osmolality
– Decreased urine osmolality or specific gravity
– Decreased urine [Na+]
– No change in total body sodium
– No change in urine sodium excretion
• The possibility of DI should be evaluated in patients who present perioperatively with
hypernatremia or excessive urine output; in particular, those who have had traumatic
injury, tumor, status post surgery in the region of the pituitary or hypothalamus, or are
pregnant.
• In patients with known DI, electrolyte abnormalities may be present perioperatively. It is
important to have recent chemistry labs done prior to anesthesia. Treatment may need to be
administered perioperatively by the anesthetist.
SYMPTOMS
• Polyuria (4–18 L/day) with acute onset, usually within 24–48 hours of neurosurgery
• Polydipsia, often with a craving for cold fluids
• Hypovolemia: Depending on whether thirst mechanism is intact
• Nocturia, enuresis in children, anorexia, fatigue
History
• Central DI usually presents abruptly in patients with pituitary/hypothalamic surgery, head
trauma, or malignancy.
• Familial nephrogenic DI presents in early childhood.
• Psychogenic polydipsia may have a long history.
Signs/Physical Exam
• Minimal typically
• Dehydration
• In rare cases, there may be bladder enlargement
TREATMENT HISTORY
When patients are awake, they can usually drink enough fluids to replace their urine losses.
Patients with inadequate thirst, however, may be treated with dextrose and water or IV fluid
that is hypoosmolar with respect to the patient’s serum. Serum sodium should not be reduced
too quickly, ideally only 0.5 mEq/L/hr.
MEDICATIONS
• ADH therapy: Desmopressin (DDAVP) is a synthetic analog to endogenous vasopressin but
with greater platelet and antidiuretic effects and decreased blood pressure effects. It binds
to V2 receptors in the renal collecting duct, causing increased water reabsorption in the
kidney (increased urine osmolality, decreased urine output, and no effect on sodium,
potassium, or creatinine reabsorption.
– Intravenous: 1–2 mcg BID, onset 15–50 minutes
– Oral: 0.05 mg BID, onset 60 minutes
– Nasal: 5–40 mcg BID
– The duration of action is highly variable and lasts from 5 to 21 hours. Additionally, it is
renally excreted; thus, renal failure will prolong its action and dosage adjustments should
be considered.
Labs/Studies
• Urine specific gravity <1.005
• Urine osmolality <200 mOsm/L
• Serum [Na+] >145 mEq/L
• A trial with desmopressin is used to distinguish between neurogenic and nephrogenic
causes. If desmopressin reduces urine output and increases osmolarity, the pituitary
production of ADH is deficient, and the kidney is normal. If the DI is due to renal pathology,
desmopressin does not change either urine output or osmolarity.
• MRI technology is being explored as a diagnostic tool.
Electrolyte abnormalities and dehydration may require optimization prior to surgery.
CLASSIFICATIONS
• Neurogenic
• Nephrogenic
• Dipsogenic
• Gestational
TREATMENT
Premedications
Consider administration of DDAVP either nasally or intravenously, if the clinical condition
dictates.
INTRAOPERATIVE CARE
No specific anesthetic choices are indicated aside from usual neuroanesthesia care and
concerns.
Monitors
• ASA monitors
• Additional monitoring should be based upon the patient disease and procedure
requirements. An arterial line (or central line) allows for serial monitoring of serum sodium
and osmolality.
• Foley catheter allows for accurate recording of fluid intake and output, and avoids
overdistension of the bladder. Also allows for serial monitoring of urine sodium and specific
gravity.
Usual neuroanesthesia induction
Maintenance
• Usual neuroanesthesia maintenance and concerns
• Fluids:
– Monitor ins and outs.
– Hypotonic IV fluids (hypoosmolar relative to the patient’s serum) should be used to match
the urine output.
– If using dextrose and water as fluid replacement, care must be taken to avoid
hyperglycemia; generally, administration should be limited to 500–750 mL/hr and glucose
levels should be monitored.
– When mannitol or furosemide must be administered to facilitate surgical conditions, it
may confuse the picture with respect to fluid losses and replacement. Close monitoring of
electrolytes, glucose, and serum osmolality as well as hemodynamic values should be used
to aid in fluid replacement, as urine specific gravity may be misleading.
• ADH therapy:
– Desmopressin 1–2 mcg/kg IV or SQ may be started or continued perioperatively.
– Re-dose if urine output remains >200–250 mL/hr for ≥2 hours with a urine specific
gravity <1.005 or urine osmolality <200 mOsm/L.
• Consider concomitant anterior pituitary insufficiency and the need for stress dose
corticosteroids.
Usual neuroanesthesia concerns
POSTOPERATIVE CARE
BED ACUITY
The patient will need a monitored setting to allow for frequent lab checks and possible
administration of DDAVP.
• DDAVP
• Careful measurement of I/Os, monitor for hypovolemia, especially if the patient is unable to
drink fluids freely
• Serial serum/urine sodium levels and serum/urine osmolality levels
• Endocrinology and neurology consults
COMPLICATIONS
If left untreated, may cause severe hypernatremia and the sequelae associated with this
derangement
REFERENCES
1. Nemergut EC, Dumond AS, Barry UT, et al. Perioperative management of patients
undergoing transsphenoidal pituitary surgery. Anesth Analg. 2005;101:1170–1181.
2. NIH. Diabetes insipidus. Publication No. 01-4620, December 2000.Saborio P, Tipton GA,
Chan JCM. Diabetes insipidus. Peds Rev. 2000;21(4):122–129.
3. Ozier Y, Bellamy L. Pharmacological agents: Antifibrinolytics and desmopressin. Best Pract
Res Clin Anaesthesiol. 2010;24:107–110. http://www.diabetesinsipidus.org/whatisdi.htm
• Hypernatremia
• Syndrome of inappropriate antidiuretic hormone (SIADH) release
• Serum osmolality
• Urine osmolality
CODES
ICD9
253.5 Diabetes insipidus
ICD10
E23.2 Diabetes insipidus
CLINICAL PEARLS
• Diabetes insipidus results from a deficiency in ADH secretion or abnormal renal response to
ADH.
• It manifests as polyuria/polydipsia with low urine osmolarity and hypernatremia.
• May present following neurosurgery, especially surgery of the pituitary or hypothalamus
• Usually presents within the first 24–48 hours postoperatively and is transient
DIABETES MELLITUS
BASICS
DESCRIPTION
• Diabetes mellitus (DM) has been increasing in the last several decades, likely due to its
strong association with obesity.
• DM is one of the leading causes of morbidity and mortality in the US population, with an
economic cost of $171 billion annually.
EPIDEMIOLOGY
Prevalence
In the US: 1.3 million new cases annually
Prevalence
In the US: 25.8 million people have the disease, accounting for 8.3% of the population.
Morbidity
A risk factor for perioperative surgical and anesthetic complications
Mortality
7th leading cause of death in the US
• Type I diabetes risk factors:
– Genetics and family history
– Infection or illness of the pancreas
• Type II diabetes risk factors:
– Obesity or overweight
– Impaired glucose tolerance
– Insulin resistance
– Hypertension
– History of gestational diabetes
– Sedentary lifestyle
– Family history
– Polycystic ovary syndrome
– Age
– Ethnic background: Diabetes occurs more often in African Americans, Hispanic Americans,
Native Americans, Asian Americans, and Pacific Islanders.
• Normally, blood glucose is tightly regulated by:
– The hormonal system which consists of a balance between the hypoglycemic insulin and
hyperglycemic counter-regulatory hormones such as glucagon, epinephrine, and cortisol.
– Neural mechanisms; glucose sensors in various organs are capable of sending messages.
– Together, these systems modulate carbohydrate metabolism by controlling endogenous
production and entrance of glucose into the cells.
• Type I diabetes is caused by the complete lack of insulin secretion from the pancreas. The
inability of cells to take in glucose leads to metabolic abnormalities, including
hyperglycemia, lipolysis, proteolysis, and ketogenesis.
• Type II diabetes is caused by insulin deficiency or insulin resistance and can result in
dehydration and a hyperosmolar state. Type II diabetes patients are usually ketosis-resistant
since their insulin concentration in the circulation is sufficient to prevent ketogenesis.
• Preoperative fasting, long-acting insulin or oral antihyperglycemics, and surgical stress can
result in episodes of hypoglycemia or hyperglycemia. Perioperative glucose testing and
treatment should be performed, as appropriate.
• Microvascular and macrovascular disease can result in end-organ damage; preoperative
evaluation should assess the involvement and severity. Maintain hemodynamic stability to
avoid hypoperfusion to the heart, brain, and kidneys.
• Consider the possibility of gastroparesis and pulmonary aspiration; if high risk, modify NPO
guidelines, premedicate to decrease gastric volume and acidity, and place a cuffed
endotracheal tube.
SYMPTOMS
• Polyuria, polydipsia, and polyphagia are associated with hyperglycemia and can suggest
new-onset diabetes.
• Autonomic neuropathy is associated with perioperative hypotension and may be suggested
by dizziness and syncope. Impotence is a sign of autonomic nervous dysfunction.
• Decrease in vision associated with diabetic retinopathy
History
• Assess metabolic control: Daily glucose level/range, usual dietary intake, physical activity,
hemoglobin A1C level, episodes of hypoglycemia or ketoacidosis, and medications.
• Assess the severity of concomitant organ dysfunction and optimize as appropriate. A prior
myocardial infarction is a clinical predictor for perioperative cardiac events. Hypertension
should be checked and controlled prior to surgery.
• Gastroparesis manifests as indigestion, nausea, vomiting, diarrhea, and abdominal
distension.
Signs/Physical Exam
• Usually nonspecific
• Abnormal physical exams are usually related to the complications associated with diabetes.
• “Stiff joint syndrome”: Limited joint mobility may be associated with a potentially difficult
tracheal intubation.
• Orthostatic hypotension or resting tachycardia associated with autonomic neuropathy
MEDICATIONS
• Exogenous insulin: The types of insulin include rapid-acting (Humalog, Novolog, Apidra),
short-acting (Regular, Velosulin), intermediate-acting (NPH, Lente), long-acting (Ultralente,
Lantus, Levemir), and pre-mixed (Humulin 70/30, Novolin 70/30, Novolog 70/30, Humulin
55/50, Humalog 75/25).
• Oral agents: Sulfonylureas stimulate the pancreas to release more insulin (glipizide,
glyburide, glimepiride). Biguanides improve the ability of insulin to move glucose
intracellularly (metformin). Thiazolidinediones improve the effectiveness of insulin
(pioglitazone, rosiglitazone). Alpha-glucosidase inhibitors block enzymes that digest starch;
they slow the rise in blood glucose (acarbose, miglitol). Meglitinides stimulate the pancreas
to release more insulin (repaglinide, nateglinide). Dipeptidyl peptidase IV inhibitors
increase insulin secretion from the pancreas and decrease glucose production from the liver
(sitagliptin, saxagliptin). Combination therapy combines the above-described mechanisms
for improved glycemic control (glyburide/metformin; glipizide/metformin;
rosiglitazone/metformin).
• ACE inhibitors or angiotensin receptor antagonists provide protective effects in diabetes
patients with CHF and renal insufficiency in addition to the treatment of hypertension. May
be associated with refractory hypotension.
Labs/Studies
• Labs: Glucose, HgA1C, BUN/Cr (renal function), electrolytes
• EKG: Silent ischemia or old infarcts
• Cardiac stress tests if indicated
• Neurologic: Cerebrovascular disease (stroke); peripheral neuropathy from direct mesangial
expansion and injury from chronic hyperglycemia
• Retinopathy is present in 28.5% of patients aged ≥40 years; it is the leading cause of new
cases of blindness in adults aged 20–74 years.
• Cardiovascular: Heart disease (comprises 68% of patients ≥65 years who died from
diabetes-related complications). Mechanisms are complex and multifactorial and are related
to both macrovascular and microvascular dysfunction. Hypertension (67% of diabetics);
progression is likely due to activation of the local renin–angiotensin system.
• Renal: Leading cause of renal failure (microvascular disease)
• Metabolic: Diabetic ketoacidosis (DKA) is the most serious acute metabolic emergency.
Hypoglycemia is more common than DKA in IDDM and is dangerous.
• Severe hypoglycemia or hyperglycemia, especially in patients with symptoms of ketoacidosis
or hyperosmolar nonketotic coma
• Acute infections
• Severe dehydration or electrolyte imbalance
CLASSIFICATIONS
• Type I diabetes (insulin-dependent) is caused by absolute insulin deficiency secondary to
immune-mediated or idiopathic causes. Patients are also prone to ketosis.
• Type II diabetes (non-insulin dependent) is usually adult onset and secondary to relative
insulin deficiency and resistance.
TREATMENT
Premedications
• Oral agents should be withheld on the morning of surgery to avoid perioperative
hypoglycemia. Metformin should be withheld for 24 hours; it has been associated with fatal
metabolic acidosis.
• Night doses of long acting insulin and morning doses are often decreased (or withheld) to
avoid hypoglycemia in the fasting patient.
• Glucose level should be checked.
INTRAOPERATIVE CARE
• Depends on the type and duration of surgery, comorbidities, and patient’s preference
• Regional anesthesia (spinal, epidural, or peripheral nerve blocks) may modulate the
secretion of insulin and catabolic hormones and block the body’s response to surgical stress
under general anesthesia. However, it may increase risks of profound hypotension
(especially in patients with autonomic neuropathy), infection, and vascular injury. There is
some evidence to suggest that local anesthetics are more toxic to peripheral nerves in
diabetics, and the standard nerve stimulator utilized for localization may exhibit reduced
effectiveness.
Monitors
• Invasive BP (in patients with severe CAD, autonomic neuropathy, and for close monitoring
of glucose during prolonged surgery under general anesthesia)
• Consider the possibility of a difficult airway in patients with stiff joint syndrome.
• Intravenous induction should be accomplished by careful titration to avoid hypotension.
– Benzodiazepines and etomidate may decrease ACTH secretion and block adrenal
steroidogenesis, respectively; this can decrease cortisol synthesis.
– Propofol may cause profound hypotension in patients with severe autonomic neuropathy.
• Rapid-sequence induction with cricoid pressure should be considered in patients with
gastroparesis to decrease the risk for pulmonary aspiration.
Maintenance
• For general anesthesia, a “balanced technique” (combination of volatile agents, narcotics,
and intravenous anesthetics) is preferable to reduce the potential metabolic disturbance
from each individual agent. Volatile agents may impair the insulin response to elevated
glucose from the sympathetic stimulation of surgery and general anesthesia.
• Total intravenous anesthesia with propofol may result in hypotension. Additionally, there
may be a decreased ability to metabolize propofol because of the impaired lipid metabolism
in diabetic patients.
• Narcotics may have the benefit of hemodynamic stability, as well as stable metabolic and
hormonal stages.
• Glucose control: Intraoperative monitoring and treatment with IV insulin (or dextrose)
should be considered, particularly in brittle diabetics (q 30–60 minutes, with intraoperative
insulin either via IV bolus or infusion). Continuous intravascular glucose monitors may aid
in tight blood glucose control perioperatively and in critically ill patients. Currently, they
are not in common use.
• Maintain normothermia; hypothermia can worsen postoperative insulin resistance.
• Ensure that patients have fully recovered from muscle relaxants or been adequately
reversed. Patients should be awake with intact protective gag reflexes prior to extubation.
• Prophylaxis for postoperative nausea and vomiting. Metoclopramide may decrease
postoperative nausea and vomiting (PONV) by enhancing gastric emptying, especially in
patients with gastroparesis.
FOLLOW-UP
BED ACUITY
• Vigilant monitoring to detect and treat hypotension, myocardial ischemia, and acute renal
failure
• In certain circumstances (brittle, high-risk surgery) hourly glucose monitoring (and
treatment) may be appropriate.
• Close monitoring for respiratory dysfunction, hypothermia, and hypoxia
• Avoid oversedation that may delay the identification of mental alteration from
hypoglycemia or ketoacidosis
COMPLICATIONS
• Metabolic abnormality (hypoglycemia, hyperglycemia, lactic acidosis)
• Perioperative aspiration
• Infection
REFERENCES
1. American Diabetes Association. Diabetes statistics. 2011.
2. Lena D, Kalfon P, Preiser JC, et al. Glycemic control in the intensive care unit and during
the postoperative period. Anesthesiology. 2001;114(2):438–444.
3. McAnulty GR, Robertshaw HJ, Hall GM. Anesthestic management of patients with diabetes
mellitus. Br J Anaesth. 2000;85(1):80–90.
4. Rigaud M, Filip P, Lirk P, et al. Guidance of block needle insertion by electrical nerve
stimulation: A pilot study of the resulting distribution of injected solution in dogs.
5. Schricker T, Wykes L, Carli F. Epidural blockade improves substrate utilization after
surgery. Am J Physiol. 2000;279:E646–E653.
6. Skjaervold NK, Solligard E, Hjelme DR, et al. Continuous measurement of blood glucose:
Validation of a new intravascular sensor. Anesthesiology. 2011;114(1):120–125.
• Hypoglycemia
• Hyperglycemia
• Hyperosmolar hyperglycemic nonketotic coma
• Postoperative renal dysfunction
CODES
ICD9
• 250.00 Diabetes mellitus without mention of complication, type II or unspecified type, not
stated as uncontrolled
• 250.01 Diabetes mellitus without mention of complication, type I [juvenile type], not stated
as uncontrolled
ICD10
• E10.9 Type 1 diabetes mellitus without complications
• E11.9 Type 2 diabetes mellitus without complications
CLINICAL PEARLS
• Patients should be scheduled early, preferably the first case.
• Patients with end-organ disease (cerebral, cardiac, renal) may not tolerate hypoxic events or
hypotension well.
DIABETIC KETOACIDOSIS
Matthew V. Satterly, MD
Ori Gottlieb, MD
BASICS
DESCRIPTION
• Diabetic ketoacidosis (DKA) is the triad of hyperglycemia, ketonemia, and acidemia.
• DKA is generally associated with type 1 diabetes mellitus (DM) but can be associated with
type 2 in cases of extreme stress (sepsis, trauma etc.).
• It is classified as mild, moderate, or severe based on the pH, serum bicarbonate, and mental
status.
• DKA is differentiated from hyperglycemic hyperosmolar non-ketotic (HHNK) coma which
usually lacks ketones and acidemia and is more common in type 2 diabetes. HHNK is often
associated with a higher serum glucose concentration that may exceed 1,000 mg/dL and the
serum osmolality may exceed 380 mOsm/kg.
EPIDEMIOLOGY
Prevalence
• In the US, there were 115,000 hospital discharges for DKA in 2003
• Annual incidence rate for DKA estimated from population-based studies ranges from 4.6 to 8
episodes per 1,000 patients with diabetes.
Mortality
Mortality <5% in experienced centers
• Most often precipitated by infection or discontinuation of insulin
• May also develop from major illness such as myocardial infarction (MI) or cerebrovascular
accident (CVA)
• Ketoacidosis may also be present with starvation or acute alcohol intoxication.
• DKA results from a relative shortage of circulating insulin in the body, resulting in impaired
glucose uptake and utilization by peripheral tissues. This can be secondary to:
– Actual deficiency (lack of insulin administration)
– Increased demand (sepsis or other hypermetabolic state)
• Gluconeogenesis: To counter the lack of insulin, and glucose available for cells, the body
responds by releasing counter-regulatory hormones (e.g., glucagon, cortisol, catecholamines,
growth hormone).
• Lipolysis: The body institutes fatty acid oxidation, or lipolysis, to provide tissues with an
energy substrate. The byproducts of lipolysis are called ketone bodies.
– B-hydroxybutyrate (technically a carboxylic acid and not a ketone)
– Acetoacetate
– Acetone: Produced by decarboxylation of acetoacetate
• Hypovolemia and electrolyte derangements: Glycosuria leads to an osmotic diuresis that
results in:
– Dehydration: On average, patients are negative by 5–8 L.
– Loss of electrolytes, most notably potassium and sodium. Potassium deficits range from
200–400 mEq due to osmotic diuresis and a chronic catabolic state. However
hyperkalemia is often present initially due to the lack of insulin (decreaes K+ intake into
the cell via Na+/K+ -ATPase) and metabolic acidosis. Sodium deficits range from 350–
600 mEq due to osmotic diuresis. However the patient often presents initially with a
hypovolemic hypernatremia derangement due to water loss in excess of sodium loss.
– Anion gap acidosis: Ketone bodies are acids that titrate the body’s buffering bases.
• Delay elective procedures: The goal is to correct the inciting factor, re-establish euvolemia,
and electrolyte levels as much as possible before going to the operating room.
• The indication for emergency surgery may be an inciting factor for DKA; thus, preoperative
correction is not always possible. In this case, initiate measures to restore euvolemia and
replete electrolytes as the first priority, then correct hyperglycemia.
• If possible, in insulin-dependent diabetes, schedule elective cases early in the day to
minimize preoperative fasting and lipolysis/ketosis from a lack of insulin.
SYMPTOMS
Weakness
History
• Evaluate diabetes severity, prior episodes of DKA, and comorbidities
• Inquire about diabetic medications: Insulin regimen and adherence as well as last dose
• Assess for precipitating factors: Sepsis, pancreatitis, MI, CVA, drugs (corticosteroids,
thiazides, sympathomimetics)
Signs/Physical Exam
• Polyuria
• Polydipsia
• Weight loss
• Vomiting
• Abdominal pain
• Dehydration
• Distinct breath odor—described as “fruity” due to presence of expired acetone
• Tachypnea early followed by deep labored breathing (Kussmaul respirations) as the acidosis
worsens
• Altered mental status
• Shock
• Coma
• Volume status: Skin turgor, dry mucus membranes
TREATMENT HISTORY
• Volume resuscitation
• Electrolyte replacement
• Acute coronary syndrome therapy if precipitating event is cardiac ischemia or infarction
• Stroke treatment if precipitating event is cerebrovascular
MEDICATIONS
• Insulin
• Antibiotics if precipitating event is sepsis or infection
• Sodium bicarbonate
Labs/Studies
• Serum glucose
• HgA1C: Poor control may suggest the presence of diabetes-related comorbidities.
• Ketonuria: Presence of β-hydroxybutyrate, acetoacetate, and/or acetone in the urine.
Measured with urine dipstick:
– Small amount <20 mg/dL
– Large amount >80 mg/dL
• Electrolyte: Hyperchloremic anion gap acidosis: AG = [Na+] – ([Cl−] + [HCO3−])
• BUN and serum creatinine
• ABG (pH)
• Serum osmolality
• CBC: Leukocytosis may be related to ketoacidosis, not necessarily infection.
• Amylase: May be elevated due to a nonpancreatic source in DKA
• Neuropathy: Autonomic nervous system dysfunction may result in difficulties with
regulating blood pressure and temperature.
• Cardiovascular disease: Perioperative morbidity and mortality with DM often results from
cardiac causes.
• Nonenzymatic glycosylation and formation of abnormal proteins may result in decreased
elastance and thus difficult intubation.
• Gastroparesis: Many consider patients with DM as a “full stomach” despite NPO status.
Delay elective procedures: The goal is to correct the inciting factor, re-establish euvolemia
and electrolyte levels as much as possible before going to the operating room.
See Table
TREATMENT
Premedications
In emergent surgeries, intensive therapy with volume resuscitation, insulin infusion, and
electrolyte replacement should be continued en route to the operating room.
• Disoriented or intubated patients cannot be consented.
• Family members should be advised about the severity of their condition, emergent nature of
the surgery, and the increased risk of mortality.
INTRAOPERATIVE CARE
Guided primarily by the procedure except in cases of altered mental status when intubation is
required for airway protection
Monitors
• Arterial line may be useful for frequent lab checks as well as to monitor beat-to-beat blood
pressure in patients who are hypovolemic or in septic shock.
• Foley catheter: Ins and outs should be carefully monitored.
• Central line access may be useful to guide fluid administration.
• Consider rapid-sequence induction/intubation if a full stomach is suspected or there is risk
for aspiration.
• Patients are hypovolemic and may become unstable with induction medications. Consider
etomidate and/or ketamine if appropriate.
• Induction agents may have effects on glucose homeostasis but are clinically insignificant.
Maintenance
• Intensive care therapy should be continued in the operating room in the same manner.
• Labs:
– Blood glucose ∼ hourly
– pH
– Electrolytes (potassium)
– Intraoperative monitoring of β-hydroxybutyrate may help trend the response to therapy
and indicate resolution.
• Volume resuscitation:
– 0.9% NaCl: 15–20 mL/kg for the first hour
– 0.45% NaCl: 4–14 mL/kg/hr if serum sodium is within or elevated above normal values
(institution-based).
– D5 0.45% NaCl should be started when the serum glucose level is <200 mg/dL.
– Lactated Ringers (LR) may also be used and may be preferable given its pH (or effect on
pH). It should also be noted that LR contains 4 mEq/L of potassium.
– Fluid replacement alone may drop the serum glucose level ∼50 mg/dL/hr.
– Adjust accordingly for cardiac and renal pathology
– Resuscitation should also factor in insensible and surgical blood loss.
– If packed red blood cells are administered, the use of washed cells may be beneficial as
acid citrate dextrose may worsen hyperglycemia.
• Insulin therapy:
– Regular insulin: 0.1–0.2 U/kg initial IV bolus
– Insulin infusion: 0.1 U/kg/hr, with the goal of decreasing serum glucose by 50–75
mg/dL/hr. If glucose does not decrease as expected, consider doubling the infusion rate.
– Continue infusion until serum glucose <200 mg/dL then reduce infusion to 0.02–0.05
mg/kg/hr and consider changing to SC management.
• Potassium replacement:
– If [K+] <3.3 mEq/L hold insulin and replete potassium
– If [K+] >5.3 mEq/L continue insulin and monitor every 2 hours
– If [K+] = 3.3–5.3 mEq/L continue to administer 20–30 mEq in each liter of fluids
• Sodium bicarbonate: Controversial and is usually not indicated; may be considered in cases
of refractory acidosis (serum pH <7.15 and [HCO3−] <10 mEq/L)
• Normothermia: Hypothermia decreases the response to insulin.
Emergence/extubation should be based on mental status, volume status, and hemodynamic
stability.
FOLLOW-UP
BED ACUITY
• ICU admission is usually required as patients may have altered mental status, hypovolemia,
or require vasopressors or an insulin infusion.
• Telemetry or floor bed may be considered if there is resolution of DKA as demonstrated by a
closing of the anion gap (<12), serum glucose <200 mg/dL, sodium bicarbonate level ≥18
mEq/L, and pH >7.3.
• Endocrine consult may be advantageous.
• Frequent blood glucose checks
• Electrolyte monitoring: Potassium moves intracellularly as the acidosis is corrected.
• Ketonemia and ketonuria may persist for 1–2 days with proper correction of acidemia.
• Once DKA has resolved and the patient is eating, consider resuming the patient’s
preoperative insulin regimen or initiating new therapy with short/long- acting agents as
necessary.
COMPLICATIONS
• Hypoglycemia may result from excess insulin therapy.
• Overly aggressive fluid resuscitation may lead to pulmonary edema and/or congestive heart
failure.
• Continued shock may occur if inadequate resuscitation is performed.
• Over-repletion of electrolytes (potassium) may lead to cardiac arrhythmia.
• Central pontine myelinolysis may result from correction of hyponatremia at a rate >10–12
mEq/hr over the first 24 hours.
REFERENCES
1. Hirsch I, McGill JB, Cryer PE, et al. Perioperative management of surgical patients with
diabetes mellitus. Anesthesiology. 1991;74:346–359.
2. Kitabchi A, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in adult patients with
diabetes. Diabetes Care. 2006;29(12):2739–2748.
3. McAnulty G, Robertshaw HJ, Hall GM. Anaesthetic management of patients with diabetes
mellitus. Br J Anaesth. 2000;85(1):80–90.
4. Milaskiewicz R, Hall GM. Diabetes and anaesthesia: The past decade. Br J Anaesth.
1992;68:198–206.
• Hypokalemia
• Hyperglycemic hyperosmolar nonketotic coma
CODES
ICD9
• 250.10 Diabetes with ketoacidosis, type II or unspecified type, not stated as uncontrolled
• 250.11 Diabetes with ketoacidosis, type I [juvenile type], not stated as uncontrolled
• 250.13 Diabetes with ketoacidosis, type I [juvenile type], uncontrolled
ICD10
• E13.10 Oth diabetes mellitus with ketoacidosis without coma
• E10.10 Type 1 diabetes mellitus with ketoacidosis without coma
CLINICAL PEARLS
• Triad of hyperglycemia, ketonemia, and acidemia
• Hypovolemia and hyperosmolarity may be life-threatening; thus, volume resuscitation is the
first priority.
• Etiology of DKA should be determined and treated.
• Preoperative evaluation should include chronic complications related to untreated diabetes
as these may have grave perioperative implications.
• Preoperative and intraoperative goal should be to mimic normal metabolism and achieve
euvolemia, normal blood glucose, pH and serum potassium, and other electrolytes through
gradual correction and careful titration with frequent monitoring.
DIASTOLE
Korrin Scott, MD
BASICS
DESCRIPTION
• Diastole describes cardiac chamber relaxation and filling with blood; it is followed by
systole, a period of contraction.
• Ventricular diastole encompasses more than half the time of the cardiac cycle and consists of
4 phases:
– Isovolumic relaxation
– Rapid early filling
– Diastasis
– Atrial contraction
• Active relaxation at the molecular level:
– At the cellular level, diastole starts when ATP is hydrolyzed and actin–myosin cross-
bridges unlink.
– This is associated with decreases in cytoplasmic calcium and dissociation of calcium from
troponin.
– Calcium sequestration into the SR is accomplished by 2 energy-consuming receptors: The
calcium adenosine triphosphate pump (SERCA-2) and sodium–calcium exchanger.
– The sarcomere rapidly returns to resting length under normal circumstances. However,
when energy supplies are diminished, the inability to sequester calcium can impair
relaxation.
• Valves, volume, and pressure during the 4 stages of diastole:
– Isovolumic relaxation time (IVRT):
Valves: Tricuspid/pulmonic on the right side of the heart and the mitral/aortic on the
left side of the heart are closed. Of note, the electromechanical onset of diastole
(beginning of relaxation) occurs even while the ventricle is ejecting blood (aortic valve
open). When the ventricular pressures drop below the aortic pressures, the aortic valve
closes and IVRT begins.
Ventricular volume: No change
Ventricular pressure: Decreases exponentially
– Rapid early filling:
Valves: Begins when the tricuspid on the right and the mitral valve on the left open
Ventricular volume: Accounts for the majority of ventricular filling (up to 80% of the
total stroke volume)
Ventricular pressure: Initially, there is little to no change with filling. Patients with
decreased compliance (e.g., fibrosis, ischemia, diastolic dysfunction) will have a greater
increase for a given volume (may also impair this passive filling process).
– Diastasis: Phase can disappear during tachycardia.
Valves: Tricuspid and mitral valves remain open; aortic and pulmonic valves are closed.
Ventricle volume: Remains approximately the same as at the end of the rapid early filling
phase
Ventricle pressure: Atrial and ventricular pressures equalize
– Atrial contraction:
Valves: Tricuspid and mitral valve open
Ventricle volume: The contribution of the “atrial kick” accounts for 15–25% of the stroke
volume.
Ventricle pressure: Creates a positive pressure gradient across the tricuspid and mitral
valve
• Pressure–volume loops can aid with the assessment of viscoelastic properties of the
ventricle. As described above, during passive filling, the slope is relatively flat; it begins to
increase as the ventricle fills.
ANATOMY
The heart consists of 2 atria and 2 ventricles that circulate blood in series.
• The right and left ventricles differ in their shape and size, as well as the pressure against
which they contract (afterload).
• Right ventricle: Pumps through the low-resistance pulmonary circulation. It is crescent-
shaped with an inflow and outflow region that contract sequentially to eject blood into the
low-pressure pulmonary circulation.
• Left ventricle: Pumps through the systemic circulation. It is ellipsoidal in shape with the
muscle fibers arranged longitudinally in the subepicardium and subendocardial layers, and
circumferentially in between these 2 layers. The LV ejects blood with a corkscrew type of
motion with the apex moving towards the base. Wall motion of regions supplied by
branches of the coronary artery can be individually assessed semi-quantitatively by
echocardiography.
• Factors that can affect the passive pressure–volume properties:
– LV chamber volume: Increases in preload (LV end diastolic volume) from volume overload
or decreased forward flow move the pressure–volume curve rightwards. This results in
smaller changes in volume will have a large change in pressure (steeper slope).
– Composition of the LV wall (endocardium and myocardium): Hypertrophy of muscle, post-
ischemic scarring, fibrosis, edema, amyloid deposition, and hemosiderin can “stiffen” the
wall and decrease compliance.
– Extrinsic factors on the ventricle: Pericardial disease, overdistention of the contralateral
ventricle, increased airway or pleural pressure, tumors, and surgical compression can
decrease LV compliance.
– Distensibility/elasticity: Active elasticity of the LV wall is a function of residual cross-
bridge activation and sarcomere contraction. This potential energy acts as a recoiling force
that restores the myocardium to its resting configuration.
• Diastolic heart failure (DHF)
– Definitions
ACC/AHA criteria: Typical signs and symptoms of heart failure; normal LV ejection
fraction (>50%); failure not explained by valvular abnormality
The European Society of Cardiology. Includes additional criteria of evidence of
dysfunction through invasive measurements (LVEDP, PCWP >16 mm Hg) or
echocardiogram parameters.
– Mechanism is multifactorial and poorly understood. It can result from either:
Intrinsic: Factors affecting ventricular muscle including myocardial relaxation and
coronary turgor
Intrinsic factors affecting external compression of the LV including RV pressure or
volume overload, pericardial disease, pleural and mediastinal pressure, and atrial
contraction
– Linking etiology with cellular mechanisms
Aging is associated with prolonged isovolumic relaxation and altered calcium
homeostasis as well as interstitial fibrosis and increased cross-linking of collagen that
can cause LV stiffness.
Chronic hypertension increases myocardial work/tension and is often compensated for
with muscle hypertrophy.
Diabetes is associated with myocyte hypertrophy and interstitial fibrosis with
microvascular disease.
• Atrial kick: The stroke volume decreases in the absence of an atrial contraction; this can be
seen with atrial fibrillation, atrial flutter, low atrial rhythms, or junctional rhythms. In
patients with decreased ventricular compliance, where passive filling is already decreased,
the stroke volume becomes more dependent on the atrial “kick.”
• Echocardiogram: LV diastolic function is assessed via pulse wave Doppler (PWD) assessment
through the mitral valve. A mid-esophageal 4-chamber view allows the beam to be aligned
parallel to blood flow and thus provides the most ideal imaging of flow and velocity. The
transmitral pattern is composed of the:
– “E” wave: Represents the rapid filling phase
– “A” wave: Represents atrial contraction. The wave is approximately 1/3} to 1/2 the size of
the E wave.
– Deceleration time (DT): Time it takes for the E wave velocity to become zero. A time
<220 ms represents good LV relaxation and a rapid decline in ventricular pressure.
• PWD classification of diastolic dysfunction
– Impaired relaxation (Grade I): This initial pattern of dysfunction is seen early in the course
of hypertension, myocardial ischemia, and hypertrophic cardiomyopathy.
Small “E” wave
Large “A” wave
E/A ratio <1
Prolonged DT (>240 ms)
– Pseudo-normal pattern (Grade II): As the disease process progresses, the LA pressure and,
hence, LA–LV gradient increases. This results in a “normal” appearing pattern. In order to
distinguish true normal from pseudonormal, maneuvers to decrease preload (e.g.,
Valsalva, nitroglycerin, etc.) can be applied to unmask a small “E” wave, large “A” wave,
and prolonged DT time.
Normal appearing “E” wave: The increased size compared to Grade I reflects the increase
in passive filling flow from the increased LA–LV gradient.
Normal appearing “A” wave: The decreased size compared to Grade I reflects the
minimal contribution of the atrial contraction.
E/A ratio >1
DT of 160–240 ms: The shortened time results from rapid equilibration pressure between
the LA and LV.
– Restrictive pattern (Grade III and IV) can be seen in decompensated heart failure, severe
coronary artery disease, constrictive pericarditis, and severe aortic and mitral
insufficiency. They result in LV filling occurring primarily in early diastole.
Very large “E” wave
Small “A” wave
E/A ratio >2
Shortened DT interval from rapid rise in the LV diastolic pressure and time to diastasis
EQUATIONS
Laplace’s law: T = (P × r)/(2 × h), where P is the intraventricular pressure, r is the
ventricular radius, and h is wall thickness.
GRAPHS/FIGURES
FIGURE 1. The 4 phases of diastole. IVRT begins with aortic valve closure and ends with mitral valve opening. RFP—
Rapid Early Filling. MVF—Mitral Valve Flow.
FIGURE 2. Doppler E and A waves from echocardiogram are superimposed. (Reproduced from Reference 3, permission
requested and pending).
REFERENCES
1. Alsaddique AA, Royse AG, Royse CF, et al. Management of diastolic heart failure following
cardiac surgery. Eur J Cardiothorac Surg. 2009;35(2):241–249.
2. Daneshvar D, Wei J, Tolstrup K, et al. Diastolic dysfunction: Improved understanding using
emerging imaging techniques. Am Heart J. 2010;160(3):394–404.
3. Hoit B. Left ventricular diastolic function. Crit Care Med. 2007;35(Suppl 8):S340–S347.
4. Mahmood F, Matyal R. Assessment of perioperative diastolic function and dysfunction. Int
Anesthesiol Clin. 2008;46(2):51–62.
5. Ouzounian M, Lee DS, Liu PP. Diastolic heart failure: Mechanisms and controversies. Nat
Clin Pract. 2008;5(7):375–386.
6. Pagel PS, Grossman W, Haering JM, et al. Left ventricular diastolic function in the normal
and diseased heart. Anesthesiology. 1993;79(5):1104–1120.
7. Satpathy C, Mishra TK, Satpathy R, et al. Diagnosis and management of diastolic
dysfunction and heart failure. Am Fam Physician. 2006;73(5):841–846.
ADDITIONAL READING
• Mahmood F, Matyal R, Subramaniam B, et al. Transmitral flow propagation velocity and
assessment of diastolic function during abdominal aortic aneurysm repair. J Cardiothorac
Vasc Anesth. 2007;21(4):486–491.
• Skubas N. Intraoperative Doppler tissue imaging is a valuable addition to cardiac
anesthesiologists’ armamentarium: A core review. Anesth Analg. 2009;108(1):48–66.
• Systole
• Pressure–volume loops
• Lusitropy
CLINICAL PEARLS
• Lusitropy (early diastolic relaxation) is an active, ATP-dependent process.
• Diastolic dysfunction is often asymptomatic, and when symptoms are present, it is often
difficult to distinguish from systolic failure. Echocardiogram can provide a noninvasive
method to categorize the type of heart failure.
• LV end-diastolic pressure can be used as a measure of preload only if the relationship
between ventricular volume and pressure (ventricular compliance) is constant.
• Patients with reduced ventricular compliance are most affected by the loss of a normally
timed atrial systole (loss of atrial kick).
DIBUCAINE NUMBER
BASICS
DESCRIPTION
• The dibucaine number (DN) is a laboratory test that indirectly determines the presence of an
atypical genetic variant of pseudocholinesterase.
– It is a qualitative (not quantitative) assessment of enzyme function.
• The duration of succinylcholine and mivacurium activity, and hence neuromuscular
blockade, is dependent on both the catalytic ability/activity (qualitative) and levels of
pseudocholinesterase (quantitative).
• Pseudocholinesterase is responsible for the hydrolysis of succinylcholine to
succinylmonocholine and choline, and hence termination of the drug’s activity.
Pseudocholinesterase (1):
– Is produced by the liver
– Is encoded by a gene on Chromosome 3
– Circulates in the plasma with a half-life of approximately 8–16 hours
– Is also known as butyrylcholinesterase or plasma cholinesterase
• Pseudocholinesterase variants (qualitative abnormality): Homozygous typical
pseudocholinesterase is most commonly found in the population. However, there is a small
subset of patients who possess an atypical variant of the gene, and will have prolonged
neuromuscular blockade when succinylcholine is administered (2).
– Heterozygous atypical: One abnormal gene
– Homozygous atypical: Both genes are abnormal
– Other gene variants exist, but are rare
• Decreased pseudocholinesterase levels (quantitative abnormality) (3,4)
– Liver disease: Even when plasma cholinesterase activity was reduced by 80% (in severe
liver disease), apnea duration was found to be approximately 9–15 minutes.
– Pregnancy: No clinically significant prolongation of action is seen.
– Malnutrition
• Dibucaine number (DN) (3)
– Dibucaine is a local anesthetic that was found to inhibit:
Typical pseudocholinesterase genotype activity by 70–80%
Heterozygous typical genotype activity by 50–60%
Homozygous atypical genotype activity by <30%
– The amount of inhibition is known as the dibucaine number.
• Dibucaine testing (3)
– DN = [1 – (pseudocholinesterase activity in the presence of inhibitor/pseudocholinesterase
activity in the absence of inhibitor)] × 100
– Measuring pseudocholinesterase activity in the absence of an inhibitor is as follows: The
substrate acetylthiocholine is added to the patient’s serum and is cleaved by
pseudocholinesterase to form acetate and thiocholine. Thiocholine reacts with Ellman’s
reagent (dithiobis-nitrobenzoic acid) to form 5-mercapto-2-nitrobenzoic acid. The amount
of absorption at specific wavelengths of light is proportional to the amount of 5-mercapto-
2-nitrobenzoic acid, and therefore proportional to the % activity of pseudocholinesterase.
– Pseudocholinesterase activity in the presence of dibucaine (inhibitor) is measured as
follows: A specified concentration of dibucaine is added to the patient’s serum, followed
by the addition of acetylthiocholine and Ellman’s agent. Light absorption is measured
(proportional to 5-mercapto-2-nitrobenzoic acid) to determine the % activity of
pseudocholinesterase.
• Quantitative measures: It is important to remember that the DN is not a quantitative test of
the amount of enzyme in the serum, but rather a test of its function.
ANATOMY
• Within the neuromuscular junction (NMJ), acetylcholine neurotransmitter is metabolized by
acetylcholinesterase (reuptake by the presynaptic membrane also occurs).
• Pseudocholinesterase circulates in the plasma. Therefore, termination of succinylcholine’s
activity requires diffusion away from the NMJ and into the plasma, where it is then
metabolized by pseudocholinesterase.
• Heterozygous atypical
• Usually clinically insignificant; with blockade being prolonged on the order of seconds or
minutes, if at all.
• DN = 50–60%
• Found in approximately 1:25 Caucasians
• Homozygous atypical
• The duration of blockade can persist for 4–8 hours (5).
• DN = ≤30%
• Found in approximately 1:2,500 Caucasians
• Atypical genotypes are rarely seen in Asians and African blacks.
• Succinylcholine is a depolarizing muscle relaxant with a rapid onset and short duration of
action. It provides profound relaxation and excellent intubating conditions, and is most
commonly used today for rapid-sequence intubation (RSI).
• With the advent of newer, intermediate- and short-acting non-depolarizing agents,
succinylcholine is used less frequently now as an infusion
• Following administration, approximately 90–95% of succinylcholine is hydrolyzed and
inactivated by pseudocholinesterase prior to reaching the NMJ. Thus, variants of
pseudocholinesterase result in higher levels reaching the NMJ as well as decreased
metabolism once they diffuse away from the junction.
• Prolonged apnea following succinylcholine administration requires supportive measures
such as the institution, or continued application, of mechanical ventilation. Other causes for
ventilatory failure should be ruled out (hypothermia, hypercarbia, CNS injury, etc.) while
further testing is undertaken.
EQUATIONS
DN = [1 – (pseudocholinesterase activity in the presence of inhibitor/pseudocholinesterase
activity in the absence of inhibitor)] × 100
REFERENCES
1. arnas ML, Procter M, Schwarz MA, et al. Concordance of butyrylcholinesterase phenotype
with genotype: Implications for biochemical reporting. Am J Clin Pathol.
2011;135(2):271–276.
2. Pantuck EJ. Plasma cholinesterase: Gene and variations. Anesth Analg. 1993;77(2):380–
386.
3. Elamin B. Dibucaine inhibition of serum cholinesterase. J Biochem Mol Biol.
2003;36(2):149–153. Green DW, Fisher M, Sockalingham I. Mivacurium compared with
succinylcholine in children with liver disease. Br J Anaesth. 1998;81(3):463–465.
4. Viby-Mogensen J. Correlation of succinylcholine duration of action with plasma
cholinesterase activity in subjects with the genotypically normal enzyme. Anesthesiology.
1980;53(6):517–520.
ADDITIONAL READING
• Jensen FS. Plasma cholinesterase and abnormal reaction to succinylcholine: Twenty years’
experience with the Danish Cholinesterase Research Unit. Acta Anaesthesiol Scand.
1995;39(2):150–156.
CLINICAL PEARLS
• Succinylcholine should be avoided, if possible, in any patient with a known history of
atypical pseudocholinesterase.
• If prolonged apnea following succinylcholine administration occurs, supportive measures
such as mechanical ventilation should be continued, while other causes for apnea are ruled
out. Heterologous blood transfusion has been used in rare instances when rapid reversal of
the blockade was required. However, this technique must carefully weigh the risks versus
the benefits.
• Many patients remain unaware of the presence of an abnormal pseudocholinesterase
genotype. This mutation is often only discovered after the patient (or a relative) develops
prolonged neuromuscular blockade after intubation, since the disorder has no other known
physiologic manifestations.
• Neostigmine and organophosphate pesticides act as potent inhibitors of
pseudocholinesterase. Patients who are given neostigmine to reverse non-depolarizing
blockade, and are subsequently re-intubated using succinylcholine, will experience a
prolonged blockade.
• While the varied terminology is somewhat confusing, pseudocholinesterase,
butyrylcholinesterase, and plasma cholinesterase are all synonymous.
• Nonspecific plasma esterases, such as those involved in the degradation of atracurium or
remifentanil, are different entities entirely.
• Acetylcholinesterase (also known as “true cholinesterase”) is found at the NMJ, and is
responsible for the hydrolysis of acetylcholine.
DIFFICULT AIRWAY
BASICS
DESCRIPTION
• Aspects of airway management that may prove to be difficult include:
– Ventilation
– Laryngoscopy
– Endotracheal tube placement
– Laryngeal mask airway (LMA) placement
• The most dangerous situation in airway management is the “cannot ventilate, cannot
intubate” scenario.
• Airway evaluation is important in predicting a difficult airway; most difficult or emergent
airways are associated with preoperative anatomic or pathologic risk factors.
• The ASA American Society of Anesthesiologists (ASA) Difficult Airway Algorithm provides a
useful approach to difficult airway management in the event that laryngoscopy or
ventilation becomes impossible (1).
• Skilled help, alternative airway tools, and surgical airway equipment may be necessary to
secure the airway.
EPIDEMIOLOGY
Prevalence
Difficult mask ventilation occurs in 5% of the adult population.
Morbidity
Most adverse outcomes relating to airway management occur at the time of induction.
Mortality
30% of deaths attributed to anesthesia involve airway management.
• Components of the airway evaluation that are associated with a difficult laryngoscopy
include the following (2,3):
– Mallampati score >2
– Thyromental distance <6 cm
– Mouth opening <4 cm
– Limited neck mobility
– Neck circumference >45 cm
– Abnormal upper teeth
– Large tongue
• A history of difficult intubation makes repeat intubation very likely to be difficult.
• Pathologic processes:
– Distortion of the airway (submandibular abscess, anaphylaxis) may make visualization of
the vocal cords difficult or impossible
– Hoarseness may indicate a vocal cord lesion
– The inability to breathe while lying flat may be the result of mass compression on the
trachea or a bronchus, which could make ventilation difficult or impossible while under
anesthesia
• Anatomic defects found in some congenital syndromes are associated with a difficult airway.
The conditions most characteristically associated with difficult airway management include
Pierre Robin Syndrome, Treacher Collins Syndrome, Menkes Disease, and acromegaly.
– Patients with Pierre Robin Syndrome have mandibular hypoplasia, micrognathia, cleft
palate, and glossoptosis. Patients will occasionally have a cleft uvula, macroglossia, or
laryngomalacia.
– Treacher Collins Syndrome is associated with hypoplasia of the maxilla and mandible,
micrognathia, and cleft palate. Airway management becomes more challenging as the
patient ages.
– Menkes Disease is a copper metabolism disease that results in micrognathia, poor bone
strength, and easily damaged teeth.
– Acromegaly is caused by excessive growth hormone, resulting in characteristic facies,
macroglossia, prognathism, and hypertrophy of laryngeal soft tissue, the epiglottis, and
the aryepiglottic folds.
• External devices may make positioning for direct laryngoscopy difficult or impossible. The
halo device is not only associated with difficult laryngoscopy, but also hinders LMA
placement and seating.
Pregnancy is associated with oropharyngeal edema, engorgement of vessels making bleeding
more likely, a full stomach, and large breasts impeding direct laryngoscopy.
• In an anesthetized patient, oropharyngeal muscle tone is lost and the soft palate, epiglottis,
and tongue can obstruct the airway. Positioning and the use of oropharyngeal or
nasopharyngeal airways may assist in adequate mask ventilation of the anesthetized patient.
• For direct visualization of the vocal cords to be possible, the tracheal and pharyngeal axes
must be in-line. This is most often accomplished by placing the patient’s head in the
“sniffing position,” a combination of flexion of the neck (usually accomplished by elevating
the head) and extension of the head.
• Care should be taken when positioning the obese patient. The use of a special ramp-shaped
pillow or series of stacked sheets will bring the tracheal and pharyngeal axes in line.
External landmarks that aid in this process are the external auditory meatus and sternum,
which should be in a straight line parallel with the ground.
• To create an appropriate airway management plan, one must perform a detailed history,
including prior difficult intubation, hoarseness, breathing difficulty, and obstructive sleep
apnea. A thorough airway evaluation, including examination of relevant anatomy, will aid
in the prediction of a difficult airway.
• When a difficult airway is suspected, alternative airway tools and skilled assistants should
be made readily available.
• When adequate ventilation seems unlikely, an awake intubation with maintenance of
spontaneous ventilation should be performed.
• Awake intubation may be via the nasal or oral routes. It involves patient cooperation and
local anesthesia of the airway, with or without intravenous sedation.
• A successful intubation is typically characterized by vocal cord visualization on
laryngoscopy, a view of the endotracheal tube passing through the cords, condensation in
the tube, bilateral breath sounds on auscultation, and confirmed end-tidal carbon dioxide.
When the vocal cords are not visualized and the usual methods to confirm endotracheal
intubation are not positive, the intubation is unsuccessful. A change in patient position or
use of an alternative laryngoscopy blade may facilitate a repeat attempt at intubation.
However, excessive repetitive attempts at laryngoscopy should be avoided to minimize
airway trauma and edema.
• When intubation fails, consider calling for help. Determine whether mask ventilation is
possible by visualizing chest rise, end-tidal carbon dioxide, bilateral breath sounds, and
maintenance of oxygen saturation.
• If mask ventilation is adequate, continue on the non-emergency pathway of the ASA
Difficult Airway Algorithm. Alternative airway equipment can be used to reattempt
intubation. If intubation proves to be impossible, the patient can be awakened or a surgical
airway can be performed.
• If mask ventilation is impossible after failure to intubate, call for help and insert an LMA. If
the LMA provides adequate ventilation, continue on the non-emergency pathway. If
ventilation is still inadequate, follow the emergency pathway. This is a “cannot intubate,
cannot ventilate” scenario.
• When a “cannot intubate, cannot ventilate” situation arises, call for help. Attempt
emergency noninvasive methods of ventilation, including transtracheal jet ventilation,
Combitube, or rigid bronchoscope. If these methods are unsuccessful, perform a
cricothyroidotomy or tracheostomy (4).
• The absence of bilateral breath sounds could be caused by an esophageal intubation,
pneumothorax, foreign body in the trachea or bronchus, large body habitus impeding
auscultation, or mainstem intubation.
• The absence of end-tidal carbon dioxide could be caused by esophageal intubation, low
cardiac output, severe bronchospasm, kinking or dislodgement of the end-tidal carbon
dioxide line, or machine failure.
TREATMENT
• Optimize patient positioning with a shoulder roll or stacked sheets.

• Attempt direct visualization with different blades. The Macintosh blade is useful for patients
with an anterior airway. Because the Macintosh blade indirectly lifts the epiglottis and the
Miller blade directly lifts it, the Miller blade is optimal for patients with a large epiglottis.
• Supraglottic devices
– The LMA is a supraglottic device that is inserted blindly. It is useful to facilitate
ventilation in a “cannot ventilate, cannot intubate” situation. Many LMAs can also
facilitate tracheal intubation (aperture is positioned over the glottic opening) via
fiberoptic techniques (see below).
– The Combitube is a double-lumen device that is inserted blindly into the trachea or
esophagus, and can ventilate the trachea based on which balloon is inflated and which
lumen is used for ventilation.
• Fiberoptic bronchoscopy (FOB)
– Awake FOB: The known or suspected difficult airway can be secured by performing an
awake fiberoptic intubation. Spontaneous ventilation is maintained and topical anesthesia
is applied to the oropharynx, hypopharynx, and larynx to blunt the response to airway
instrumentation.
– Asleep FOB: In patients where ventilation appears feasible, an asleep approach can be
utilized.
– The LMA-Aintree technique begins with insertion of the LMA and confirmation of
ventilation. An Aintree Intubation Catheter (AIC) is fiberoptically guided through the LMA
into the trachea. The LMA and fiberoptic scope are removed while the AIC is left in place.
The endotracheal tube is passed over the AIC and the AIC is removed.
• Bougie catheter: If the vocal cords are not visualized, a Bougie catheter may be placed into
the trachea with laryngoscopy guidance or blindly. The tracheal rings can be felt and the
endotracheal tube is then passed over the Bougie.
• Video laryngoscopes include the CMAC and GlideScope. These devices provide a view of the
vocal cords that may not be possible with direct laryngoscopy, especially in the anterior
airway.
• Surgical airway
– A cricothyroidotomy can be performed by an experienced provider in less than a minute.
It can provide a stable airway for 24 hours before being converted to a tracheostomy.
– A tracheostomy is a surgical airway that takes longer to perform as compared with a
cricothyroidotomy. Given its more inferior position, risks include damage to the recurrent
laryngeal nerves, nearby vascular structures, and the thyroid gland.
FOLLOW-UP
• When a difficult intubation occurs, inform the patient in writing. Emphasize the importance
of alerting the surgical and anesthesia teams for future procedures.
• Document the details regarding the airway and how it was secured and maintain this
information in the patient’s medical record.
CLOSED CLAIMS DATA
• The time periods 1985–1992 and 1993–1999 were most recently compared. Death/brain
death occurred most often at the time of induction, but there was a decrease in the
incidence at induction during the later time period. This improvement is likely a result of
widespread adoption of the 1993 Difficult Airway Guidelines (5).
• Claims during maintenance, extubation, and recovery remained the same for both time
periods.
• The odds of death/brain death increased with airway emergency and multiple attempts at
laryngoscopy.
• A delay in alternative emergency airway management or surgical airway placement led to
worse outcomes.
• Since 1993, the airway guidelines were used in 8% of cases to defend anesthetic care and in
3% of cases to criticize care.
REFERENCES
1. American Society of Anesthesiologists. Practice guidelines for management of the difficult
airway: An updated report by the American Society of Anesthesiologists Task Force on
Management of the Difficult Airway. Anesthesiology. 2003;98(5):1269–1277.
2. Langeron O, Masso E, Huraux C, et al. Prediction of difficult mask ventilation.
Anesthesiology. 2000;92(5):1229–1236.
3. Ezri T, Gewurtz G, Sessler D, et al. Prediction of difficult laryngoscopy in obese patients by
ultrasound quantification of anterior neck soft tissue. Anaesthesia. 2003;58(11):1111–
1114.
4. Benumof JL, Scheller MS. The importance of transtracheal jet ventilation in the
management of the difficult airway. Anesthesiology. 1989;71(5):769–778.
5. Peterson GN, Domino KB, Caplan RA, et al. Management of the difficult airway: A closed
claims analysis. Anesthesiology. 2005;103(1):33–39.
ADDITIONAL READING
• ASA Difficult Airway Algorithm
• Acromegaly
• Jet ventilation
• Tracheostomy
• Cricothyrotomy
• Laryngeal mask airway
CLINICAL PEARLS
• A thorough history and physical exam prior to induction will help the anesthesia care team
plan an appropriate airway management strategy.
• When an airway cannot be easily secured, call for help early and follow the ASA Difficult
Airway Algorithm. Avoid repetitive intubation attempts, which may cause airway trauma.
DIFFICULT PERIPHERAL INTRAVENOUS ACCESS
Bradley A. Stone, MD
BASICS
DESCRIPTION
• Intravenous (IV) access is required for:
– Venous blood testing
– Contrast enhanced imaging
– Fluid resuscitation
– Medication administration
– Blood product transfusion
– Short-term parenteral nutrition
• IV access is considered difficult if it requires:
– Multiple attempts
– Staff with unique expertise (IV team, anesthesia department, transport team)
– Enhanced vein visualization technology
EPIDEMIOLOGY
Prevalence
5% of the general population
Morbidity
• Phlebitis:
– Mechanical
– Infectious
– Chemical
• Infiltration (non-vesicant)
• Extravasation (vesicant medication)
• Thrombosis
• Nerve injury
• Hematoma
• Compartment syndrome
• Unrecognized intra-arterial placement
• Pain
• Anxiety
• Low patient satisfaction
Mortality
In hypovolemic shock or when life-saving medications are urgently needed, the failure to
establish a peripheral IV can become life-threatening.
• Veins difficult to visualize:
– Obesity
– Dark skin
– Skin disease
• Small veins:
– Age <3 years
– Decreased peripheral perfusion
• Fragile veins:
– Elderly
– Malnourished
• Medications:
– Warfarin
– Antithrombotics
– Corticosteroids
• Uncooperative patient
• Limited sites:
– Previous phlebitis from multiple previous venous catheters or IV drug abuse
– Planned extremity surgery
– Previous mastectomy or axillary lymph node dissection
– Shunts/arteriovenous fistulae
• IV access requires a relatively straight vein section and distention with adequate pressure of
blood so that the vein is visible and/or palpable.
• Preferred sites for IV access:
– Upper extremity
Metacarpal, dorsal venous network
Forearm: Cephalic, basilica, median antebrachial
Antecubital fossa: Cephalic, basilic, median cubital
– Foot (mostly in children): Greater saphenous, lesser saphenous, dorsal venous network
– Scalp (mostly age <6 months)
– Umbilical (neonate)
– External jugular
• Avoid the following sites for IV access:
– Proximal sites: Usually start with more distal sites and work proximally, if necessary
– Sites over a joint: Flexion and extension will increase phlebitis and infiltration.
– Distal cephalic vein in forearm is adjacent to the radial nerve (Infusion Nurses Society
Guideline).
– Veins on palmar side of wrist: Adjacent to median nerve (Infusion Nurses Society
Guideline)
– Visible valves
• Preserve and avoid the following veins in the non-dominant arm for future dialysis in
patients with chronic kidney disease (National Kidney Foundation Guideline):
– Cephalic vein at wrist
– Cephalic vein antecubital space
– Brachial basilic vein
• If difficult IV access is anticipated, consider using the following techniques to enhance
success:
– Search extensively to find the best target vein before attempting an IV
– Increase vein size
Use a tourniquet or blood pressure cuff 8 cm above the site, with pressure less than the
arterial diastolic pressure
Place the extremity in the dependent position
Use light tapping of the vein
– If insufficient consider:
Warming extremity (1)[A]
Vasodilator: Nitroglycerin ointment topical (2)[B]
• Sedation for uncooperative patients
– Oral: Midazolam, clonidine, ketamine
– Intranasal: Midazolam, dexmedetomidine
– Intramuscular: Ketamine
– Inhaled: Nitrous oxide, sevoflurane
• Use local anesthetic to prevent pain and subsequent patient movement
– Intradermal lidocaine
– Transdermal lidocaine/prilocaine (EMLA)
– Iontophoresis lidocaine (Numby Stuff)
• Stabilize the vein with skin traction
• Insert the needle with bevel up (3)[B]
• Verify correct IV placement of the catheter
– Aspirate blood from catheter
– Fluid should infuse with minimal pressure.
– Tourniquet applied proximally slows infusion rate.
– No pain and no swelling with infusion
– Infrared imaging and ultrasound may be able to detect infiltration.
After 2 failed attempts refer to staff with advanced IV skills
TREATMENT
Utilize vein visualization technology if needed

• Transillumination involves utilizing a very bright light through the hand or placed adjacent
to the vein site (4)[B].
– Works well for superficial veins
– Least expensive method
– Requires darkened room
– Device contacts skin.
– One hand of the technician must hold the light.
– Less effective with darker skin tones
– Burns have resulted with non-approved devices.
• Near infrared imaging.
– Works well for superficial veins
– More expensive
– Does not require darkened room
– Device does not contact skin.
– Hands-free option for the technician
– Not affected by skin tone
– 2-dimensional image limits perception of vein depth.
• Ultrasound (5)[A]
– Works well for deeper veins
– Most expensive; however, many anesthesia or emergency departments already own one.
– Does not require darkened room
– Device does contact skin and requires gel applied to skin.
– One hand must hold ultrasound transducer.
– Brachial veins adjacent to brachial artery and median nerve can be cannulated by
experienced practitioners.
– Deep veins may require longer catheters and/or guidewire techniques.
• Emergent or alternative IV access can be attained as follows:
– Central line placement in the internal jugular, subclavian, or femoral veins
– Intraosseous
– Tracheal; appropriate for some medications but not fluids. “NAVEL” mnemonic drugs
include naloxone, atropine, vasopressin, epinephrine, and lidocaine.
– Venous cutdown requires a longer insertion time.
FOLLOW-UP
If IV access cannot be established, consider:

• Alternate type of vascular access such as central line or intraosseous
• Alternative routes for medication administration (oral, subcutaneous, and intramuscular)
CLOSED CLAIMS DATA
• Most common complications related to IV catheters (140 total claims):
– Skin slough or necrosis: 28%
– Swelling/inflammation/infection: 17%
– Nerve damage: 17%
– Fasciotomy scars from compartment syndrome: 16%
– Air embolism: 8% (most claims for air embolism resulted from air in blood bags from cell
savers)
– Burns due to heat compresses used to treat IV infiltrations: 3%
• 55% of IV complications were related to the extravasation of drugs or fluids, most
commonly:
– Thiopental
– Vasopressors (dopamine, dobutamine, epinephrine)
– Calcium chloride
• Interestingly, there were no claims for complications of IV catheters in patients who had
previously had an axillary node dissection on the ipsilateral arm.
• Overall median payment was $47,475.
REFERENCES
1. Lenhardt R, Seybold T, Kimberger O, et al. Local warming and insertion of peripheral
venous cannulas. Br Med J. 2002;325:409–412.
2. Andrew M, Barker D, Laing R. The use of glyceryl trinitrate ointment with EMLA cream for
IV cannulation in children undergoing routine surgery. Anaesth Intens Care.
2002;30(3):321–325.
3. Black JL, Pusic MV, Harmidy D, et al. Pediatric intravenous insertion in the emergency
department bevel up or bevel down? Pediatr Emerg Care. 2005;21(11):707–711.
4. Katsogridakis YL, Seshadri R, Sullivan C, et al. Veinlite transillumination in the pediatric
emergency department. Pediatr Emerg Care. 2008;24(2):83–88.
5. Constantino TG, Parikh AK, Satz WA, et al. Ultrasonography-guided peripheral intravenous
access versus traditional approaches in patients with difficult intravenous access. Ann
Emerg Med. 2005;46:456–461.
ADDITIONAL READING
• American Society of Anesthesiologists Closed Claims Project: Bhananker SM, Liau DW,
Kooner PK, et al. Liability related to peripheral venous and arterial catheterization: A closed
claims analysis. Anesth Analg. 2009;109(1):124–129.
• Infusion Nurses Society. 2011. Infusion Nursing Standards of Practice.
• National Kidney Foundation. 2006. Updates: Clinical Practice Guidelines Recommendations:
Vascular Access.
CLINICAL PEARLS
• Be aware of the Infusion Nurses Society and National Kidney Foundation guidelines that
outline which IV access sites to avoid.
• Warming the extremity is effective in dilating veins.
• Transillumination and infrared imaging facilitate superficial vein access.
• Ultrasound is very effective for visualizing deeper veins.
DIFFUSION
Vijay Tarnal, MBBS, FRCA
BASICS
DESCRIPTION
• Diffusion is the process by which molecules of a solute transfer through a layer or surface of
a solution. It is a passive process, and the net movement of solutes occurs down a
concentration (or electrical) gradient.
• Laws defining diffusion:
– Fick’s law states that the rate of diffusion of a substance across a unit area is proportional
to the concentration gradient. This applies to a single homogenous phase, and the rate of
diffusion is equal to flow multiplied by concentration. In a non-homogenous medium, the
rate of diffusion is proportional to the tension gradient (diffusion of gas into solution).
– Graham’s law of diffusion states that the rate of diffusion of a gas is inversely proportional
to the square root of its molecular weight.
• The transport of water and other molecules across biological membranes is essential to
many processes in the human body.
• Diffusion can be described as:
– Simple: A passive process by which solutes move from a region of higher concentration to
one of lower concentration (down a concentration gradient). Oxygen, nitrogen, carbon
dioxide, urea, steroids, and fatty acids are transported across membranes by simple
diffusion.
– Ion channel mediated: Ions channels are comprised of polypeptide subunits that are
embedded in the phospholipid bilayer of the cell membrane. These ion channels render
the cell membrane selectively permeable to certain ions such as Na+, K+, Ca2+ and Cl−
(the positive or negative charge would otherwise preclude movement across the bilipid
membrane). Opening and closing of these ion channels allows rapid changes to ion
concentration on either side of the cell membrane.
– Active transport: This involves movement of molecules against a concentration gradient,
and is mediated by integral membrane proteins or carriers. Carriers can be uniport
(specific substance), anti-port (exchange one substance for another), or symport (transport
more than one substance); they require the expenditure of chemical energy (ATP). An
example is the Na+-K+-ATPase carrier, which maintains a transmembrane gradient of
Na+ and K+ ions. Secondary active transport involves transport of a substance and an ion
together. The carrier has 2 separate binding sites. An example of this is glucose and Na+
transport across the intestinal mucosa.
– Facilitated: A misnomer, as this describes the passive transport of substances from higher
to lower concentration, which is facilitated by integral transport proteins. No energy is
utilized. Glucose is transported into cells by this mechanism.
Tonicity Effects on the Red Blood Cell
• Osmosis is a specific type of diffusion, and involves the net movement of water across
different concentrations. Tonicity is the measure of an osmotic pressure gradient produced
between 2 compartments when separated by a semi-permeable membrane.
– Isotonicity describes a solution where the concentration of solute is the same both inside
and outside of the cell, with equivalent water movement into and out of the cell.
– Hypertonicity describes a higher concentration of solute outside the cell, with net water
movement out of the cell.
– Hypotonicity describes a lower concentration of solute outside the cell, with net water
movement into the cell.
• Diffusion across the alveolar–capillary membrane: Gas diffuses between the alveoli and
capillaries based on partial pressure gradients, blood solubility, tissue surface area, and
tissue thickness. In the blood, gas may dissolve and reach an equilibrium state based upon
its solubility coefficient. The rate of gas transfer is directly proportional to tissue surface
area.
– Oxygen and carbon dioxide transfer occurs via simple diffusion between alveoli and
capillary blood, as well as systemic capillary blood and tissue cells.
– Red blood cells take 0.75 seconds to pass through the pulmonary circulation. Carbon
dioxide reaches equilibrium in <0.1 seconds, whereas oxygen takes slightly longer due to
its slower diffusion and binding to hemoglobin.
• Neuromuscular transmission results from chemical messengers (acetylcholine), voltage-gated
receptors, or mechanical stretch receptors of membranes.
– Acetylcholine (ACh) release from the presynaptic membrane diffuses across the
neuromuscular junction and binds to ACh receptors located on the postsynaptic
membrane. This binding elicits ion channel mediated Na+ and K+ conductance down
their gradient. The sudden influx of Na+ produces a positive end plate potential; if an
action potential is reached/generated, it triggers excitation/contraction coupling in the
muscle and brings about muscle contraction.
ANATOMY
• Phospholipid membranes of cells
• Lung units: Alveolar–pulmonary capillary membrane
• Nervous system: Blood–brain barrier, axons of neurons
• Placenta
• Tissue edema and interstitial lung disease (e.g., interstitial fibrosis) decrease the diffusion
capacity and increase the distance between the alveolar membrane and diffusing gases. This
results in increased Alveolar-arterial oxygen gradients (and ratios).
• Acute tubular necrosis describes damage to the renal tubules from exposure to toxins or
ischemia. It can impair diffusion of water or urea across the tubular membrane.
• Nitrous oxide (N2O) and expansion of confined air spaces. N2O diffuses out of the blood and
into pockets of trapped gas within the patient. However, because nitrogen is poorly soluble
in blood (1/34th the solubility compared to nitrous oxide), it takes longer for it to diffuse
out of the air space and into the blood. This “lag time” results in larger amounts of nitrous
entering the air space and an increase in volume and/or pressure within the confined space.
In patients with intestinal obstruction, pneumothorax, pneumocephalus, or undergoing
middle ear or eye surgery, this may cause serious damage. Endotracheal tube cuffs can also
expand and have the potential to compromise tracheal mucosal perfusion, leading to edema
and ischemia. Avoid using N2O in decompression sickness.
• Second gas effect: When N2O is administered in high concentration with a volatile
inhalational agent of low solubility, the rapid N2O diffusion out of the alveoli into the
pulmonary capillaries produces an increasing concentration of the second agent (volatile
agent) within the alveoli. As a result, there will then be an increased uptake of the second
agent into the pulmonary capillaries, due to the higher partial pressure gradient between
the 2 compartments.
• Diffusion hypoxia: When N2O administration is discontinued, the rapid diffusion of N2O out
of the pulmonary capillaries and into the alveoli will reduce the alveolar oxygen
concentration. There will be a decreased O2 partial pressure driving gradient from the
alveoli to the pulmonary capillaries (and hemoglobin molecules), with the potential for
tissue hypoxia. Increasing the fractional inspired concentration of oxygen can prevent and
correct transient hypoxemia.
• Local anesthetics should be injected in close proximity to the nerves that are to be blocked
in order to improve diffusion into nerves (enhanced onset, strength, and duration of block).
Vasoconstrictor additives decrease systemic uptake, leaving more drug at the site of action.
• Blood brain barrier (BBB): Serves as both a physical barrier and a system for cellular
transport mechanisms. Solutes move across the BBB by all of the 4 basic mechanisms of
diffusion (simple, facilitated, ion channel mediated, and active transport). As a result, the
BBB provides tight control over ion concentrations in the brain, as well as protects against
toxins and changes in blood glucose. Drugs such as mannitol and hypertonic saline are used
in the treatment of increased intracranial pressure (ICP); its therapeutic application is based
upon establishing a hypertonic environment in the systemic vasculature, across the
semipermeable BBB. Because water then moves freely by osmosis (down the osmolar
concentration gradient), there is a net movement out of the intracellular and interstitial
spaces of the BBB and into the systemic vasculature. This results in a decrease in
intracranial volume, and hence pressure.
• Absorption of drugs by enteric, sublingual, rectal, nasal, intramuscular, subcutaneous,
transmucosal, and transdermal routes is dependent on the following factors:
– Permeability coefficient which is related to the solubility of the drug in the tissue between
the site of administration and the blood draining the tissue
– Concentration gradient which is maintained by a high concentration of drug at the site of
administration and rapid blood flow
– Increased temperature enhances the rate of diffusion secondary to increased molecular
movement.
• The placenta is, in effect, a lipid bilayer.
– Some nutrients cross the placental barrier via active transport process.
– Drugs cross via passive diffusion. However, protein binding and ionization on either side
of the membrane affects the transfer of drugs.
– Ion trapping: Fetal blood has a lower pH than that of the maternal blood. Weak bases,
such as opioid analgesics and local anesthetics, become more ionized once they enter the
fetal circulation. Because ions cannot cross the placenta, they are trapped on the fetal side
of circulation. Ionized drug accumulation can occur in fetal distress where the pH
becomes even lower.
– General anesthesia for Cesarean sections is induced after prepping and with the surgeons
scrubbed and ready for incision in order to decrease the effect of induction medications
and volatile agents that can diffuse across the placenta.
REFERENCES
1. Sleath GW, Jenkins LC, Graves HB. Diffusion in anaesthesia. Can Anaesth Soc J.
1963;10:72–82.
2. Fanning GL, Colgan FJ. Diffusion hypoxia following nitrous oxide anesthesia. Anesth
Analg. 1971;50:86–91.
3. Munson ES. Transfer of nitrous oxide into body air cavities. Br J Anaesth. 1974;46(3):202–
209.
ADDITIONAL READING
• Davis PD, Parbrook GD, Kenny GNC. Basics of physics and measurement in anaesthesia, 4th
ed. Butterworth Heinemann Co.
• Pneumothorax
CLINICAL PEARLS
• Exercise caution when using nitrous oxide for middle ear surgery, bowel surgery, or
craniotomy.
• Barring neuromuscular agents (high molecular weight and quaternary ammonium
compounds), most drugs used in anesthesia practice can cross the placental barrier.
• Inclusion of epinephrine with local anesthetics can prolong the block and reduce the risk of
systemic toxicity by decreasing diffusion of drug from the injection site.
DOUBLE LUMEN TUBE (DLT)
Siamak Rahman, MD
BASICS
DESCRIPTION
• Double lumen endotracheal tubes (DLT) are the most commonly used technique for one lung
ventilation (OLV) or lung isolation. Other techniques utilize a single lumen endotracheal
tube with:
– An enclosed bronchial blocker (Univent)
– A wire-guided endobronchial blocker (Arndt blocker)
– A Fogarty catheter as a bronchial blocker
• Double lumen tubes are advanced into the airway and the distal lumen is positioned in
either the right or left main bronchus; the proximal lumen is positioned in the trachea. By
inflating the tracheal and bronchial cuffs, each lung will be ventilated through a different
lumen of the tube, and lung isolation can be obtained by only ventilating the desired lumen
at the proximal connector of the double lumen tube.
• Indications for OLV include:
– Isolating one lung from the other, in the case of bleeding, abscess, or bronchopleural
fistula
– Collapsing the right or left lung independently to aid with surgical visualization
• Double lumen tubes are designed to isolate ventilation; they have the added benefit over
other techniques of facilitating deflation and suctioning, and administering continuous
positive airway pressure (CPAP) to the deflated lung. The DLT consists of:
– A tracheal and bronchial lumen
– Cuffs on both lumens
– Right or left sidedness
FIGURE 1. Double lumen tube showing a connector, stylet, 2 pilot balloons, lumens (tracheal and bronchial), and different
color cuffs.
• Tracheal lumen: Shorter in length than the bronchial lumen. Designed to allow ventilation
through its lumen above the carina. The tracheal lumen internal diameter sizes are 4.5 mm
and 4.7 mm for 35F and 37F double lumen tubes, respectively; they are 2 mm larger than
their bronchial lumens. The internal diameter of tracheal and bronchial lumens are equal in
39F and 41F double lumen tubes, at 4.9 mm and 5.4 mm, respectively.
• Bronchial lumen: Longer in length than the tracheal lumen; distal tip is at a fixed distance
from the trachea. Designed to allow ventilation through its lumen into the mainstem
bronchus.
• Cuffs: Respective pilot balloons are used to inflate and deflate the distal cuffs of the tracheal
and bronchial lumens. The bronchial cuff is typically blue in color to aid with identifying its
location (when bronchoscopy is performed through the tracheal lumen).
ANATOMY
• The tracheobronchial tree begins with the trachea at the level of the cricoid cartilage; it is
approximately 11–13 cm long in the normal adult. It divides into right and left mainstem
bronchi at the level of the carina (T5).
• Left main bronchus: Takes a 45° angle off the trachea and bifurcates after 5 cm into the
upper and lower lobes.
• Right main bronchus: Takes a 25° angle off the trachea and bifurcates at a shorter distance
in the normal adult (∼1–2.5 cm) into the upper, middle, and lower lobes.
• Vocal cord injury
• Edema
• Trauma
• Preparation: The placement of a DLT can be challenging due to its larger diameter and the
need to be positioned into a specific mainstem bronchus.
– In addition to a detailed airway examination, the anaesthetist should review films and
images of the neck and thorax for changes in airway lumen, abnormal anatomy, masses,
effusions and abscesses, hemorrhage and hematomas, if available.
– Review pulmonary function. Patients with severe restrictive lung disease and very poor
DLCO generally do not tolerate OLV.
– Discuss surgical plan with the surgeon. Some patients will need to be kept intubated
postoperatively with a single lumen tube (requiring a tube exchange) while others will
need continued selective ventilation (leaving DLT in place and utilizing two different
ventilators).
– Equipment: Different sized laryngoscope blades and a fiberoptic scope. Consider having an
indirect video laryngoscope, tube exchanger, or gum bougie available.
– Difficult airway: In the event of a suspected (or unsuspected) difficult airway, it is better
to place a single lumen tube and isolate the lung with a bronchial blocker. However, when
a DLT is necessary, a single lumen tube can be placed and a tube exchanger can then be
used to switch to a DLT. A fiberoptic scope should be used to confirm proper positioning.
– Size: The Robert-Shaw is the most commonly used DLT. They are available in sizes 35, 37,
39, and 41F and refer to the outer diameter. Some proponents recommend choosing the
largest tube that will fit in order to decrease the chance of migration and obstruction,
which can result in hypoxemia, lung isolation failure, increased airway resistance,
difficulty of passing a fiberoptic scope, or tracheal obstruction. Others propose inserting a
smaller than conventional size to decrease trauma with insertion. One study demonstrated
that choosing a smaller size did not influence the incidence of hypoxemia, need for
repositioning, or success of lung isolation (1)[A]. Some studies suggest that measurement
of the tracheal size from available CT or MRI imaging films can be used as a guide to
choose DLT size (2)[A]. In general, most male adults take a size 37F or 39F and most
female adults take a size 35F or 37F.
– Sidedness: Left-sided DLTs are used for most cases that require lung isolation and OLV. If a
left pneumonectomy is planned, the left DLT can be withdrawn back to the trachea before
the surgeon staples the bronchus. Right-sided double lumen tube placement is more
challenging because of the early branching of the right upper lobe and the proper
positioning of the opening for ventilation (Murphy eye) of the endobronchial lumen at its
origin (3)[B]. They were created primarily for left lung surgeries.
FIGURE 2. Correct placement. In both instances, the proximal tracheal lumen is located within the trachea. The left-sided
DLT has the (distal) bronchial lumen located in the left mainstem bronchus. Notice the longer distance before the left
upper lobe take-off; thus providing an increased margin for error. The right-sided DLT has the (distal) bronchial lumen
located in the right mainstem bronchus. The shorter distance before the right upper lobe take-off decreases the margin for
error.
• Insertion: The tip of the tube is inserted just through the vocal cords and then immediately
rotated 90° in the direction of the bronchus that one is aiming to intubate (4)[B].
• Confirming position:
– Auscultation of the lungs and manual ventilation while the tracheal and bronchial lumens
are selectively clamped and unclamped is one technique of determining proper positioning
of the double lumen tube (5)[B].
– A fiberoptic scope is considered the gold standard, however, to confirm proper position of
the double lumen tube (1)[B]. The fiberoptic scope is advanced through the tracheal
lumen, and adequate positioning of the DLT is determined when the carina is visualized
and the inflated blue cuff is observed in the desired bronchus (barely seen at the carina).
For a proper right side DLT placement, it is necessary to look through the bronchial lumen
with the fiberoptic scope to position the lateral slit of the Murphy eye at the site where
the right upper lobe branches out.
FIGURE 3. View from fiberoptic bronchoscope inserted through the tracheal lumen above the carina on a correctly placed
left-sided DLT.
REFERENCES
1. Amar D, Desiderio DP, Heerdt PM, et al. Practice patterns in choice of double-lumen tube
size for thoracic surgery. Anesth Analg. 2008;106(2):379–383.
2. Brodsky JB, Macario A, Mark JBD. Tracheal diameter predicts double-lumen tube size: A
method for selecting left double-lumen tubes. Anesth Analg. 1996;82:861–864.
3. Campos JH, Massa C, Kernstine KH. The incidence of right upper-lobe collapse when
comparing a right-sided double-lumen tube versus a modified left double-lumen tube for
left-sided thoracic surgery. Anesth Analg. 2000;90:535–540.
4. Koshy T, Nair SG. Positioning of double-lumen endobronchial tubes: Correlation between
clinical and bronchoscopic findings. Indian J Anaesth. 2003;47(2):116–119.
5. Alliaume B, Coddens J, Deloof T. Reliability of auscultation in positioning of double-lumen
endobronchial tubes. Can J Anaesth. 1992;39(7):687–690.
ADDITIONAL READING
• Lohser J. Evidence-based management of one-lung ventilation. Anesthesiol Clin.
2008;26(2):241–272.
• Pulmonary ventilation
• Perfusion matching
CLINICAL PEARLS
• The choice of a smaller than conventional DLT has not been associated with adverse
outcomes such as hypoxemia, need for higher balloon cuff inflation pressures, or increased
incidence of repositioning.
• DLT should be advanced slowly, especially if a larger than conventional size is selected, to
prevent damage to and rupture of the bronchi.
• Placing a double lumen tube on a patient with a known difficult airway can make the
process more challenging since the tubes are bulky and harder to place.
• A left DLT can be technically used for all cases of lung isolation (3)[A].
DUCHENNE’S MUSCULAR DYSTROPHY (DMD)
Jorge A. Galvez, MD
BASICS
DESCRIPTION
• Duchenne’s muscular dystrophy (DMD) is a progressive neuromuscular disease.
– Initially presents in early childhood as weakness and motor delay
– Progresses to significant disability
– Follows an X-linked recessive inheritance with female carriers and males being affected
• Advances in cardiopulmonary therapy have improved survival and increased the need to
undergo procedures that may require sedation or general anesthesia.
• Succinylcholine is an absolute contraindication. Binding to extrajunctional receptors can
result in acute hyperkalemia with resultant cardiac arrhythmias. Because muscular
dystrophy disorders may go undiagnosed in the 1st and 2nd decades of life, succinylcholine
should be avoided for routine airway management due to the risk of fatal reactions.
• Mimics malignant hyperthermia where exposure to inhaled volatile agents (halothane,
isoflurane, sevoflurane, desflurane) in patients with DMD may result in hyperthermia,
hyperkalemia, and sudden death from cardiac arrest.
EPIDEMIOLOGY
Prevalence
• Most common of all muscular dystrophies
• Live male births: 1 in 3,500
• X-linked recessive inheritance
Prevalence
Increased survival due to cardiopulmonary therapy advances
Mortality
• Mean survival approximately 25 years
• Death usually from progressive cardiomyopathy and/or ventilatory insufficiency
• X-linked recessive inheritance of dystrophin gene
• Phenotype expressed in males
• Females not affected, only carriers
• Dystrophin is responsible for connecting the cytoskeleton of each muscle fiber to the
underlying basal lamina or extracellular matrix through a protein complex composed of
several subunits. It prevents unregulated and unrestricted calcium entry into the
mitochondria.
• In DMD, the recessive mutation on the X-chromosome prevents normal formation of
dystrophin. Calcium can abnormally pass through the cell membrane or sarcolemma of
mitochondria, resulting in increased osmotic effects and mitochondrial lysis.
– Characterized by a complete loss of dystrophin
– Becker’s muscular dystrophy is a less severe dystrophy caused by partial functioning of the
dystrophin protein.
• Malignant hyperthermia and DMD are genetically distinct diseases.
• Avoid potentially fatal drug reactions, volatile anesthetics (halothane, sevoflurane,
isoflurane, desflurane), succinylcholine. Patients should be scheduled as first starts, and if
the anesthesia machine is utilized, it should be appropriately flushed, and the carbon
dioxide absorber changed.
• Assessment of baseline pulmonary dysfunction is critical. Goals should include avoidance of
upper airway obstruction, hypoventilation, and atelectasis. Postoperative mechanical
ventilation may be necessary, as well as deep inspiratory maneuvers and pulmonary toilet.
• Operations with major blood loss or fluid shifts may result in compromised cardiac and
respiratory function during recovery. Consider invasive monitoring for guidance.
SYMPTOMS
• Almost all DMD patients are symptomatic by 6 years of age: Difficulty running, jumping,
climbing steps, waddling gait
• Loss of ability to ambulate by 14 years of age
• Snoring
• GI reflux
• Scoliosis with thoracic insufficiency
History
• Presents in early childhood as weakness and motor delay
• Delayed walking beyond 15 months of age
• Progressive lower extremity weakness
Signs/Physical Exam
• Gower’s sign: Patients use their arms when they get up from the floor.
• Pseudo-hypertrophy of calves
• Accessory muscle use
• Proximal muscle weakness
• Macroglossia
TREATMENT HISTORY
• Spine fusion for scoliosis, thoracic insufficiency
• Gastrostomy or Nissen fundoplication for dysphagia
• Tracheostomy with ventilator dependence for respiratory insufficiency
MEDICATIONS
• Glucocorticoids may preserve respiratory muscle strength.
• GI medications: H2 receptor antagonists, proton pump inhibitors, motility agents, laxatives
for management of constipation
• Cardiac medications can include angiotensin-converting enzyme (ACE) inhibitors,
antiarrhythmics, and diuretics.
Labs/Studies
• Pulmonary function tests demonstrate a restrictive pattern:
– Pulse oximetry: If <95%, consider measuring end-tidal CO2
– Spirometry: A restrictive pattern is seen with a decreased forced vital capacity (FVC) and a
normal or increased FEV1/FVC (FVC may decrease to a greater extent than the FEV1).
Measurements of the FVC may have predictive value for the risk of postoperative
pulmonary complication (PPC). PPC is increased when the FVC <50%; it is significantly
increased when <30%. Additionally, some suggest measuring a supine and upright FVC; a
decreased FVC while supine may be more predictive of PPC.
– Flow volume loops: Curve shifts rightward on the x-axis secondary to a decreased total
lung capacity; all volumes are reduced; peak expiratory flow (PEF), maximal expiratory
flow (MEF), and maximal inspiratory flow (MIF) are all reduced; however, flow reduction
is congruent over the inspiratory and expiratory loops and the MEF50 ∼ MIP50.
• Markedly elevated creatinine kinase (CK) levels
• Neurologic: Normal
• Cardiac: Dilated cardiomyopathy, conduction defects, pulmonary hypertension, congestive
heart failure
– Patients have a limited ability to increase cardiac output in response to stress.
– Dilated cardiomyopathy is present in up to 1/3rd of patients by age 14 years; reaches
100% by age 18 years.
• ENT: Macroglossia, weak upper respiratory dilator muscles
• Respiratory: Restrictive lung disease due to progressive deterioration in respiratory muscle
strength (diaphragm, intercostal, and accessory muscles)
– Hypoventilation
– Impaired cough, predisposes to atelectasis and respiratory failure
• Gastrointestinal: Dysphagia, dysmotility, aspiration risk, malnutrition (poor wound healing,
muscle weakness, electrolyte abnormalities); may impair respiratory function if abdominal
distention is present and not controlled.
FVC <30%; consider delay for training in noninvasive respiratory support
TREATMENT
Premedications
Use with caution as patients are very sensitive to sedative effects. The resultant
hypoventilation may lead to rapid cardiopulmonary deterioration.
• Review resuscitation guidelines and advanced directives for individual patients, as goals of
care may vary depending on disease severity/stage.
• Decisions regarding resuscitation parameters, attitudes toward prolonged dependency on
mechanical ventilation, and tracheostomy should be clearly articulated and accessible in the
medical record.
INTRAOPERATIVE CARE
• Consider alternatives to sedation and general anesthesia whenever possible.
• When general anesthesia is necessary, total intravenous anesthesia should be utilized.
Monitors
• Arterial line may help assess blood gases.
• Major operations with expected high blood loss or fluid shifts (e.g., spine fusion) may
warrant invasive monitors to guide resuscitation and postoperative management.
• Airway support options depend on baseline pulmonary status. Intubation and mechanical
ventilation may be necessary or preferred if:
– Poor respiratory muscle strength
– Ventilator dependent
– Tracheostomy in situ
– High risk for aspiration
– Macroglossia, snoring is severe; patients are prone to airway obstruction with sedation.
• The limited mobility of the mandible and C-spine: Makes jaw-thrust a less effective
maneuver at receiving airway obstruction; may hinder vocal cord visualization on
laryngoscopy.
• Total intravenous anesthesia for induction
• Muscle relaxation for intubation may not be necessary, given the baseline muscle weakness.
Succinylcholine is absolutely contraindicated.
• Other potential airway devices include noninvasive positive pressure ventilation, laryngeal
mask airway, mechanical ventilation with mouthpiece, tracheostomy, BiPAP (bilevel
positive pressure ventilator) with face-mask or nasal interface.
Maintenance
• For GA cases, total intravenous anesthesia for maintenance. Muscle relaxation may not be
necessary.
• For MAC cases, titrate sedation cautiously and relieve airway obstruction.
• Consider noninvasive respiratory support to facilitate extubation (BiPAP or CPAP)
• For FVC <50% (especially FVC <30%), consider:
– Extubation directly to non-invasive respiratory support
– Delaying extubation until respiratory secretions are well controlled
– Delaying extubation until the SpO2 is normal or baseline
FOLLOW-UP
BED ACUITY
• ICU setting is often necessary in order to provide:
– Careful assessment of respiratory parameters such as hypoxemia due to hypoventilation,
atelectasis
– Secretion management, chest percussions
– Manual assisted cough and mechanical insufflation-exsufflation (MI-E) device
postoperatively
– Mechanical ventilation
• Optimize pain control. If sedation or hypoventilation occurs, delay ETT extubation 24–48
hours or use noninvasive positive pressure ventilation.
• Consider enteral feeding with nasogastric or nasoduodenal tube in patients who cannot
achieve adequate oral nutrition 24–48 hours postoperative.
• Consider total parenteral nutrition in patients who develop ileus.
• Pulmonary and cardiology evaluation as needed
• Nutrition assessment, consider strategies for dysphagia
COMPLICATIONS
• Pulmonary: Increased when the FVC <50%, especially high when the FVC <30%. They
include aspiration, weakness, atelectasis and decreased functional residual capacity
(hypoxemia), and failure to wean from mechanical ventilation.
• Cardiovascular: Hypotension and arrhythmias
• Gastrointestinal: Postoperative gastroparesis, intestinal dysmotility, constipation; may be
exacerbated by opioid analgesics.
• Rhabdomyolysis secondary to depolarizing muscle relaxants (succinylcholine)
• Malignant hyperthermia: Increased risk
REFERENCES
1. Hayes J, Veyckemans F, Bissonnette B. Duchenne muscular dystrophy: An old anesthesia
problem revisited. Pediatr Anesth. 2008;18:100–106.
2. Birnkrant DJ, Panitch HB, Benditt JO, et al. American College of Chest Physicians
consensus statement on the respiratory and related management of patients with Duchenne
muscular dystrophy undergoing anesthesia or sedation. Chest. 2007;132(6):1977–1986.
3. Gurnaney H, Brown A, Litman RS. Malignant hyperthermia and muscular dystrophies.
Pediatr Anesthesiol 2009;109(4):1043–1048.
4. Hopkins PM. Anaesthesia and the sex-linked dystrophies: Between a rock and a hard place.
Br J Anaesth. 2010;104(4):397–400.
ADDITIONAL READING
• Muscular Dystrophy Association. http://www.mdausa.org/
• Flow volume loops
• Spirometry
• Hyperkalemia
CODES
ICD9
359.1 Hereditary progressive muscular dystrophy
ICD10
G71.0 Muscular dystrophy
CLINICAL PEARLS
• High risk of cardiac and pulmonary complications with sedation or anesthesia. Alternatives
such as local anesthesia or minimally invasive procedures should be considered.
• Avoid succinylcholine and volatile anesthetic gases (halothane, sevoflurane, isoflurane,
sevoflurane) due to potentially fatal hyperkalemia and rhabdomyolysis, respectively.
• Postoperative mechanical ventilation may be needed. Noninvasive positive pressure
ventilation can facilitate extubation in patients with low FVC (<30%).
DYSPHAGIA
John Henao, MD
BASICS
DESCRIPTION
• Dysphagia describes abnormal deglutition from impaired coordination, obstruction, or
weakness affecting swallowing biomechanics.
– Odynophagia: Painful swallowing
– Globus (hystericus): Sensation of a lump in the throat
• Dysphagia is often associated with significant comorbidities, including difficult airways, and
also poses a risk for aspiration.
• Patients with certain comorbidities frequently suffer from undiagnosed dysphagia.
EPIDEMIOLOGY
Incidence
Overall lifetime incidence: 7%
Prevalence
• Patients with CVA: >30% (1)
• Patients 65 years or older: 40% (1)
• Patients with Parkinson’s: 52–82% (1)
• Patients with Alzheimer’s: 84% (1)
• Institutionalized elderly: >60% (1)
Morbidity
• In general, aspiration pneumonia occurs in 4–8 of every 1,000 patients admitted to a
hospital in the US (2).
• Aspiration occurs in up to 40% of patients with dysphagia, but rates vary by etiology.
Mortality
• Dependent upon underlying etiology of dysphagia
• Aspiration carries a risk of 3.8–4.6%.
• Chronic gastroesophageal reflux
• Developmental disability
• Increased age
• Infection (botulism, diphtheria, Lyme, HIV, Candida, herpes, CMV, syphilis)
• Medications: Anticholinergics, HMG-CoA reductase inhibitors, metoclopramide,
chemotherapy agents, sedatives, antipsychotics, neuroleptics, antacids, antihistamines, and
NSAIDS
• Neurologic impairment (cervical spinal injuries anterior > posterior, CVA, dementia, TBI)
• Neuromuscular degeneration (ALS, multiple sclerosis, myopathies)
• Respiratory (intubation >48 hours, tracheostomy, ventilator dependency)
• Substances (alcohol, cigarettes)
• Surgery related (head and neck or esophageal, cervical spine, intracranial, thoracic, post-
radiation effects)
PATHOPHYSIOLOGY
• Deglutition consists of 3 phases based on functional and anatomic characteristics.
– Oral phase (preparatory and propulsive portions) alters the food bolus size, shape, volume,
and pH. It involves voluntary and involuntary mechanisms controlled by CN V, VII, and
XII, and is dependent on the lips, muscles of mastication, saliva, and tongue. Dysfunction
is most frequently a result of poor tongue control.
– Pharyngeal phase consists of the elevation of the entire pharyngeal tube including the
larynx. This reflex is controlled by CN IX and X and is dependent on the epiglottis, hyoid
bone, larynx, pharyngeal walls, soft palate, tongue, and vocal folds. Dysfunction of the
pharyngeal phase represents the most common cause of aspiration.
– Esophageal phase involves relaxation of the cricopharyngeal muscle and facilitates passage
into the esophagus, after which the bolus is transported via primary peristalsis. This reflex
is controlled by the medulla and is dependent on peristalsis and relaxation of the lower
esophageal sphincter.
• Patients may be hypovolemic. Reduced oral intake can result in hypernatremia with
associated hypertonic hyperosmolality and intracellular compartment shrinkage. Assess
volume status and create a fluid management plan.
• Anticipate a difficult airway, as dysphagia is often the result of distorted anatomy.
• Use caution when passing equipment (NG, OG, esophageal stethoscope, TEE).
• Increased risk of aspiration makes a rapid-sequence intubation appropriate in certain cases
(including pharyngeal disorders such as Zenker’s diverticulum or GERD).
SYMPTOMS
• Oral or pharyngeal dysphagia: Aspiration pneumonia, change in voice or speech, difficulty
initiating swallow, excessive salivation, nasal regurgitation, swallow followed by coughing,
choking, or sensation of food sticking in the back of throat, reflexive cough combined with a
wet voice (gurgling sounds produced on phonation of a prolonged “e”; has an 84% positive
predictive value) (2), and weight loss
• Esophageal dysphagia: Aspiration pneumonia, heartburn, pain during swallowing,
regurgitation of food particles, swallow followed by sensation of food sticking in the throat
or the upper chest, and weight loss
• Absence of symptoms may indicate silent aspiration (more common in older males).
History
• Time of onset or frequency of symptoms; rapidity of progression
• Association with liquids versus solids
• Changes in dietary habits
• Presence of pain
• Drooling or facial muscular weakness
• Weight loss or failure to thrive
• Presence of halitosis
• Aspiration or recurrent pneumonias
• Trauma involving the head, neck, or chest
• Neurologic or neuromuscular disorder
• Ingestion of acidic material or foreign body
Dysphagia more commonly presents in children with multiple impairments. Additional
history may include discussion of growth and development of the swallowing aperture;
development of normal oromotor reflexes; maturation of feeding behavior; and acquisition of
adequate nutrition for somatic growth.
Signs/Physical Exam
• General: Syndromal/non-syndromal and craniofacial anomalies
• Nose: Choanal atresia, congenital mass
• Oral cavity: Dentition, gag reflex, palate, tongue, tonsils
• Hypopharynx: Mass effect, pooling of secretions
• Larynx: Congenital anomaly, mass, vocal fold mobility, voice quality
• Neck: Osteophytes, presence of mass, thyroid gland
• Pediatrics: Observe feeding and sucking and assess esophageal patency (consider passing an
NG tube)
TREATMENT HISTORY
• Previous gastric tube placement to avoid aspiration from oral feedings
• Botulism toxin injections for achalasia
MEDICATIONS
• Nitrates, CCBs, sildenafil, or botulism toxin injections for treatment of achalasia (3)
• Topical steroids or leukotriene receptor inhibitors for treatment of eosinophilic esophagitis
Labs/Studies
• Modified barium swallow (MBS) or fiberoptic endoscopic evaluation of swallowing
(FEES)/with sensory testing (FEEST): Evaluate mechanical disorder. This is the gold
standard for identifying patients who have the potential to develop pneumonia and for
diagnosing aspiration and swallowing problems.
• Upper endoscopy (EGD): Evaluate mechanical disorder
• X-ray: Evaluate aspiration (patchy opacity, lower lobe infiltrate, air space disease) or
motility disorder (air–fluid levels vs. absence of stomach bubble) (3)
• Manometry: Evaluate motility disorder (3)
• pH monitoring: Evaluate reflux
• CT head and chest: Evaluate masses (3)
• See “Etiology/Risk Factors”
• Suspected pneumonia from aspiration
• Hypovolemia and hypernatremia
• Newly suspected dysphagia. Absent swallow response on command, inability to manage oral
pharyngeal secretions
CLASSIFICATIONS
• Penetration: Material enters the laryngeal area to the level of the true vocal folds.
• Aspiration: Material moves below the true vocal folds and enters the trachea.
TREATMENT
Premedications
Consider IV fluid boluses if patient is suspected to be hypovolemic.
Decreased cognitive function; may need consent from family member or power of attorney
INTRAOPERATIVE CARE
• Depends on type of surgery and patient comorbidities:
– If general anesthesia is chosen, an endotracheal tube should be considered in patients at
– If sedation is chosen, goals of sedation should be established; oversedation can result in
aspiration, particularly in the supine position.
Monitors
Difficult intubation should be anticipated in the oral phase disorders such as hypertrophic
tonsils, and those with congenital defects.
Maintenance
• Gastric suctioning to decrease stomach volume and risk of aspiration. It may be difficult to
direct equipment to the esophagus in patients with velopharyngeal insufficiency as well as
esophageal strictures, masses, or Schatzki’s ring.
• Replete fluid deficits while balancing the risk of fluid overload that could exacerbate
comorbidities.
• Patient positioning with the head elevated to prevent upper airway obstruction or aspiration
• Ensure full reversal of neuromuscular blockade
• Elderly or patients with Parkinson’s disease or Alzheimer’s may experience postoperative
delirium, further increasing risk of aspiration.
• Frequent assessments of airway patency
POSTOPERATIVE CARE
BED ACUITY
Dependent upon the surgery, ability to maintain proper nutrition and hydration, and risk for
aspiration, as well as the presence of comorbid disease
Consult: ENT, GI, speech language pathology (SLP), dietician, PT, and OT [B]. 66.8% of
patients with dysphagia secondary to neurogenic causes experience improved swallow
function after SLP services (4).
COMPLICATIONS
• Airway obstruction
• Aspiration pneumonia
• Bronchospasm
• Chronic chest infections
• Death
• Dehydration
• Malnutrition
• Pediatric complications: Apnea, bradycardia, choking episodes, chronic noisy breathing,
reactive airway disease, bronchitis, atelectasis
REFERENCES
1. Rofes L, Arreola V, Almirall J, et al. Diagnosis and management of oropharyngeal
dysphagia and its nutritional and respiratory complications in the elderly. Gastroenterol
Res Pract. 2011:818979.
2. Smith-Hammond CA, Goldstein LB. Cough and aspiration of food and liquids due to oral-
pharyngeal dysphagia: ACCP evidence-based clinical practice guidelines. Chest.
2006;129:154–168.
3. Lawal A, Shaker R. Esophageal dysphagia. Phys Med Rehabil Clin N Am. 2008;19(4):729–
745.
4. Ashford J, McCabe D, Wheeler-Hegland K, et al. Evidence-based systematic review:
Oropharyngeal dysphagia behavioral treatments. Part III: Impact of dysphagia treatments
on populations with neurological disorders. J Rehabil Res Dev. 2009;46(2):195–204.
• Aspiration
• Gastroesophageal reflux disease (GERD)
• Duchenne’s muscular dystrophy
CODES
ICD9
• 787.20 Dysphagia, unspecified
• 787.21 Dysphagia, oral phase
• 787.22 Dysphagia, oropharyngeal phase
ICD10
• R13.10 Dysphagia, unspecified
• R13.11 Dysphagia, oral phase
• R13.12 Dysphagia, oropharyngeal phase
CLINICAL PEARLS
• Abnormal swallowing can cause aspiration and increases the likelihood of pneumonia.
• History and symptoms concerning for malignancy: Worsening dysphagia, weight loss,
alcohol or tobacco use, and long-standing GERD
• JCAHO mandates that all stroke patients be screened for dysphagia before initiating an oral
diet.
• Despite normal EGD findings, esophageal biopsies need to be considered in the patient with
intermittent solid-food dysphagia to rule out eosinophilic esophagitis.
• MBS and FEES are the best tests available to evaluate dysphagia.
• In the geriatric population, diagnosis is frequently delayed because dysphagia may present
with atypical symptoms, or the symptoms may be attributed to other coexisting disorders.
Additionally, elderly patients are less likely to seek medical care as they often tolerate
symptoms better.
ECLAMPSIA
Daniel Mulcrone, MD
BASICS
DESCRIPTION
Eclampsia describes new-onset convulsions or coma during pregnancy. It is
• An emergency and carries a high risk of morbidity and mortality. Definitive treatment is
delivery of the fetus.
• Often a complication of severe preeclampsia; however, it can also occur in patients without
hypertension and proteinuria
• Can occur in the ante-, intra-, or postpartum period
EPIDEMIOLOGY
Prevalence
Can occur in ∼5 per 10,000 live births (1,2); may be higher (5–100 per 10,000 live births) in
developing countries (3)
Prevalence
• Antepartum: ∼40–50%
• Intrapartum: ∼20–40%
• Postpartum: ∼10–40%
Morbidity
• Preterm delivery (∼50%)
• HELLP syndrome (hemolysis, elevated liver enzymes, low platelets, ∼10–15%)
• Placental abruption (∼7–10%)
• Acute renal failure (∼5–10%)
• Disseminated intravascular coagulation (∼5%)
• Cardiopulmonary arrest (∼5%)
• Pulmonary edema (∼3–5%)
• Aspiration pneumonia (∼2%)
• Liver hematoma (∼1%)
• Stroke (ischemic or hemorrhagic, ∼0.02%)
Mortality
• Maternal mortality ∼10% (63,000 maternal deaths annually)
• Neonatal mortality ∼10%
• Etiology unclear
• Maternal risk factors:
– Demographics: Age >40 years old, African American ethnicity
– Pregnancy associated: Nulliparity, multiple gestations, molar pregnancy
– Comorbidities: Hypertension, renal disease, diabetes mellitus, factor V Leiden deficiency
– Smoking: (Note: Surprisingly has been associated with a decreased risk of preeclampsia)
• Fetal risk factors:
– Gestational age <28 weeks
• Paternal risk factors:
– History of fathering a preeclamptic pregnancy with another woman
– Mother with preeclampsia during gestation
• The etiology of eclamptic seizures remains unclear. Theories include systemic hypertension
resulting in:
– Cerebral over-regulation (vasoconstriction/vasospasm) which leads to hypoperfusion of
the brain and localized ischemia
– Loss of cerebral autoregulation leading to hyperperfusion and endothelial damage with
edematous sequelae
– Oxidative stress
• Control seizures and monitor for neurologic deficits which could signify an intracranial
hemorrhage
• Ensure maternal oxygenation, prevent maternal aspiration, and control hypertension (target
SBP <160 mm Hg; DBP <110 mm Hg)
• Prepare for urgent/emergent delivery
SYMPTOMS
• May be asymptomatic prior to seizure
• Preeclampsia symptoms: Visual disturbances (photophobia/blurred vision), headache, right
upper quadrant pain, epigastric pain, altered mental status
History
• Eclampsia risk factors
• Neurologic or seizure disorder
Signs/Physical Exam
• Seizures: Generalized tonic–clonic seizures lasting ∼60 seconds
• Coma
MEDICATIONS
• Antiepileptics, magnesium
Labs/Studies
• Labs:
– Urinalysis for proteinuria
– CBC, especially platelets and Hct
– CMP, including Mg2+
– Coagulation studies, including PT/INR, PTT, and fibrinogen
– Type and Cross
• Imaging studies:
– CT head: Useful in identifying cerebral edema, loss of cortical sulci, and/or cerebral
hemorrhage
• Central nervous system (CNS): Risk of cerebral edema, cerebral hemorrhage, and/or
alterations in cerebral autoregulation
• Cardiovascular: Decreased central venous pressure (CVP), increased peripheral vascular
resistance (PVR), coronary vasospasm, left ventricular hypertrophy, and/or increased
sensitivity to catecholamines
• Pulmonary: Airway edema, pulmonary edema, and/or increased risk of gastric aspiration
• Renal: Acute renal failure, decreased glomerular filtration rate, and/or decreased clearance
of uric acid
• Hematologic: Hemoconcentration, increased blood viscosity, thrombocytopenia, and/or
coagulopathy
• Hepatic: Risk of liver hematoma, hepatocellular damage, and/or periportal hepatic necrosis
• Placental: Uteroplacental insufficiency may lead to fetal hypoxia and/or intrauterine growth
restriction. There is an increased risk of placental abruption and/or premature labor.
Delivery may be delayed if the parturient is stable and reassuring fetal heart tones are
present.
TREATMENT
Premedications
• Magnesium sulfate (first line for seizures)
– Dosing: 4–6 g IV bolus over 15 minutes, followed by 1–2 g/hr for seizure prophylaxis
– Therapeutic level: ∼6–8 mEq/mL
– Contraindications: Heart block, Addison’s disease, hepatitis, myasthenia gravis, markedly
reduced renal function
– Pregnancy class A
– Possible interactions: Nifedipine (hypotension) and non-depolarizing neuromuscular
blockade (prolonged duration)
– Toxicity manifests with hyporeflexia and/or respiratory depression. Calcium gluconate (1
g IV) counteracts effects of magnesium.
• Phenytoin (second line for seizures)
– Dosing: 10 mg/kg dose over 1 hour
– Contraindications: 2nd or 3rd degree AV block, bradycardia, Adams–Stokes syndrome
– Pregnancy class D
– Adverse reactions: Blood dyscrasia, bullous or purpuric skin rash, QRS widening, cardiac
arrest (rapid infusion), hyperglycemia, and hepatic dysfunction
• Diazepam (second line for seizures)
– Dosing: 5–10 mg IV over 15 minutes; may be repeated every 15 minutes for a maximum
dose of 30 mg
– Contraindications: Narrow-angle glaucoma, hepatic failure, renal failure
– Pregnancy class D: Freely crosses the placenta and accumulates in the fetal circulation
– Adverse reactions: Cardiac arrest (rapid infusion), neonatal hypotonia, floppy infant
syndrome, infantile kernicterus
• Lorazepam (second line for seizures)
– Dosing: 4 mg IV infused over 5 minutes; repeat in 10 minutes for a maximum dose of 8
mg IV in a 12-hour period
– Contraindications: Narrow-angle glaucoma, hepatic failure, renal failure
– Pregnancy class D: Freely crosses the placenta and accumulates in fetal circulation
– Adverse reactions: Cardiac arrest (rapid infusion), neonatal hypotonia, floppy infant
syndrome, infantile kernicterus
• Hydralazine (first line for BP control)
– Dosing: 5–10 mg IV every 15 minutes
– Pregnancy class C
– Possible interactions: Severe hypotension may occur if co-administered with MAOIs
and/or beta-blockers.
– Adverse reactions: Uterine hypoperfusion, reflex tachycardia
• Labetalol (first line for BP control)
– Dosing: 20 mg IV every 10 minutes up to a maximum dose of 300 mg
– Contraindications: Cardiogenic shock, bradycardia, pulmonary edema, AV nodal block,
reactive airway disease, and CHF
– Adverse reactions: Neonatal bradycardia
• Nifedipine (second line for BP control)
– Dosing: 10 mg PO TID titrated to effect for a maximum dose of 120 mg/day
– Possible interactions: May cause severe hypotension if administered with magnesium
sulfate
Surrogate consent may be necessary if the patient is in a postictal state or is comatose.
INTRAOPERATIVE CARE
• Neuraxial anesthesia (spinal or epidural)—if platelets and coagulation are normal. If an
epidural catheter is already in place and properly functioning, the anesthetist may consider
bolusing with a fast onset local anesthetic (chloroprocaine, lidocaine with bicarbonate, etc.)
to avoid general anesthesia.
– Hypotension may accompany initiation or bolusing of neuraxial anesthesia. Patients with
preeclampsia are often intravascularly volume depleted (increased systemic vascular
resistance).
• General anesthesia may be necessary in emergent deliveries or if the patient has coagulation
abnormalities.
– Severe hypertension, with resultant intracranial hemorrhage, may accompany
laryngoscopy.
– Airway edema may increase difficulty of laryngoscopy.
– Prolonged duration of non-depolarizing neuromuscular blockade in parturients on
magnesium sulfate
Monitors
• Pulse oximetry: Decrease in SpO2 in the setting of pulmonary edema, respiratory depression,
and/or pulmonary aspiration
• Blood pressure monitoring: Consider invasive blood pressure monitoring in the setting of
refractory hypertension (BP >180/120)
• CVP: May be useful in determining volume status and for infusion of vasodilators
• EKG
• Fetal heart tracing
• General anesthesia for emergent deliveries
– Rapid-sequence intubation with cricoid pressure to minimize risk of aspiration
– Avoid hypertensive response to laryngoscopy with deepening of intravenous or
inhalational anesthetic, opioids (e.g., remifentanil), beta blockers (esmolol has a short
duration of action), or vasodilators (e.g., nitroglycern, calcium channel blockers).
Maintenance
• General anesthesia is maintained with a combination of volatile anesthetic and nitrous
oxide.
– Following delivery of fetus, decrease volatile anesthetic to <0.5 MAC to minimize
decreases in uterine tone.
– IV opioids can be given following clamping of the cord.
Standard extubation criteria; may be precluded by airway edema. Additionally, ensure that
the mother is awake, alert, and capable of protecting their airway.
FOLLOW-UP
BED ACUITY
Consider ICU admission in patients with evidence of end-organ damage and/or need for
mechanical ventilation
• Continue antihypertensive therapy until the blood pressure normalizes
• Continue seizure prophylaxis for 24 hours following the last seizure
• Labs: Follow Cr/BUN, platelets, INR/PT until values normalize
• Consider consulting neurology, pediatrics, and/or maternal fetal medicine
COMPLICATIONS
• Recurrent seizures
• Cerebral dysfunction
• Pulmonary edema
• Hepatic dysfunction
• Disseminated intravascular coagulation
• Placental abruption
• Maternal death
• Fetal death
REFERENCES
1. Katz VL, Farmer R, Kuller JA. Preeclampsia into eclamspia: Toward a new paradigm. Am J
Obstet Gynecol. 2000;182:1389–1396.
2. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol.
2005;105(2):402–410.
3. Morriss MC, Twickler DM, Hatab MR, et al. Cerebral blood flow and cranial magnetic
resonance imaging in eclampsia and severe pre-eclampsia. Obstet Gynecol. 1997;89:561–
568.
4. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin
for the prevention of eclampsia. N Engl J Med. 1995;333(4):201–205.
5. McDonald SD, Malinowski A, Zhou Q, et al. Cardiovascular sequelae of preeclampsia/
eclampsia: A systematic review and meta-analysis. Am Heart J. 2008;156:918–930.
6. Vigil-De Gracia P, Silvia S, Montufar C, et al. Anesthesia in pregnant women with HELLP
syndrome. Int J Gynaecol Obstet. 2001;74:23–27.
• Preeclampsia
• Magnesium
CODES
ICD9
• 642.60 Eclampsia, unspecified as to episode of care or not applicable
• 642.61 Eclampsia, delivered, with or without mention of antepartum condition
• 642.62 Eclampsia, delivered, with mention of postpartum complication
ICD10
• O15.00 Eclampsia in pregnancy, unspecified trimester
• O15.02 Eclampsia in pregnancy, second trimester
• O15.9 Eclampsia, unspecified as to time period
CLINICAL PEARLS
• Molar pregnancy or antiphospholipid syndrome should be suspected if eclampsia presents in
the first trimester of pregnancy.
• Eclampsia may not necessarily be a continuum of preeclampsia and may exhibit no signs or
symptoms of preeclampsia before onset of seizure activity.
• Definitive treatment of eclampsia is delivery of the fetus. However, onset of eclampsia may
still occur in the postpartum period.
• Primary anesthetic objectives are cessation of the seizure, avoidance of maternal hypoxia,
prevention of aspiration pneumonia/pneumonitis, management of hypertension, and
prompt preparation for emergent delivery.
EJECTION FRACTION
Amrik Singh, MD
BASICS
DESCRIPTION
• The ejection fraction (EF) is defined as the percentage of end diastolic volume that is ejected
during ventricular systole. EF usually applies to the left ventricle (LV).
• Normal EF ranges from 55% to 70%.
• Ejection fraction: EF = (EDV – ESV) / EDV
– End diastolic volume (EDV): The volume of blood within the ventricle immediately prior
to systole
– End systolic volume (ESV): The volume of blood within the ventricle immediately after
systole
– Alternatively, the stroke volume is equal to the difference between the EDV and ESV (SV
= EDV – ESV)
EF = SV / EDV
• As the LV pressure becomes higher than the aortic pressure during systolic contraction, the
aortic valve opens. A portion/fraction of the EDV is ejected into the aorta until the aortic
valve closes again and the LV begins its isovolemic relaxation phase. Even at a constant
contractility, the measured EF can vary with varying preload and afterload.
• Frank Starling Law: A larger LV end diastolic volume leads to increased cardiac muscle
length with a higher force of contraction that consequently results in an increased EF. This
mechanism is exhausted in failing hearts.
• Echocardiography is the most frequently used technique to measure EF using M-mode, 2D
and 3D modalities.
– M-mode measures the fractional shortening (FS) of the mid-LV end diastolic internal
diameter during systole. Doubling the FS value can be used to obtain a rough estimate of
EF in the absence of optimal images or in the interest of time. Its accuracy is decreased in
a ventricle with asymmetric contractility along different planes. The normal range for FS
is 25–45%.
– 2D echocardiography uses Simpson’s method to calculate EDV and ESV of the LV. The
method is based on the division of the LV into multiple discs and summation of individual
disc volumes. The data is acquired from apical (transthoracic) or mid-esophageal (TEE) 2-
and 4-chamber views and is less affected by abnormal size or asymmetry of the ventricle.
Fractional area change (FAC), which is a rough estimation of EF, measures percent change
in the area during systole and is calculated by tracing the end diastolic and systolic area of
the mid-LV. It is not accurate in a ventricle with asymmetric contractility along its long
axis.
– 3D echocardiography eliminates some of the inherent geometrical assumptions and
mathematical modeling needed in the M-mode and 2D methods because the LV image is
acquired in its true shape and provides more accurate assessment in the presence of
regional dysfunction.
• Left ventriculography:
– A contrast agent is injected directly into the LV cavity and images are obtained during
diastole and systole, most commonly in a 30° right anterior oblique view.
– This method is commonly used during diagnostic or therapeutic cardiac
catheterization/angiography.
– Contraindicated in patients at risk for contrast-induced nephropathy
• Magnetic resonance imaging:
– Has a high accuracy due to excellent resolution with minimal inter-observer variability
and is considered the gold standard
– It also uses Simpson’s method to calculate LV volume.
– Associated with minimal adverse effects
• Computed tomography:
– Requires IV contrast administration
– A slow sinus rhythm is necessary to obtain good quality images.
– Can also evaluate any calcification in the coronary arteries
• Nuclear medicine technique:
– Involves injection of radiotracer material intravenously and analyzing recorded cardiac
images
– For example, a patient’s red blood cells are labeled with Technetium-99 and re-injected
intravenously followed by imaging of the LV at a high frame rate.
ANATOMY
• Depolarization leads to calcium influx into the myocardial cells. The amount of calcium
influx coupled with preload (length of cardiac muscle) and afterload (systemic vascular
resistance, blood viscosity, aortic valve stenosis) determine the force of contraction.
• The heart works as a closed circuit; therefore left and right ventricles, although different in
size, thickness, and chamber pressure, have identical EF.
• Regional wall motion and aneurysmal abnormalities will impact EF calculations that use
linear measurements.
• EF is a good clinical indicator of LV systolic function. A low EF indicates systolic dysfunction
due to myocardial ischemia or non-ischemic cardiomyopathy and often leads to signs and
symptoms of congestive heart failure (CHF). CHF in the presence of normal EF indicates
significant diastolic dysfunction. The lifetime risk of developing CHF is 20% for both men
and women.
• In the presence of normal ventricular contractility, a higher EDV (e.g., increased venous
return or aortic insufficiency) will result in increased EF. Therefore, it is important to report
the preload status at the time of the EF measurement.
• Low afterload (e.g., low systemic vascular resistance or severe mitral regurgitation) will also
result in a higher EF. A normal measured EF in these conditions may actually indicate
contractile dysfunction.
• The primary goal in patients with low EF is to:
– Focus on the etiology of systolic dysfunction
– Optimize preoperative cardiovascular status
– Maintain baseline hemodynamics
– Minimize cardiovascular stress
– In patients with ischemic heart disease, optimize preoperative medical management,
decrease preoperative anxiety, and decrease myocardial oxygen demand by controlling
heart rate, contractility, and wall tension. Improve myocardial oxygen supply by
maintaining optimal hemoglobin levels, oxygenation, and coronary perfusion pressure
(CPP).
• Elective surgery should be delayed in the presence of active heart failure.
• Avoid excessive myocardial suppression by anesthetic agents; expect slow circulation time
for all drugs and slow emergence from anesthesia.
• Invasive cardiovascular monitoring may be necessary to guide intravascular volume status
and control hemodynamics closely.
• Patients with significantly low EF (<35%) may have had cardiac resynchronization therapy
and/or an implantable cardioverter-defibrillator device placed that will need to be managed
appropriately.
• Patients with chronic CHF have down-regulation of β-1 receptors that might make them less
responsive to β-agonist therapy in improving contractility and EF. Chronic β-blocker
therapy up-regulates β-1 receptors in these patients and has been shown to improve
survival.
• The prevalence of diastolic heart failure increases with age. LV hypertrophy from chronic
hypertension or aortic stenosis also contributes to increased stiffness and decreased
compliance. Maintain preload and adequate diastolic time. Lusitropic agents such as
milrinone may be effective in improving cardiac output. Most anesthetic agents do not
impair diastolic function.
The myocardium in children, especially neonates, is less compliant compared to an adult
heart. Therefore, it is much more sensitive to small changes in in heart rate, preload, and
afterload
EQUATIONS
• SV = EDV − ESV; where SV is stroke volume, EDV is end diastolic volume, and ESV is end
systolic volume
• EF = (100 × SV) / EDV; where EF is ejection fraction, SV is stroke volume, and EDV is end
diastolic volume
• FS (Fractional Shortening) = 100 × [(LV diastolic diameter) – (LV systolic diameter)] / (LV
diastolic diameter)
• FAC (Fractional Area Change) = 100 × [(LV diastolic area) – (LV systolic area)] / (LV
diastolic area)
• CPP (Coronary Perfusion Pressure) = (Diastolic blood pressure) – (Left ventricular end
diastolic pressure)
GRAPHS/FIGURES
See Table
REFERENCES
1. Lloyd-Jones DM, Larson MG, Leip EP, et al. Lifetime risk for developing congestive heart
failure: The Framingham Heart Study. Circulation. 2002;106:3068–3072.
2. Ramani GV, Uber PA, Mehra MR. Chronic heart failure: Contemporary diagnosis and
management. Mayo Clin Proc. 2010;85:180–195.
3. San Román JA, Candell-Riera J, Arnold R, et al. Quantitative analysis of left ventricular
function as a tool in clinical research: Theoretical basis and methodology. Rev Esp Cardiol.
2009;62:535–551.
• Cardiac output
CLINICAL PEARLS
• EF is a measure of systolic function of the heart.
• A low EF often indicates ischemic or non-ischemic cardiac disease.
• A normal EF does not rule out heart failure, and is seen with diastolic dysfunction.
• Assure preoperative optimization and maintain a positive myocardial oxygen supply and
demand ratio perioperatively.
• Be aware of low cardiovascular reserve and excessive myocardial depression by anesthetic
agents.
ELECTRICAL SAFETY IN THE OPERATING ROOM
David P. Frey, DO
Adam Thaler, DO
BASICS
DESCRIPTION
• An electrical shock or injury occurs when a person is part of, or completes, an electrical
circuit.
• Electrical hazards in the operating room (OR) are numerous, making proficiency in safety
imperative.
• Electrical injury is classified as:
– Macroshock: Large amounts of current; results range from discomfort to death
– Microshock: Minute, imperceptible amounts of current that are capable of death in
electrically susceptible patients
• A standard power cord consists of a:
– Hot wire: Carries current from the source to equipment
– Neutral wire: Carries current from equipment back to the source
– Ground wire: A third wire, positioned at the lowest position, and functions as a safety
device. Its prong is longest to ensure that it is the first to plug into an outlet.
• Grounding is a confusing term since it has 2 separate meanings in reference to power and to
equipment.
EPIDEMIOLOGY
Prevalence
40% of electrical accidents in hospitals occur in the OR (1).
Morbidity
Burns, seizures, muscle contraction, respiratory paralysis, and ventricular fibrillation (Vfib)
Mortality
Not available
• Any piece of electrical equipment is a source of potential hazard that demands
understanding of electrical safety from all members of the care team. Some examples
include:
– Ungrounded equipment; if the ground wire to a piece of equipment is damaged, it is
possible for charge to build on the case of the equipment and eventually discharge to a
patient, provider, or both.
– Damaged power cords
– Internal cardiac devices (ICDs)
– Esophageal temperature probes
– Conductive fluids
– Electrosurgical units (ESUs)
– Lasers
– EKG leads
• Electrically susceptible patients: Refers to a person with some kind of conducting device in
direct contact with the heart over a small area (pacing wire, central catheter, etc.).
• Electricity is commonly thought of as a flow of charge through a conducting material. It
requires a source of voltage, 2 points at differing electric potentials, and a closed circuit that
is able to conduct charge.
• Ohm’s law: States that voltage is equal to the current multiplied by resistance: V = I × R
(for DC current); similar to the cardiovascular system where pressure is equal to cardiac
output times resistance.
– Voltage (V): The force driving current against the resistance in a circuit; measured in volts.
It is the potential difference of charge (high potential versus low potential). It is similar to
pressure.
– Current (I): The flow of charge measured in amperes. It is traditionally thought of as the
flow of positive charge from a high potential (positive terminal) to low potential (negative
terminal). However, current is measured as the flow of negatively charged electrons; thus,
electron flow is opposite (from low to high potential) of the positive charge flow. Current
is classified as Direct (DC; flows in one direction only) or Alternating (AC; changes
directions periodically; what is supplied by utility companies). It is similar to cardiac
output.
– Resistance (R): Can be thought of as the opposition to the flow of current; unit is Ohms.
Human tissue is inherently resistant to current. The higher the resistance, the more
voltage that is necessary for current to pass.
– Impedance (Z): For AC, resistance is referred to as impedance (V = I × Z).
• Radio frequency: Measured in Hertz (Hz) and refers to the number of times in 1 second that
an AC reverses direction. Power from the utility company is AC of 120 V at 60 Hz. Common
radio frequencies (5):
– 60 Hz: Household appliances
– 200 kHz–3.3 MHz: Electrosurgical equipment
– 54–880 MHz: Television signal
• The severity of injury is dependent on the amount of current, the duration of flow, and
current density (the amount of current applied per unit area). Current density is increased
when there is an increase in the current or when it is applied to a smaller area. ESUs
operate on this principle by concentrating current at the ESU tip.
• Macroshock: Refers to large amounts of current flowing through a person. The effect of a 60
Hz current on an average person for 1 second (2):
– 1 mA: Threshold of perception
– 5 mA: Maximal harmless current
– 10–20 mA: “Let go” current before sustained muscle contraction
– 50 mA: Pain, fainting, mechanical energy; heartbeat and respiration continue
– 100–300 mA: Ventricular fibrillation; respiratory center intact
• Microshock: Minute amounts of current that can result in injury or death only in electrically
susceptible patients.
– 0.1 mA: Ventricular fibrillation (Note: the threshold for perception with macroshock is 1
mA).
– 0.01 mA: Recommended maximal leakage current for OR devices
• DC is generally considered safer than AC; it takes approximately 3 times the DC current to
produce the injuries seen with AC at 60 Hz. This, however, does not mean that DC is benign
as death can still result.
• Temperature: Current passing through any type of resistance will raise the temperature of
that substance, potentially leading to thermal injury ranging from cell destruction to burns.
• Electrosurgery: The high frequency used will not cause cardiac fibrillation, only burns.
– Unipolar: Current will pass through the patient, through the attached return plate, and
back to the ESU (completing a circuit). The return plate (large blue adhesive pad) is a
dispersive electrode with a large surface area that provides a low current density pathway.
If incorrectly applied, it is possible for a high current density to develop and burn the
patient. If not applied or a wire is broken, it is possible that the current will find a
different route through the operator, EKG leads, prosthetic devices, etc., and result in
injury.
– Bipolar: This device only passes current between the 2 tips of an electrode resembling a
forceps. The active and return electrodes are the 2 blades, so there is no need for a return
plate and much less power is needed compared to a unipolar electrode.
• ICD interference: The current may be misperceived by the device as an arrhythmia and elicit
anti-tachycardic pacing or shock delivery. Newer devices have improved insulation, and the
development of frequency-based devices will be able to recognize interference. However,
the ASA recommends reprogramming the device directly or turning off with a magnet
before surgery.
• Differences exist in the electrical safety measures built into operating rooms that the
anaesthetist should be aware of.
• Isolated power system: Most OR power sources are built with an isolation transformer that
separates the outlet from the actual power source. It greatly diminishes the risk of shock by
requiring that a person be in contact with both lines of an isolated power system to
complete the circuit. In contrast, for a non-isolated power source, standing on the ground
completes a circuit; thus, a person standing in contact with the ground will complete a
circuit by touching the hot wire (3,4).
• Line isolation monitor (LIM): Continuously monitors the integrity of the isolated system. The
isolation is degraded with every device that is connected, secondary to inherent leakage
currents. Integrity of the system is displayed in milliamperes (mA) and alarms if the total
leakage current is 2–5 mA. This is not a value of current flowing; it is the current that would
be able to flow during a fault. So the alarm does not necessarily signal an emergent
situation but rather a degradation of isolation. Devices will continue to function but the
safety of the isolated system is gone. It should be noted that the LIM is not designed to
protect against microshock, as its threshold is set above 1 mA (3,4,5).
• Ground wire: The third and lowest prong of a power cord is meant to offer a path of lowest
resistance in case of a fault. Most of the current will return along the ground wire away
from the person. If this is not present or if it is broken, the person will experience a
considerable, and perhaps lethal, shock. In addition, it dissipates leakage current that is
potentially lethal to electrically susceptible patients.
• Hospital-grade outlets: Identifiable by a green dot. Have been shown to have greater
integrity in ground wire connection than non-hospital-grade outlets.
• Emergency outlets: Identifiable by a red outlet. These outlets provide power from a backup
generator in case of a power outage (2).
• Hospital-grade plugs: Allow for visible inspection of ground wire integrity through the use
of clear plastic or easy disassembly (2)
• Emergency power: All hospitals are required to have backup power. Generators should start
within a few seconds of detecting loss of power from the utility company. As such,
generators may not turn on if power is lost only to isolated rooms within the hospital (2).
• Damaged equipment and power cords should not be used until repaired. All equipments
must undergo regular maintenance and inspection (2).
• Grasp cords by their plugs when removing.
• Keep cords off of the ground in order to avoid puddles of conductive liquids and damage
from rolling equipment in addition to their potential to trip members of the care team.
• Multi-outlet extension boxes are prone to fluid contamination. They should be avoided, if at
all possible.
• Electrosurgery: Ensure proper placement of the return plate. Encourage the use of a bipolar
electrodes in electrically susceptible patients. Bipolar electrodes create little, to no, sparking
and have not been recorded as a cause of fire.
• LIM-equipped rooms will alarm at a preset limit of leakage current, usually 2–5 mA.
• Microshock will result in Vfib on EKG in electrically susceptible patients.
• The need for higher settings on the ESU may signal an improperly placed or faulty return
pad.
TREATMENT
• In the event of a LIM alarm:

– Systematically unplug the last piece of equipment connected, as it is probably the faulty
one. Faulty equipment should be removed and serviced.
– If the equipment is life-sustaining and essential, it could continue to remain in use.
However, the system is no longer isolated and there is a potential for serious shock.
– It is possible that no equipment is faulty and there are simply too many devices since
leakage current is additive. Excessive use of extension cords will also increase the leakage
current.
– If the offending device cannot be found, the search should expand to the actual outlets,
extension boxes, and environmental hazards such as puddles.
• In the event of a power outage:
– Most times, the emergency generator will provide power, but a contingency plan should
already exist with necessary equipment.
– Battery-supplied light sources: Laryngoscopes and cell phones can serve as light until
flashlights are located.
– Battery-powered monitors and workstation: Prepare for hand ventilation. Inhaled
anesthetics, other than desflurane, will continue to be vaporized pneumatically.
FOLLOW-UP
Patients should be informed if they are involved in a perioperative electrical outage or

accident and be provided necessary care.
REFERENCES
1. runer J, Aronow S, Cavicchi R. Electrical incidents in a large hospital: A 42 month register.
J Assoc Adv Med Instr. 1972;6:222–230.
2. Raftery EB, Green HL, Yacoub MH. Disturbances of heart rhythm produced by 50-Hz
leakage currents in human subjects. Cardiovasc Res. 1975;9:263–265.
3. Hutchisson B, Baird MG, Wagner S. Electrosurgical safety. AORN J. 1998;68(5):829–830.
4. Bernstein MS. Isolated power and line isolation monitors. Biomed Instrum Technol.
1990;24:221.
5. Massarweh NN, Cosgriff N, Slakey DP. Electrosurgery: History, principles, and current and
future uses. J Am Coll Surg. 2006;202(3):520–530.
ADDITIONAL READING
• Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia, 5th ed. Philadelphia, PA:
Lippincott Williams & Wilkins, 2006.
• Burns
• Fire in the operating room
CODES
ICD9
994.8 Electrocution and nonfatal effects of electric current
ICD10
T75.4XXA Electrocution, initial encounter
CLINICAL PEARLS
• Manufacturers can accomplish leakage current standards by keeping their power cords
short. By using an extension cord you are increasing the leakage current.
• LIMs do not protect against microshocks.
ELECTROCONVULSIVE THERAPY (ECT)
Stephen M. McHugh, MD
Li Meng, MD, MPH
BASICS
DESCRIPTION
General
• Electroconvulsive therapy (ECT) is the transcutaneous delivery of an electrical stimulus to a
patient’s brain in order to produce a generalized seizure. It was first developed in the 1930s
as a treatment for schizophrenia, and performed without anesthesia until the 1960s.
• Current indications include major depression, bipolar disorder, and certain subtypes of
schizophrenia.
• The typical course of therapy includes 2–3 sessions per week for 3–4 weeks followed by
weekly or monthly maintenance sessions.
• Leads are usually placed in a bitemporal or right unilateral configuration. After the
electroshock is delivered by the psychiatrist, monitoring of both the central and peripheral
nervous systems is performed.
• CNS effects are desired. EEG monitoring typically reveals a latent period (2–3 seconds) that
is followed by a tonic (10–12 seconds) and then a clonic (30–50 seconds) phase. A seizure
length of at least 25 seconds is considered necessary for therapeutic effect. The first session
often includes an upward titration of the electrical stimulus to determine the dose required
to achieve the desired seizure length.
• The peripheral effects are “side effects” that are monitored and minimized to prevent harm
to the patient. They include autonomic nervous system discharge as well as uncontrolled
motor activity.
– Autonomic nervous system: Electrical stimulation of the brain is associated with an
increased parasympathetic discharge (corresponds with the tonic phase; 10–15 seconds)
followed by an increased sympathetic discharge (corresponds with the beginning of the
clonic phase, but lasts 5–7 minutes).
• Contraindications include:
– Absolute: Pheochromocytoma
– Relative: MI in past 3 months, CVA in past 3 months, intracranial mass, elevated ICP (ECT
can significantly increase cerebral blood flow), cardiac conduction abnormalities,
aortic/cerebral aneurysms, high-risk pregnancy
Position
• Supine
• Left uterine displacement should be used for all parturients in the second and third
trimesters.
Incision
None
Approximate Time
Less than 20 minutes
EBL Expected
None
Hospital Stay
Less than 1 day
• Electrical leads to produce seizure
• Electromyogram (EMG)
• Second blood pressure cuff or tourniquet
EPIDEMIOLOGY
Prevalence
• 14 million Americans are diagnosed with depression each year.
• Approximately 400,000 ECT treatments are performed each year.
Prevalence
• Lifetime risk of major depression is 17%.
• Depression resistant to pharmacotherapy is present in up to 50% of patients.
Morbidity
Dental injury is the most common complication.
Mortality
4 in 10,000 procedures; cardiac events comprise 67% of deaths.
• Rapid loss of consciousness and recovery for a short duration procedure; often an out-of-OR
procedure.
• Airway management is usually non-invasive with a bag-mask device (Ambu, Jackson-Reese).
• Anticipate and prevent adverse peripheral effects including hemodynamic changes and the
potential for biting or extremity injury
• Avoidance of medications that increase seizure threshold or decrease duration; the majority
of anesthetic drugs have effects on the threshold.
SYMPTOMS
Depression, mania, psychosis, and catatonia
History
• Psychiatric illness including major depression, bipolar disorder, and schizophrenia
• Focused cardiac and neurologic system history to look for relative contraindications as well
as patients who are at increased risk for adverse events
Signs/Physical Exam
• Careful airway exam to assess the ability to ventilate as well as intubate
• A dental exam should document any baseline damage and be confirmed with the patient.
• Focused cardiac and neurologic exam as indicated by the history
MEDICATIONS
• Antidepressants (MAOIs, TCAs, SSRIs, SNRIs, and atypical antidepressants); direct acting
sympathomimetics may have an exaggerated effect in patients taking TCAs.
• Lithium is usually held for 3 days prior to ECT as it can interfere with effects of
neuromuscular blocking drugs, barbiturates, and benzodiazepines.
• Antipsychotic medications
• Antihypertensive medications should be continued to avoid extreme hypertensive events
during the procedure.
• Anticonvulsant medications should be held on the morning of the procedure.
Labs/Studies
• EKG to screen for relative contraindications including arrhythmias and evidence of
myocardial ischemia
• CXR if history or exam shows evidence of pulmonary disease that could affect ventilation
during procedure
• Non-contrast head CT if concern for possible intracranial mass
• Blood glucose if patient requires insulin for DM
• Potassium level if patient has renal failure, is taking a potassium-sparing diuretic, or has
other risks for hyperkalemia
• Special attention should be paid to cardiac and neurologic comorbidities.
• ECT has been reported to convert atrial fibrillation to sinus rhythm. Because of this, all
patients undergoing ECT with AF should be fully anticoagulated for at least 3 weeks prior to
ECT.
• Pregnancy is not a contraindication to ECT and is considered safe in all trimesters (1)[C].
TREATMENT
Premedications
• Glycopyrrolate (0.2 mg IV) can decrease secretions and the risk of bradyarrhythmias.
• Benzodiazepines should be avoided as they increase the seizure threshold.
• In patients at increased risk of aspiration pneumonitis, consider H2 blockers, non-particulate
antacids, and promotility drugs.
• Ketorolac, PO NSAIDs, or acetaminophen can be given prophylactically to patients
experiencing headache or myalgias after previous ECT treatments.
• Caffeine may occasionally be given intravenously to increase seizure duration.
• Communicate the potential for post-procedure amnesia, headaches, myalgias, and dental
injuries.
• Patients with severe psychiatric disorders may not be able to consent for themselves.
Antibiotics are not indicated.
INTRAOPERATIVE CARE
• Most commonly performed with general anesthesia using an IV induction agent,
succinylcholine, and bag-mask ventilation.
– The “gold standard” induction agent is still considered methohexital (0.75–1.0 mg/kg) due
to its minimal effect on seizure threshold and short duration of action. However, shortages
and lack of availability often make it necessary to utilize other medications.
– Propofol (0.75 mg/kg) is associated with decreased hypertension and equal seizure quality
as compared to methohexital (2)[A].
– Thiopental, etomidate, and ketamine have also been used successfully.
– Remifentanil (1 mcg/kg) can reduce the dose of IV induction agent needed and increase
the likelihood of adequate seizure duration (3)[A].
– Avoid barbiturates in patients with acute intermittent porphyria.
• Mask induction with sevoflurane has been used successfully for patients with difficult IV
access; however, this may be associated with prolonged induction and recovery times.
Monitors
• A second BP cuff (or tourniquet) is usually placed on the non-IV arm or lower extremity and
is inflated above the systolic BP prior to induction. This technique prevents neuromuscular
blockade distally and allows observation of motor duration of the seizure.
• BIS monitoring may be useful for predicting the seizure duration (4)[B].
• AICDs must be deactivated as seizure activity may be mistaken for a cardiac arrhythmia and
a back-up defibrillator should be available. Pacemakers should be set to a fixed-rate
(demand mode) pacing prior to ECT.
• Standard induction with an IV agent following pre-oxygenation.
– Mask ventilation with an oral or nasal airway as needed; hyperventilation can be used to
decrease the seizure threshold.
– A bite block or mouth guard should be used to avoid dental injury during the seizure.
– Succinylcholine (1 mg/kg) is given after induction. In the event that a depolarizing agent
is contraindicated, a non-depolarizing neuromuscular blocking drug should be used. This
may result in prolonged procedure duration. Avoid excessive doses of succinylcholine to
prevent ongoing paralysis after the patient regains consciousness.
• Intubation may be necessary for patients at risk for airway obstruction/difficulty with bag
mask ventilation. A rapid-sequence intubation with cricoid pressure is indicated for patients
at increased risk of aspiration.
• A full array of emergency airway equipment must always be available.
Maintenance
• Parasympathetic discharge occurs first and can present as bradyarrhythmias or asystole.
Treatment with an anticholinergic medication may be appropriate.
• Sympathetic discharge follows, typically with hypertension and tachycardia. Ventricular
tachycardia is also possible. These conditions are usually transient and stop with completion
of the seizure, but short-acting drugs such as esmolol, labetalol, nitroglycerin, or nicardipine
may be necessary.
ALERT
Hypotension should not be treated with mixed-acting sympathomimetics (e.g., ephedrine) in
patients taking MAOIs.
Reverse non-depolarizing neuromuscular blocking drugs if used
FOLLOW-UP
BED ACUITY
• Standard PACU bed
• AICDs must be reactivated and pacemakers reset.
ANALGESIA
Headache and myalgias can be treated with IV or PO NSAIDs or acetaminophen.
COMPLICATIONS
• Anterograde and retrograde amnesia are usually limited to immediate peri-procedure
memories.
• Post-procedure delirium
• Dental damage due to direct stimulation of masseter muscles
• Skeletal fractures from inadequate neuromuscular blockade
PROGNOSIS
• ECT is more effective than pharmacotherapy in achieving remission of depression; studies
have shown a 90% response rate.
• Maintenance sessions are usually required at gradually increasing time intervals.
• Clinical improvement is usually evident after 3–5 sessions.
REFERENCES
1. Yonkers KA, Wisner KL, Stewart DE, et al. The management of depression during
pregnancy: A report from the American Psychiatric Association and the American College
of Obstetricians and Gynecologists. Obstet Gynecol. 2009;114(3):703–713.
2. Geretsegger C, Nickel M, Judendorfer B, et al. Propofol and methohexital as anesthetic
agents for electroconvulsive therapy: A randomized, double-blind comparison of
electroconvulsive therapy seizure quality, therapeutic efficacy, and cognitive performance.
J ECT. 2007;23(4):239–243.
3. Akcaboy ZN, Akcaboy EY, Yigitbas B, et al. Effects of remifentanil and alfentanil on seizure
duration, stimulus amplitudes and recovery parameters during ECT. Acta Anaesthesiol
Scand. 2005;49(8):1068–1071.
4. Gombar S, Aggarwal D, Khanna AK, et al. The bispectral encephalogram during modified
electroconvulsive therapy under propofol anesthesia-relation with seizure duration and
awakening. J ECT. 2011;27(2):114–118.
• Increased intracranial pressure
• Pacemakers/ICDs
CODES
ICD9
• 295.90 Unspecified schizophrenia, unspecified
• 296.20 Major depressive affective disorder, single episode, unspecified
• 296.80 Bipolar disorder, unspecified
ICD10
• F20.9 Schizophrenia, unspecified
• F31.9 Bipolar disorder, unspecified
• F32.9 Major depressive disorder, single episode, unspecified
CLINICAL PEARLS
• Patients respond similarly to subsequent sessions of ECT, so accurate record-keeping is vital.
Prior records should be checked for medications used and patient responses.
• The initial ECT session often requires multiple electrical stimulations to determine seizure
threshold, and this can increase the potential for parasympathetically mediated side effects
such as bradycardia and asystole.
ELECTROENCEPHALOGRAM (EEG)
BASICS
DESCRIPTION
• The raw EEG is a reflection of cortical brain activity.
• EEG monitoring may be utilized in the perioperative period to assess the depth of anesthesia
and attainment of burst suppression, as well as indirectly monitor for cortical ischemia
during surgical procedures (aneurysm clipping, carotid endarterectomy).
• Analysis of the EEG requires knowledge of the differing waveforms. However, the
complexity can mislead even sophisticated quantitative monitors and can lead to erroneous
clinical decisions.
• Modern monitors, such as the Bispectral Index (BIS) and Spectral Entropy (M-entropy),
attempt to quantify this raw EEG, yielding an easy-to-interpret number.
• The EEG is influenced not only by the medications administered, but also by a myriad of
factors in the patient’s physiology and underlying pathology.
• An accurate assessment of the depth of anesthesia via the raw EEG may reduce the
incidence of awareness and improve recovery from anesthesia.
• Classically, patients require a full “montage” of electrodes covering the entire scalp to
capture the whole spectrum of EEG generated. This is especially true when looking for
regional ischemia (e.g., during carotid endarterectomy, and clipping of cerebral aneurysms)
due to surgical interventions to guide further surgical decisions.
• For the purpose of depth of anesthesia, monitoring 3 or 4 electrodes placed on the forehead
close to the hairline will obtain an EEG sufficient to assess the depth of anesthesia (positive,
negative, and reference). The rest of the scalp may be “neglected” since the frontal aspect is
more resistant to pharmacologic sleep than the more posterior aspects (frontal
predominance); allows for a margin of safety.
• The surface electrodes pick up voltage fluctuations in the synaptic activity of the dendrites,
and the sum of a large number of these is reflected in each EEG electrode. They are not
specific to the voltage generated by dendritic cells, and will pick up signals generated by
other, unwanted current sources such as facial, eye, and heart muscles, and electrical
sources. The understanding of these noise generators is crucial in making clinical decisions.
– Myogenic activity can be distinguished from the EEG by causing the waveform to
“wander” above and below the baseline. Patient blinking and facial movement will cause
a similar deviation from baseline and will make identification of these noise generators
easy.
– Muscle relaxants will eliminate the myogenic artifact. However, one must be careful to
administer paralytics to patients who are only marginally asleep to avoid recall. Studies
have shown that, even in the absence of myogenic artifact, the EEG is depressed by
administering paralytics. This is likely due to reduction in the afferent input to the brain
from muscle spindles, slowing the EEG.
– Electrical interference from line currents have a frequency of 60 Hz and are easy to detect;
the highest frequency of EEG encountered is typically 30 Hz
• EEG patterns (see Table 1).
– Awake: High frequency and low voltage; the tracing will appear as a blurred line on the
monitor.
– Sedation: Loss of fast α activity and an increase in β activity.
– Deep sedation: Slowing of β activity, appearance of spindle activity. Eventually, α and β
activity disappears, and θ activity appears.
– General anesthesia: θ waves predominate. α and β activity disappear, and with increasing
depth, slow waves (Δ) predominate.
– Deep levels of general anesthesia: Isoelectric EEG interrupted by “bursts” of electrical
activity (burst suppression).
– Further deepening of anesthesia: Increase the length spent suppressed and reduce the
number of “bursts.” Eventually, isoelectricity will prevail without “bursts.”
– Characteristics may not be easily evident with rapid transition between phases (i.e.,
during induction of general anesthesia)
– Physiologic sleep and anesthetic sleep are similar, but not identical
– Different anesthetic agents will produce different EEG patterns.
• Physiologic sleep and anesthetic sleep are similar, but not identical. Different anesthetic
agents will produce different EEG patterns.
ANATOMY
• Extrapyramidal neurons are arranged in the cerebral cortex.
• Synaptic activity in the dendrites causes electrical activity, which changes over time and
place.
• These fluctuations in potentials in the dendritic trees of pyramidal neurons are summed up
by overlying electrodes on the scalp.
• Baseline EEGs in the awake patient aid with establishing “normal” and differentiating
pathology intraoperatively.
– Low-amplitude EEG can be drug induced, genetically determined, pathologic, or metabolic
(e.g., hypoglycemia).
– Healthy patients in an awake state can demonstrate very slow EEGs.
– Dementia patients may display increased slow wave activity and decreased fast activity.
– Schizophrenics have an increase in frontal slow waves, and a decrease in α waves.
– Alcohol generally increases α waves, and severe intoxication can cause burst suppression.
– Cocaine and cannabis increase α activity.
– Cerebrovascular disease causes slowing.
– Severe brain injury and cerebral palsy cause significant EEG slowing.
• Cerebral ischemia. EEG monitoring to detect cerebral ischemia (e.g. during carotid
endarterectomy, aneurysm clipping) is well established. Slowing of the EEG during a stable
anesthetic and stable surgical stimulation should alert one to cerebral ischemia if the blood
pressure is marginal.
• Changes in EEG pattern: Hypoglycemia, hypothermia, and hypotension will cause EEG
slowing and even progress to an isoelectric EEG
• Δ pattern
– There may be periods of time where despite a stable level of anesthesia and no change in
surgical stimulation, patients will transition to a predominately Δ pattern, indicating a
very deep level of anesthesia. The cause of this is unknown, and the significance of this is
also not known. One must be vigilant and pursue possible causes for this (e.g., cerebral
ischemia) if this pattern persists despite lightening of anesthetic depth.
– May paradoxically appear during sudden noxious stimuli; the cause remains unknown.
This appearance may give the appearance of actually increasing anesthetic depth, yet the
patient is actually transitioning into a lighter plane of anesthesia.
• The EEG can be used as a gauge of anesthetic depth and possibly reduce the risk of
awareness as well as improve the recovery from anesthesia, and identify risk of cerebral
ischemia.
• The EEG can be used as an indicator of cerebral perfusion (e.g., during carotid
endarterectomy, cerebral aneurysm clipping). Changes to look for would be a sudden
slowing or isoelectricity with clamp application.
• The EEG is a poor predictor of movement. There are several reasons for this. The EEG
reflects cortical activity, and movement during anesthesia is not a cortical phenomenon, but
controlled at deeper levels of the brain, and also at the level of the spinal cord. A patient
can be judged to be “deep” yet move. The sequence of events will be that the EEG is deep, a
noxious stimulus is administered to the patient, generators at the spinal cord or deep brain
level will initiate patient movement, and eventually these stimuli will transition to the
cortical level. The EEG will display a “lighter” level of anesthesia AFTER the patient has
moved. If the brain activity is recorded in deeper structures (such as near the thalamus) a
much better correlation between depth and patient movement can be obtained.
• The EEG is useful in situations where patients are at greatest risk for awareness and recall.
Groups at risk are traditionally trauma patients, women having emergent Cesarean sections,
and patients undergoing cardiac surgery. In these scenarios, either because of the
intolerance to adequate anesthesia, or the urgency for a rapid induction, patients may be at
higher risk for awareness. The EEG can be an adjunct to other parameters correlating with
patient depth (blink reflex, movement, blood pressure, heart rate, etc.) (3).
• Barbiturates initially produce fast EEG waves, and then successively slower waves
culminating in isoelectricity with increasing doses. The initial “rapid response” is only seen
if very small doses are given. It is not seen with typical induction doses.
• Isoflurane at subanesthetic doses will yield fast activation, and slowing of the EEG with
increasing concentration. Isoflurane can produce isoelectricity.
• Sevoflurane is very similar to isoflurane in its effect on the EEG, but has been observed to
cause seizure-like movements at high concentrations.
• Ketamine, an NMDA receptor antagonist, causes an increase in the frequency of the EEG.
This may mislead the practitioner to erroneously interpret this as lighter anesthesia, and
overdose the patient. This will also lead to higher numbers on quantitative EEG monitors
such as the BIS.
• Nitrous oxide has a minimal effect on the EEG. Therefore, a patient on a nitrous oxide–
volatile anesthetic can actually be deeper than a patient who is on a volatile anesthetic
alone despite the fact that the EEG indicates the patient to be more lightly anesthetized.
Nitrous oxide may also cause a decrease in the frequency of the EEG several minutes after
discontinuation.
• Opioids in small doses have a minimal effect on the EEG, but produce slowing at larger
doses. Opioids will either slow an EEG or reduce the likelihood of movement at a stable
EEG. Alfentanil may produce seizure-like activity, or unmask epileptiform foci.
• Epinephrine and ephedrine can cause increasing frequencies on the EEG.
• α-2 agonists, such as clonidine and dexmedetomidine, have similar effects on the EEG as
barbiturates, propofol, and etomidate.
GRAPHS/FIGURES
Table 1 Summary of EEG Frequencies at Different States of Anesthesia
REFERENCES
1. Bennett C, Voss LJ, Barnard JPM, et al. Practical use of the raw electroencephalogram
waveform during general anesthesia: The art and science. Anesth Analg. 2009;109(2):539–
550.
2. Avidan MS, Zhang L, Burnside BA, et al. Anesthesia awareness and the bispectral index. N
Engl J Med. 2008;358(11):1097–1108.
3. Ekman A, Lindholm ML, Lenmarken C, et al. Reduction in the incidence of awareness using
BIS monitoring. Acta Anaesthesiol Scand. 2004;48(1):20–26.
ADDITIONAL READING
• American Society of Anesthesiologists Task Force on Intraoperative Awareness. Practice
advisory for intraoperative awareness and brain function monitoring. A report.
Anesthesiology. 2006;104(4):847–864.
• Hypoglycemia
CLINICAL PEARLS
• The EEG is a very useful tool in judging anesthetic depth if one interprets the EEG using
clinical judgment, patient factors, clinical situation, and drugs administered.
• The use of quantitative EEG monitors such as the BIS cannot be advocated if they are used
in a vacuum without interpreting the raw EEG and other patient factors.
• The EEG is the gold standard for identifying brain ischemia. A sudden slowing of the EEG
during carotid endarterectomy or cerebral aneurysm clipping has to prompt immediate
reassessment of the surgical intervention.
• The EEG is relatively insensitive to opioid and nitrous oxide administration, but very
sensitive to halogenated volatile agents. Therefore, a patient who is undergoing a procedure
with a balanced anesthetic including nitrous oxide and an opioid is less likely to move than
a patient who is receiving an exclusively volatile anesthetic at any given depth of
anesthesia.
ELECTROMYOGRAPHY (EMG)
BASICS
DESCRIPTION
• Electromyography (EMG) is a special type of motor monitoring that has been used
intraoperatively since the mid-1970s.
• It allows real-time identification and functional assessment of vulnerable nerves during
surgery. Prior to its common use, surgeons relied on the Stagnara wake-up test or ankle
clonus. These tests were less than ideal: They were disruptive to the surgery, potentially
dangerous and traumatic to the patient, and could not be performed continually.
• Additionally, perioperative nerve injuries such as ulnar nerve damage may warrant EMG
evaluation.
• EMG is the recording of electrical muscle activity; the tracings allow interpretation as to the
function of the nerve. This is similar to the electrocardiogram of the heart where electrical
depolarization and repolarization can be detected by electrodes.
• Electrodes are shaped as probes, needles, or wires capable of stimulating muscle contraction
and/or detecting muscle activity.
• Interactive software is able to process and display the electrophysiological signals as they
are picked up by the recording electrodes.
• Spontaneous EMG monitoring involves the placement of multiple needle electrodes into the
muscle that is being examined. The EMG detects and records muscle electrical activity
continually. Mechanical irritation of roots or peripheral nerves can trigger motor unit
potential discharges. This aids with identifying nerves as well as inadvertent manipulation
during dissection, retraction, or electrocautery use.
• Evoked EMG monitoring involves placement of needle electrodes at a stimulating site (e.g.,
transcranially at the motor cortex [tcMEP], filum terminale) and also over peripheral
muscles to record contraction. Supraphysiologic current is applied at chosen times and
muscle contraction is recorded; therefore, evoked EMG assesses the integrity of the nerve
fibers between the stimulating site and the muscle.
• EMG allows for intraoperative, indirect neuromonitoring as well as aids in the diagnosis and
assessment of peripheral nerve injuries.
• Factors affecting change in the signal: Anesthesia, tissue temperature, surgical stage, tissue
stresses, and previous pathology.
Table 1 Effect of certain agents or conditions on EMG monitoring
• Spontaneous (continuous) EMG in anesthetized patients:
– The free-run EMG shows no muscle activity (a flat line), and the speaker connected to the
amplifier remains silent.
– Manipulation of peripheral nerves or roots (such as stretching, contusion, compression,
and rubbing) results in EMG bursts called neurotonic discharges.
– Mechanical irritation is translated and displayed on the monitor screen and produces a
crispy noise in the speakers that provide immediate auditory feedback to the surgeon.
– Limitations of the method:
During surgery, it is possible to record spontaneous EMG activity not related to the
intervention, such as propagated end plate potentials, fibrillations, positive sharp waves,
complex repetitive discharges, fasciculation, and myokymia. This can occur in 12–16%
of cases (false positives).
Failure to assess non-irritative mechanisms of nerve damage such as ischemia, and
remarkably sharp nerve transection (false negative)
• Evoked EMG in anesthetized patients is typically in the form of motor evoked potentials
(MEP) and are used to monitor nerve conduction in the anterior motor tracts of the spinal
cord.
– SSEPs (somatosensory evoked potentials) were initially used to assess the integrity of the
dorsal column and lateral sensory tract function. However, injury to the anterior column
of the spinal cord (motor fibers) will have no, or a possibly delayed, change in SSEP
signals. Therefore, MEPs are employed in combination with SSEPs to afford a higher
sensitivity for anterior spinal cord injury.
– When motor nerve fibers are electrically stimulated, they trigger a contraction in the
muscles of the corresponding myotome. The electrodes placed in these muscles record the
muscle contraction as a compound muscle action potential. Evoked EMG assesses the
integrity of the nerve fibers between the stimulating site and the muscle.
– Any drug or physical parameter that changes impulse conduction along an axon may
change the evoked potential waveform.
• During head and neck surgery, the small space combined with a number of cranial nerves
traversing this space can result in inadvertent nerve injury:
– Parotidectomies, mastoidectomies, and acoustic neuromas: Facial nerve (VII) provides
motor innervation to the muscles of facial expression, posterior belly of the digastric
muscle, and stapedius muscle. Injury can result in paralysis of one side of the face, facial
droop, impairment of taste, and sensitivity to sound (hyperacusis). Facial nerve
monitoring involves placement of needle electrodes in the obicularis oculi and obicularis
muscles that can indicate irritation of CN 7.
– Thyroidectomies and parathyroidectomies: The recurrent laryngeal nerve (RLN) and
superior laryngeal nerve (SLN) innervate the laryngeal muscles; injury can result in vocal
cord paralysis. A special endotracheal tube is utilized that can detect vocal cord
movement to aid with nerve localization and detect irritation.
– Radical neck dissections: The accessory nerve (XI) innervates the trapezius muscle; injury
can result in shoulder dysfunction.
• Neurosurgery
– Tethered cord release can result in injuries to lower extremity motor neurons that
innervate the quadriceps femoris, tibialis anterior, and gastrocnemius muscles. Evoked
EMG stimulates the filum terminale and anal and urethral sphincter tone are measured.
– Acoustic neuroma procedures can result in damage to CN 7 and CN 8. EMG monitoring
and brainstem auditory evoked potentials (BAEPs) may be implemented. BAEPs involve
delivering clicks (in lieu of delivering current to stimulate muscle fibers); it is relatively
resistant to anesthetic agents.
• Vascular surgery
– Carotid endarterectomy may use MEPs to assess for ischemia to the motor cortex from
emboli or impaired perfusion during clamping.
– Thoracic or abdominal aneurysm repair use MEPs to assess for spinal cord injury that can
result from damage to the artery of Adamkiewicz or decreased perfusion during cross
clamping.
• Orthopedic surgery
– Spine procedures utilize MEPs to detect direct injury to the spinal cord, nerve roots, or
blood supply.
• Anesthetic medications
– Inhaled anesthetics decrease the waveform amplitude and increase latency. IV anesthetics
have the same effect but to a lesser degree.
– The best anesthetic regimen for surgery involving intraoperative monitoring is
controversial.
– Although total intravenous anesthesia most dependably allows signal attainment, it is
often costly, requires multiple infusion pumps, and may not be easily titrated.
– The safest plan is to create a stable anesthetic milieu prior to baseline signal attainment
and attempt to minimize changes, particularly at critical moments where nerve injury can
occur (e.g., placement of screws, dissection).
– Communication regarding change in anesthetic technique or bolus administration is
important.
– Acceptable anesthetic agents include total IV anesthesia technique with short-acting
narcotic and propofol infusion, nitrous oxide and anesthetic agents, and short-acting
muscle relaxants (for induction).
– Neuromuscular blocking agents and local anesthetics should be avoided.
• Regional anesthesia should be avoided when intraoperative neuromonitoring is planned.
• EMG can be used as a diagnostic tool following complications in regional anesthesia.
Although peripheral nerve or spinal cord injury is rare, it is a significant complication of
regional anesthesia.
– In the event of complete or incomplete absence of nerve function beyond the duration of
the anesthetic or the progression of neurologic deficit (in addition to neurosurgical
consultation and radiologic imaging), electrophysiological studies such as EMG should be
done.
– Consideration should be given to bilateral examination and early studies to establish
baseline, pre-existing lesions, and prognosis.
REFERENCES
1. Denier S. Highlights of anesthetics considerations for intraoperative neuromonitoring.
Semin Cardiothorac Vasc Anesth. 2010;14(1):51–53.
2. Dillon FX. Electromyographic (EMG) neuromonitoring in otolaryngology-head and neck
surgery. Anesthesiol Clin. 2010;28:423–442.
3. Gorji R. Anesthesia and neuromuscular monitoring: Electroencephalography and evoked
potentials. Available at: www.neuroanesthesia.net/ep-manual.pdf
4. Guerit JM. Neuromonitoring in the operating room, why, when and how to monitor?
Electroencephalogr Clin Neurophysiol. 1998;106:1–21.
5. Liem L. Intraoperative neurophysiologic monitoring. Available at:
http://emedicien.medscape.com/article/1137763-overview
6. Neal J, Bernards C, Hadzic A, et al. ASRA practice advisory on neurologic complications in
regional anesthesia and pain medicine. Reg Anesth Pain Med. 2008;33(5):404–415.
7. Paradiso G, Lee G, Sarjeant R, et al. Multi-modality neurophysiological monitoring during
surgery for adult tethered cord syndrome. J Neurosci. 2005;12(8):934–936.
8. Sorenson EJ. Neurologic injuries associated with regional anesthesia. Reg Anesth Pain Med.
2008;33(5):442–448.
• Somatosensory and motor evoked potentials (SSEPs/MEPs)
• Parathyroidectomy
• Thyroidectomy
CLINICAL PEARLS
• Following the use of neuromuscular blocking agents, the return of 4 muscle twitches on
train-of-four testing is sufficient to perform a consistent EMG run/recording.
• Transcranial motor evoked potentials (tcMEP): Stimulation of the motor cortex through the
scalp with recordings over the corresponding muscles
• Cortical motor evoked potentials (cMEP): direct stimulation of the motor cortex during a
craniotomy with recordings over the corresponding muscles
END STAGE LIVER DISEASE
Vadim Gudzenko, MD
Anahat Dhillon, MD
BASICS
DESCRIPTION
End-stage liver disease (ESLD) is usually manifested by cirrhosis of the liver (fibronodular
hyperplasia and bridging fibrosis). Functionally, ESLD is characterized by impaired synthetic
function, cholestasis, and portal hypertension (1).
EPIDEMIOLOGY
Prevalence
Exact prevalence is unknown, but it is estimated that 0.15% of the population has liver
cirrhosis.
Mortality
Perioperative mortality in patients with cirrhosis varies from 8.3% to 25% depending on the
severity of disease and type of surgery (2).
Viral hepatitis (primarily B and C), alcohol abuse, autoimmune conditions, drug reactions,
cholestasis, genetic metabolic aberrations, and inflammatory disease of bile tracts
• Impaired synthetic function. Fibronodular hyperplasia and bridging fibrosis cause damage to
hepatocellular units; consequently, glycogenolysis, gluconeogenesis, protein synthesis, and
metabolism of byproducts/medications are impaired. This manifests clinically as decreased
albumin production, malnutrition, muscle wasting, coagulopathy, cholestasis, and
bilirubinemia.
• Portal hypertension. Fibronodular hyperplasia and fibrosis also cause sinusoidal obliteration
and prevent effective portal venous blood flow. This results in venous congestion of the
spleen (platelet sequestration), small bowel, and colon as well as esophageal varices and
gastropathy from accessory drainage along the diaphragm, mediastinum, and esophagus.
Portal hypertension in combination with hypoalbuminemia cause ascites and pleural
effusions.
• Coagulopathy. General malnutrition, poor absorption of vitamin K (secondary to severe
cholestasis), and impaired synthesis of coagulation factors result in impaired coagulation
(1).
Assessment of concomitant organ dysfunction and optimization. Patients have an increased
risk of morbidity and mortality.
SYMPTOMS
Malaise and fatigue, jaundice, loss of appetite, itching, and bruising
History
• Risk factors: Alcohol abuse, illicit drug use, and a history of blood transfusions
• Family history of jaundice, anemia, or hereditary liver disease
• In a patient with confirmed liver cirrhosis, assess for the presence of ascites or edema,
severity of encephalopathy, and variceal bleeding.
Signs/Physical Exam
Temporal wasting, jaundice, spider nevi, gynecomastia, testicular atrophy, ascites,
hepatomegaly, palmar erythema, and asterixis (3)
TREATMENT HISTORY
Transjugular intrahepatic portosystemic shunt (TIPS), esophageal banding, and paracentesis
MEDICATIONS
• Lactulose, rifaximin, and neomycin are taken for management of hepatic encephalopathy.
• Furosemide and spironolactone are used for the management of ascites.
• Non-selective beta blockers (propranolol and nadolol) are used for control of portal
hypertension and prevention of variceal bleeding.
• Octreotide, a splanchnic vasoconstrictor, is used for acute variceal bleeding.
Labs/Studies
• Routine screening labs in patients without risk factors, history, or suspicion of liver disease
are not recommended.
• For a patient with an established diagnosis of ESLD/cirrhosis:
– CBC with platelet count, creatinine, coagulation panel (PT/INR, PTT), LFTs (ALT, AST,
and bilirubin), and albumin
– Transthoracic echocardiography to evaluate for the presence of pulmonary hypertension
and cardiomyopathy
• Hepatic encephalopathy is a spectrum of neuropsychiatric conditions varying from mild
confusion to deep coma; the exact mechanism is unknown. It can be precipitated by
infection, GI bleeding, hypoxia, azotemia, and other stressful states. Elevated levels of
ammonia are associated with encephalopathy; however, the level does not have a direct
correlation with severity (1,2).
• Pulmonary dysfunction (hepatopulmonary syndrome) from intrapulmonary arteriovenous
shunts can result in hypoxia. Hallmarks include orthodeoxia and platypnea (desaturation
and dyspnea in the supine position).
• Renal dysfunction (hepatorenal syndrome): Develops with advanced portal hypertension and
is associated with profound splanchnic vasodilatation, leading to decreased renal perfusion
and renal insufficiency. Hepatorenal syndrome is usually reversible after liver
transplantation.
• Child–Turcotte–Pugh (CTP) scores: Elective surgery for class A is well tolerated, class B is
permissible with optimization, and class C should not be considered for elective surgery due
to prohibitively high perioperative mortality (1).
• Ascites increases the risk for perioperative pulmonary complications, postoperative wound
infection, and dehiscence. Moderate-to-severe ascites can be treated with large volume
paracentesis and intravenous administration of albumin (4).
• Worsening hepatic encephalopathy should be optimized with medical therapy (lactulose,
rifaximin, or neomycin) before elective surgery.
• Coagulopathy and thrombocytopenia should be corrected before major surgery to decrease
the risk of major bleeding, but transfusion of large volumes of FFP might be detrimental
secondary to volume overload.
CLASSIFICATIONS
• CTP class includes 2 clinical signs (ascites and encephalopathy) and 3 lab values (albumin,
bilirubin, and PT/INR). Combination of points for each feature defines class: A—mild, B—
moderate, and C—severe (1,4).
• MELD score (Model for End-stage Liver Disease) takes into account creatinine, bilirubin, and
INR and was originally devised as a prognostic tool of short-term mortality of patients with
cirrhosis undergoing TIPS procedure. MELD has been validated as a predictor of
perioperative morbidity and mortality for a variety of surgeries. Higher scores (>14) are
correlated with high perioperative mortality. In 2002, the United Network for Organ
Sharing (UNOS) adopted MELD for donor liver allocation (3).
TREATMENT
Premedications
• Parenteral vitamin K should be considered.
• FFP, platelets, and cryoprecipitate are used to correct coagulopathy and thrombocytopenia.
• Benzodiazepines and opioids should be used judiciously because the metabolism of
midazolam, diazepam, and morphine is significantly impaired and can worsen
encephalopathy (2).
INTRAOPERATIVE CARE
• Regional anesthesia may be considered if coagulopathy is not present.
• General anesthesia with an ETT is typically preferred when there is increased risk of
aspiration.
• Monitored anesthesia care should be considered whenever appropriate for the procedure.
Monitors
• Arterial line for monitoring blood pressure, blood sugars, and acidosis may be needed.
• Central venous catheters have been shown to be safe with coagulopathy and may be
necessary when large volumes of fluid resuscitation are anticipated (to guide and avoid
over-resuscitation which can lead to further liver damage). Ultrasound placement may
reduce inadvertent arterial injury.
• Transesophageal echocardiography should be used with extreme caution due to the risk of
rupturing esophageal and gastric varices.
• Rapid-sequence induction with succinylcholine is most commonly used.
Pseudocholinesterase levels may be decreased resulting in a prolonged duration of paralysis.
• Induction agents should be titrated slowly and to effect due to altered pharmacokinetics/
pharmacodynamics (increased volume of distribution, decreased protein binding, decreased
clearance, increased hemodynamic and central nervous system sensitivity).
• Nasotracheal intubation or nasal airway manipulation should be done with extreme caution.
Maintenance
• Maintenance agents: Typically volatile agent +/– nitrous oxide with the goal of maintaining
hemodynamics and MAP within baseline. Cirrhotic liver is extremely susceptible to ischemic
injury in the setting of even mild hypotension. Modern volatile anesthetics (desflurane and
sevoflurane) do not directly affect hepatic perfusion (unlike halothane which significantly
reduces hepatic artery blood flow).
• Although single doses of induction agents such as etomidate, propofol, and methohexital
have similar pharmacokinetic properties in ESLD, recovery from propofol infusion might be
prolonged.
• Morphine and meperidine (primarily metabolized by the liver) can prolong encephalopathy.
Pharmacokinetics of fentanyl and its derivatives (alfentanil and sufentanil) are less affected.
• Steroidal muscle relaxants (vecuronium, rocuronium, and pancuronium) have an increased
volume of distribution that requires higher induction dosing. If primarily metabolized by
the liver, the duration of action may be prolonged. Atracurium and cisatracurium, which
are metabolized by plasma esterases, are not affected in ESLD.
Determined by preoperative liver function, type of surgery, and medications administered.
Patients with ESLD are at increased risk for prolonged emergence.
FOLLOW-UP
BED ACUITY
Monitored floor or ICU management should be considered in CTP class B and C or following
major surgery.
• Sedatives and pain medications that are predominantly metabolized by the liver should be
avoided because they can precipitate and exacerbate hepatic encephalopathy.
• Maintaining cardiovascular stability is crucial to maintain hepatic perfusion.
• Venous pressure should be maintained on the lower side to avoid venous congestion of liver.
If using CVP monitoring, keep CVP <10 mm Hg.
• Early nutrition is extremely important in recovery of intestinal and hepatic function. Enteral
nutrition is preferable.
• Probability of perioperative renal failure is increased; therefore maintaining stable renal
perfusion is key. Renal protective strategies, such as dopamine, nesiritide, fenoldopam
infusion, or mucomyst, have not shown improved outcomes in clinical trials.
• Low threshold for antibiotic administration should be used since patients with ESLD are
susceptible to infections and are at increased risk for perioperative sepsis and wound
infections.
• Coagulopathy and thrombocytopenia should be corrected aggressively.
COMPLICATIONS
• Most common: Hemorrhage, sepsis, liver failure, fluid overload, and hepatorenal syndrome.
• Surgical wound complications include infection, dehiscence, fistula, abscess, and surgical
site bleeding.
• General complications include pneumonia/ARDS, ventilation dependence, chronic heart
failure, arrhythmia, myocardial infarction, urinary tract infections, paralytic ileus,
pulmonary embolism, and death (2).
REFERENCES
1. Wiklund RA. Preoperative preparation of patients with advanced liver disease. Crit Care
Med. 2004;32(Suppl 4):S106–S115.
2. Hanje AJ, Patel T. Preoperative evaluation of patients with liver disease. Nat Clin Pract
Gastroenterol Hepatol. 2007;4(5):266–276.
3. Millwala F, Nguyen GC, Thuluvath PJ. Outcomes of patients with cirrhosis undergoing
non-hepatic surgery: Risk assessment and management. World J Gastroenterol.
2007;13(30):4056–4063.
4. Ziser A, Plevak DJ. Morbidity and mortality in cirrhotic patients undergoing anesthesia and
surgery. Curr Opin Anaesthesiol. 2001;14(6):707–711.
ADDITIONAL READING
• Ginès P, Cárdenas A, Arroyo V, et al. Management of cirrhosis and ascites. N Engl J Med.
2004;350(16):1646–1654.
• Hemprich U, Papadakos PJ, Lachmann B. Respiratory failure and hypoxemia in the cirrhotic
patient including hepatopulmonary syndrome. Curr Opin Anaesthesiol. 2010;23(2):133–
138.
• Meltzer J, Brentjens TE. Renal failure in patients with cirrhosis: Hepatorenal syndrome and
renal support strategies. Curr Opin Anaesthesiol. 2010;23(2):139–144.
• Ramsay M. Portopulmonary hypertension and right heart failure in patients with cirrhosis.
Curr Opin Anaesthesiol. 2010;23(2):145–150.
• Cirrhosis
CODES
ICD9
• 571.5 Cirrhosis of liver without mention of alcohol
• 573.9 Unspecified disorder of liver
ICD10
• K74.60 Unspecified cirrhosis of liver
• K76.9 Liver disease, unspecified
CLINICAL PEARLS
• Perioperative mortality after abdominal surgery in patients with CTP class C is 70–80%.
Emergent surgery is an independent risk factor of mortality.
• Acute liver failure might develop on postoperative day 2 or 3 in patients with stable liver
disease secondary to perioperative hepatic hypoperfusion.
• Perioperative fluid overload is detrimental due to an increase in venous pressure and venous
congestion which leads to hepatic hypoperfusion.
END TIDAL CARBON DIOXIDE (ETCO2)
Siamak Rahman, MD
BASICS
DESCRIPTION
• ETCO2 is the partial pressure or maximal concentration of carbon dioxide (CO2) at the end
of an exhaled breath; it is expressed as a percentage of CO2 or mm Hg. Normal values are 5–
6% CO2, which is equivalent to 35–45 mm Hg. A capnogram is the ETCO2 plotted against
time.
• ETCO2 is used as a noninvasive estimate of alveolar and hence arterial carbon dioxide
partial pressures (or percentages). This is based on 2 assumptions:
– ETCO2 is approximately 4–5 mm Hg lower than PaCO2 in the awake state. This normal
gap signifies the magnitude of the physiological dead space (sum of the anatomical and
alveolar dead spaces).
– A change in one causes an equal change in the other, in the same direction, thus leading
to a constant gradient.
• Pathological or apparatus dead space can further increase the gap between ETCO2 and
PaCO2.
• As recommended by the ASA House of Delegates, the adequacy of ventilation shall be
evaluated by continual observation of qualitative clinical signs and ETCO2 monitoring when
endotracheal tube or laryngeal mask airway is used as well as during moderate or deep
sedation unless precluded or invalidated by the nature of the patient, procedure, or
equipment.
• CO2 elimination depends upon 3 interrelated variables. If 2 of these variables are held
constant, any change in ETCO2 reflects an alteration in the third variable:
– CO2 production
– Alveolar ventilation
– Cardiac output
• Monitoring of end-tidal carbon dioxide tension (ETCO2) is routinely used in different fields
of medicine (emergency medicine, anesthesiology, and critical care medicine).
• ETCO2 monitors are either semi-quantitative changes (relies on changes in pH and color of
the paper) or quantitative changes (based on infrared absorption of the light passing
through the gas). The quantitative method uses either in-line measurement or a side stream
sampling of the exhaled air. The measured ETCO2 in non-intubated patients (side stream
sampling technique) via a nasal cannula or an oxygen mask is a sign of breathing. It may
also correlate to the actual ETCO2, depending on the device used to deliver oxygen and the
flow of oxygen.
• Capnogram is the ETCO2 plotted against time.
– Phase I (a→b): Inspiration and the first portion of exhalation (gas from large airways).
Under normal circumstances, there is no CO2 during inspiration, and during the beginning
of exhalation, gas from the large airways empties first (devoid of CO2).
– Phase II (b→c): Expiration continues and marks the transition between airway and
alveolar gas. CO2 is seen as a rapid upstroke toward the alveolar plateau.
– Phase III (c→d): Expiration of alveolar gas, known as the alveolar plateau. Under normal
circumstances, it is flat.
– Phase IV (d→e): Onset of inspiration and represented as a down slope. Of note, the ETCO2
value is the highest value, and often measured at the d point.
Normal capnogram
ANATOMY
• ETCO2 sampling monitors locations.
– Distal: Decreased dead space, resulting in decreased gap. Cardiac oscillations are often
smoothed over when the sampling port is more distal to the airways (deeper tracheal or
bronchial areas).
• CO2 production:
– Decreased production, and hence ETCO2, may be seen with hypothermia.
– Increased production, and hence ETCO2, may be seen with hypermetabolic states such as
malignant hyperthermia, thyroid storm, fever, sepsis, or shivering.
• Alveolar ventilation:
– Decreased minute ventilation, and hence ETCO2, may be seen with inadequate ventilator
settings, or in spontaneously ventilating patients with narcotics, residual paralysis,
metabolic alkalosis, or other IV or volatile anesthetic agents, affecting tidal volume and/or
respiratory rate.
– Increased minute ventilation, and hence ETCO2, may be seen with inadequate ventilator
settings, pain, metabolic acidosis, or awareness under anesthesia.
– Atelectasis and other situations in which the alveoli are perfused, but not ventilated
(pneumonia, mucus plug, and pulmonary edema), have little effect on ETCO2 because CO2
is highly soluble and will diffuse out almost completely in better ventilated alveoli. Thus,
shunting has only a minor effect on the ETCO2 and PaCO2 gradient.
– Airway obstruction can result from bronchospasm, upper airway obstruction, biting, or
excessive mucus production. The capnogram may demonstrate a delayed alveolar
emptying with a slow rise of expired CO2, leading to failure to obtain a true plateau
(sloping of phase II). It does not normally change the ETCO2 value.
• Cardiac output: ETCO2 can function as an indicator of profound hypotension and cardiac
arrest. Dead space ventilation results in V/Q mismatching secondary to impaired pulmonary
blood flow and exhalation of CO2. Thus, despite decreases in the ETCO2, the PaCO2
continues to rise, resulting in an increased gap.
– During cardiac arrest, the ETCO2 falls close to zero; when cardiopulmonary resuscitation
starts, the ETCO2 increases and correlates to pulmonary blood flow.
– Pulmonary emboli from air, clot, fat, or amniotic fluid also impair pulmonary blood flow,
and a decreased ETCO2 can signal this occurrence (low specificity).
• Endotracheal tube placement confirmation is the most common use of ETCO2 detection. This
is done by a calorimetric ETCO2 detector in emergency situations and outside of the
operating room. After esophageal intubation, ETCO2 may be initially detected but will taper
off; thus, sustained ETCO2 should be noted over several breaths.
• Hypoventilation and obstruction during spontaneous breathing and sedation cases can be
detected early with ETCO2.
• Circuit disconnect: In addition to low-pressure alarms which are often used to detect the
drop in peak inspiratory pressure (PIP) that occurs when a patient becomes disconnected
from a ventilator, lack of ETCO2 detection could be a sign of circuit disconnect.
• Diaphragmatic paralysis: Curare notch is the early sign of reversal of muscle paralysis.
Curare notch, diaphragmatic movement, or attempted spontaneous ventilation
Phase I second elevation can represent diaphragmatic efforts or attempted breaths
• Malignant hyperthermia: Early detection is of utmost importance, and a rise in ETCO2 is one
of the earliest signs. ETCO2 trends could also be efficacious in monitoring the treatment.
• Elevated baseline or partial rebreathing represents CO2 in the inspired gas. The return of
ETCO2 close to zero depends mostly on the proper functioning of the breathing circuit,
valves, and CO2 absorber. Abnormalities may be seen with a low fresh gas flow, faulty
expiratory valve, and exhausted CO2 absorber.
Phase I elevated, with Phase III sloping signifies increasing inspired CO2 and expired CO2. Can be seen when the absorbent
is depleted or faulty unidirectional valve
• Cardiogenic oscillations: Synchronous changes in pulmonary blood flow during slow

expiration and mechanical agitation of different lung regions induced by cardiac activity
and pulmonary blood flow contribute to the creation of ripples. This is often observed in a
repetitive pattern during the alveolar plateau in synchrony with the heartbeat.
Cardiac oscillations that will correlate to heart rate
• Sudden loss of ETCO2 waveform during anesthesia could be due to a lack of respiratory
effort, airway obstruction, unintentional extubation, or circuit disconnect.
Decreasing ETCO2 with each breath may be seen with esophageal intubation, profound hypotension, or cardiac arrest
• Profound hypotension: In addition to palpating a pulse, rechecking noninvasive blood

pressure cuff, a sudden decrease in the ETCO2 can be a useful tool to confirm the diagnosis
of low cardiac output and allow for early treatment.
• Mechanical forces during thoracic or abdominal surgery may be seen during phase 1.
Phase I irregularities may be seen with mechanical forces on the thorax or abdomen that get transmitted as tiny oscillation
to the end of the endotracheal tube
REFERENCE
1. Dubin A, Murias G, Estenssoro E, et al. End-tidal CO2 pressure determinants during
hemorrhagic shock. Intensive Care Med. 2000;26(11):1619–1623.
ADDITIONAL READING
• American Society of Anesthesiologists. Standards for basic anesthetic monitoring. Available
at: http://www.asahq.org/
• Dead space
• Pulmonary ventilation and perfusion matching
• Cardiac output
CLINICAL PEARLS
• End-tidal CO2 is the partial pressure of CO2 at the end of expiration during tidal breathing.
It is assumed to be representative of alveolar gas but it is lower than alveolar PCO2 (the
alveolar dead space dilutes and lowers the end-tidal PCO2).
• Mixed expired PCO2 (PETCO2) is the partial pressure of CO2 in the expired gas during a tidal
breath. It is much lower than ETCO2 because the CO2-free gas from anatomical dead space
dilutes even further.
• There is only a subtle difference between PETCO2 and ETCO2 so ETCO2 is a valid substitute
for PETCO2.
ENDOSCOPIC RETROGRADE
CHOLANGIOPANCREATOGRAPHY (ERCP)
Basavana G. Goudra, MD, FRCA, FCARCSI
Vinay Chandrasekhara, MD
BASICS
DESCRIPTION
General
• Endoscopic retrograde cholangiography (ERCP) is a diagnostic and therapeutic procedure
performed with a flexible endoscope and fluoroscopy to examine the biliary tree and/or the
pancreatic ducts.
• Indications include obstructive jaundice due to common bile duct stones/strictures, papillary
stenosis, or a pancreatic head mass. It is also indicated for the treatment of pancreatic duct
abnormalities associated with recurrent or chronic pancreatitis (pancreatic duct strictures or
stones), bile duct and pancreatic duct leaks (either traumatic or iatrogenic), cholangitis
(infection of the bile duct from prolonged biliary stasis), and for evaluation of ampullary
tumors.
• A side-viewing endoscope is inserted through the mouth into the second portion of the
duodenum where the major papilla is identified. Using a catheter with or without the
assistance of a guidewire, the duct of choice (biliary, pancreatic, or both) is cannulated. The
duct(s) are visualized by injecting contrast dye along with simultaneous fluoroscopy.
• Based on the findings, a variety of therapeutic procedures can be performed. Endoscopic
sphincterotomy or cutting of the sphincter of Oddi muscle is routinely performed to allow
for improved drainage and flow of bile and pancreatic secretions. Additionally, stents can be
placed either in the biliary or in the pancreatic duct to facilitate drainage. Biliary stones can
be extracted with the use of a balloon catheter or a basket or can be crushed with a
mechanical lithotriptor.
Position
• Usually prone with the head laterally rotated to the left
• Occasionally lateral or supine if the patient is unable to tolerate the prone position
(comorbidities, recent abdominal surgery)
Approximate Time
30–60 minutes, depending on the endoscopist’s experience and the procedural indication
EBL Expected
None
Hospital Stay
• Can be performed in an outpatient setting; hospital stays are not mandated unless a
complication arises.
• May be performed for inpatients as a semi-urgent procedure. These patients are often ASA 3
or 4 and may present with complex hepatobiliary issues or sepsis due to cholangitis.
May include guidewires, exchange platforms, stone extraction devices, biliary and pancreatic
stents and dilators
EPIDEMIOLOGY
Incidence
• Gallstone disease is estimated to affect >20 million adults in the US at an annual cost of
$6.2 billion (1).
• 5–10% of those undergoing laparoscopic cholecystectomy for symptomatic cholelithiasis and
18–33% of patients with acute biliary pancreatitis will also have choledocholithiasis (2).
• Pancreatic cancer is the 10th most common site of new cancer, but is the 4th leading cause of
cancer death in the US and worldwide.
Prevalence
• An estimated 1.41% of men and women will be diagnosed with cancer of the pancreas; in
2010 an estimated 43,140 new cases were diagnosed in the US, accounting for 2.8% of all
cancers (3).
• Roughly 2,000–3,000 new cases of extrahepatic cholangiocarcinomas are diagnosed in the
US each year.
Morbidity
Low; can include bleeding, cholangitis, perforation, and pancreatitis
Mortality
The overall mortality related to complications from ERCP is 0.6%.
• ERCPs present a unique challenge to the anesthesia provider:
– They are often performed in an out-of-OR location.
– Patients often lack a secure airway and are expected to maintain spontaneous ventilation
(SV).
– The airway is shared with the endoscopist.
– Patients are in the prone position.
– IV anesthetic techniques are implemented.
– The intensity of stimulation could be similar to minor surgery.
• Multiple IV techniques may be utilized with a goal of maintaining spontaneous ventilation
and hemodynamic stability while rendering the patient unresponsive to stimulation.
• Significant liver disease requires dosing modification since it can affect the volume of
distribution, have prolonged duration of action (hepatically cleared drugs), and increase the
availability of free (active) drug (decreases in albumin and other plasma proteins).
• Unlike intravenous administration of contrast, injection of contrast into the bile duct or
pancreatic duct is not commonly associated with renal failure and does not require pre-
procedural creatinine levels to be checked.
SYMPTOMS
• Abdominal or back pain
• Jaundice
• Loss of weight
• Cachexia
• Ascites
• Psychological anxiety, depression
History
• Recent or planned cholecystectomy, bile leak
• Weight loss, jaundice, abdomen and back pain if pancreatic mass or cholangiocarcinoma is
suspected
• Recent pancreatitis, gallstones, alcohol use, chronic pancreatitis
• Primary sclerosing cholangitis
• Hepatitis B or C
Signs/Physical Exam
• Charcot’s triad of cholangitis: Jaundice, fever, right upper quadrant pain
• Evaluate for signs of chronic liver disease
• Airway exam must be performed in the event that the airway needs to be supported or
secured.
MEDICATIONS
Recent or chronic opioid use may increase anesthetic requirements.
Labs/Studies
Liver function tests and markers of hepatic function (INR, platelet count)
• Hepatic decompensation leading to encephalopathy, renal failure, or cardiopulmonary
compromise may occur.
• Pancreatic insufficiency
TREATMENT
Premedications
• Anxiolytics may be appropriate.
• Analgesics may be considered for patients with acute or chronic pain.
• Risk of aspiration, sepsis, bleeding from airway interventions
• Discuss deep sedation and realistic goals. Patients are not typically going to be “knocked
out.”
Coverage for biliary infections may be required for patients with cholangitis or persistent
biliary obstruction. Typical antibiotics include fluoroquinolones with or without
metronidazole or a combination of beta-lactam/beta-lactamase inhibitor (e.g., ampicillin–
sulbactam or piperacillin–tazobactam).
INTRAOPERATIVE CARE
• Deep sedation is commonly preferred with a total IV technique. Although frequently
considered as “MAC,” as the patient neither recalls nor responds to the procedural
stimulation, it can also be classified as general anesthesia and consented as such. Propofol is
commonly used in combination 1. with a potent opioid or ketamine with titration to SV.
• General endotracheal anesthesia is used infrequently and is dependent on the anesthesia
provider’s comfort with the patient’s airway (e.g., Mallampati 4, risk of aspiration, morbid
obesity) as well as difficulty and anticipated length of the procedure.
Monitors
• In sick inpatients, continue invasive monitoring, if already established.
– Deep sedation with propofol and fentanyl
– Nasal trumpets may be inserted to provide a conduit (bypasses oropharynx and
endoscope) to deliver an FIO2 of 1.0 at high flows into the hypopharynx.
By using an endotracheal tube connector and Mapleson C or other portable circuit, one
can provide some degree of positive pressure ventilation when the endoscope is in situ.
• A jet ventilator can be used supraglottically to provide intermittent or continuous high-
frequency ventilation. This would allow maintenance of oxygenation and permits deeper
sedation.
• General endotracheal anesthesia is induced in standard manner, in the supine position, after
appropriate pre-oxygenation. Consider a rapid-sequence induction, as appropriate. After
confirming tube location and securing it appropriately, the patient is positioned, with
careful attention to pressure points.
Maintenance
• Deep sedation: A multitude of regimens exist, often with propofol at the core. When
supplemented, a reduction in dosing should be anticipated. Although the anesthetic drugs
may be combined in the same syringe or bag, this limits the ability to titrate one medication
upwards or downwards.
– Propofol is a GABA receptor agonist that provides sedation; at higher doses it can result in
loss of consciousness and amnesia. However, it has a 300% pharmacokinetic and
pharmacodynamic variability, can lead to unanticipated apnea, and does not provide
analgesia (or amnesia reliably).
– Ketamine provides analgesia while maintaining SV. However, it can cause tachycardia,
excessive salivation (which can provoke laryngospasm), and emergence phenomenon.
– Remifentanil is a potent analgesic (mu receptor). However, respiratory depression,
bradycardia, nausea/vomiting, and chest wall rigidity limit its use as a sole drug in
endoscopy.
– Dexmedetomidine can provide sedation and analgesia. However, its use in the endoscopy
suite is limited due to its long onset time and increased duration of action. Additionally, it
can cause intense bradycardia and hypotension.
• Titration to effect at various levels of stimulation while maintaining a spontaneously
ventilating patient is more important than the drug or technique used.
With the use of potent, short-term hypnotics and opioids, patients usually “wake up” within
5–7 minutes after termination of the anesthetic. The use of longer-acting medications or
decreased drug clearance capacity can prolong the time to emergence.
POSTOPERATIVE CARE
BED ACUITY
• Most are performed on an outpatient basis.
• Comorbid conditions and vital signs should dictate the level of care for inpatients.
ANALGESIA
Not typically needed
COMPLICATIONS
• Common surgical complications:
– Bleeding
– Infection
– Perforation
– Pancreatitis
– Cramps in the abdomen usually disappear after the gas used for insufflation is absorbed.
• Common anesthetic complications:
– Postoperative nausea and vomiting
– Respiratory depression, hypoxia, desaturation.
REFERENCES
1. Everhart JE, Ruhl CE. Burden of digestive diseases in the United States. Part 1: Overall and
upper gastrointestinal diseases. Gastroenterology. 2009;136:376–386.
2. ASGE Standards of Practice Committee. The role of endoscopy in the evaluation of
suspected choledocholithiasis. Gastrointest Endosc. 2010;71:1–9.
3. merican Cancer Society. Cancer facts & figures. Atlanta: American Cancer Society, 2010.
ADDITIONAL READING
• Adler DG, Baron TH, Davila RE, et al. ASGE guideline: The role of ERCP in diseases of the
biliary tract and pancreas. Gastrointest Endosc. 2005;62:1–8.
• Colonoscopy
• End stage liver disease
• Cholecystectomy
CLINICAL PEARLS
• Nasal trumpet contraindications include antiplatelet medications and coagulopathies from
liver disease.
• Given the extended procedure duration and need for deeper levels of sedation compared to
other routine endoscopic procedures, most centers rely on an anesthesia care team-directed
propofol sedation rather than IV conscious sedation.
ENDOSCOPIC SINUS SURGERY
Shannon M. Gossett-Popovich, MD
BASICS
DESCRIPTION
General
• Also known as FESS (functional endoscopic sinus surgery). It serves as a diagnostic and
therapeutic procedure in which limited surgical intervention can improve ventilation and
drainage of the ostiomeatal complex (also known as the “Messerklinger technique”).
– Indications include:
Chronic sinus infection refractory to medical management
Recurrent sinusitis
Nasal polyposis
Control of epistaxis
Sinus mucoceles
Excision of nasal tumors
– Involves insertion of a rigid, nasal endoscope into the nose for direct visualization of the
sinus openings
– The procedure allows for removal of tissue obstructing the ostiomeatal complex, allowing
for drainage of mucus, while protecting normal, non-obstructing anatomy and mucous
membranes.
• Other indications include:
– Skull base surgery
CSF leak closure
Endoscopic pituitary surgery
– Orbital surgery
Orbital decompression
Dacryocystorhinostomy
Optic nerve decompression
Position
• Supine with the bed at a 90° or 180° position.
• Reverse Trendelenburg with the head up 30–40° to allow for decreased arterial pressure and
prevention of venous congestion (improves surgical conditions and decreases blood loss).
There is a potential risk of venous air embolism in the head-up position during ESS.
Incision
Endoscope inserted into the nose. It is a minimally invasive technique that alllows for a
thorough examination of the nose from the anterior nare to the postnasal space.
Approximate Time
1–3 hours
EBL Expected
100–300 mL
Hospital Stay
Outpatient or overnight hospital stay
• Rigid fiberoptic nasal endoscope
• Vasoconstricting agents (cocaine or local anesthetic solution with epinephrine) aid in
decreasing bleeding in the surgical field.
• Intraoperative image-guidance systems
EPIDEMIOLOGY
Prevalence
Sinusitis is a very common condition (31 million Americans affected each year).
Prevalence
Increased likelihood of surgical intervention needed in patients with a history of asthma,
allergic disorders, deviated nasal septum, and previous nasal surgery
Morbidity
Major complications: 0.44% incidence (versus 1.4% in non-endoscopic procedures). CSF leaks
comprise almost half of all major complications (0.2%).
Mortality
Extremely low risk of death
• The airway should be protected from contamination.
• Adequately addressing postoperative pain and avoiding postoperative nausea and vomiting
can facilitate expeditious recovery and discharge.
• Provide optimal surgical conditions and minimize risk of bleeding
SYMPTOMS
Chronic sinusitis, nasal polyps, epistaxis, olfactory disturbances, nasal obstruction, postnasal
discharge, headaches, mid-facial pain
History
• Previous nasal surgery, nasal polyps, deviated nasal septum
• Asthma, allergic disorders
• Active infection/inflammation
• Gastroesophageal reflux disease (GERD)
• Presence of vascular tumors
Signs/Physical Exam
• Head and neck exam: Airway/nasal abnormalities
• Cardiopulmonary exam: Wheezing, breathing obstruction
MEDICATIONS
• Preoperative steroids can improve operating conditions in patients with rhinosinusitis and
polyposis.
• Preoperative antibiotics may be considered to decrease infection and inflammation.
• Medications that increase the risk of perioperative bleeding (anticoagulation and antiplatelet
drugs) should be withheld prior to surgery (but the risks of stopping these should be
carefully considered given the patient’s history).
– Aspirin, NSAIDs, vitamin E, ginkgo biloba, ginseng, and garlic should be withheld 7 days
prior to surgery.
Labs/Studies
• CBC, PT/PTT, INR, Type & Screen
• CT scan of the sinuses to identify disease extent and pathological tissue (aids in surgical
planning)
• Radiographic embolization of vascular tumors should be considered, if present, to decrease
the risk of bleeding.
Pulmonary disorders
TREATMENT
Premedications
Vasoconstriction, with cocaine or a local anesthetic with epinephrine, is administered by the
surgeon prior to endoscopy to decrease blood flow to the nasal sinus tissue.
While unlikely, it may be prudent to obtain consent for possible blood transfusion if deemed
necessary during the procedure.
• Cephalosporins are chosen most commonly to provide Staphylococcus coverage.
• 57% of surgeons preferred antibiotic prophylaxis, despite lack of solid evidence to support
use of prophylactic antibiotics.
INTRAOPERATIVE CARE
• Local anesthesia with mild sedative: Careful patient selection is necessary and extreme
caution should be used due to blood/secretions that may accumulate in the airway.
• General anesthesia with an endotracheal tube (ETT) or laryngeal mask airway (LMA)
Monitors
• Standard ASA monitors: A noninvasive BP cuff is usually adequate unless the patient’s
comorbidities necessitate an arterial line.
• One large-bore, well-functioning IV
• Eyes should remain uncovered during surgery. Surgeon will continually monitor for orbital
swelling, afferent papillary defect, or eyelid bruising.
• Slow controlled induction (unless the patient requires rapid-sequence induction)
• ETT versus LMA
– ETT requires higher anesthetic depth to maintain a target BP. Local anesthetic can be
applied to the vocal cords prior to intubation to decrease the risk of postoperative
laryngospasm. Avoid tight ETT ties; minimize positive end expiratory pressure to keep the
central venous pressure and venous congestion at a minimum.
– LMA provides excellent operating conditions. It allows for decreased sympathetic
stimulation on insertion, protects the upper airway from contamination, and allows for
smoother emergence. It will not, however, protect against regurgitation; thus,
contraindications include hiatal hernia, GERD, obesity, and a full stomach.
Maintenance
• Total intravenous anesthesia (TIVA): Propofol and remifentanil are commonly utilized as
they are easily titratable to HR and BP goals and provide a smooth and rapid emergence.
Remifentanil has the benefit of providing hemodynamic stability, while inducing slight
hypotension. It lowers BP via decreasing cardiac output without peripheral vasodilation.
However, it can cause PONV.
• Neuromuscular blockade can be used as needed to facilitate placement of the ETT and/or
positive pressure ventilation.
• Fluids should be administered with caution and care to avoid overloading the patient,
raising the BP, and allowing for controlled hypotension if the patient is a good candidate for
this method of anesthesia.
• Consider controlled hypotension methods to decrease blood loss and improve surgical
conditions.
– A preoperative dose of alpha-2 agonist clonidine (5 mcg/kg) may be helpful in some
patients.
– Vasodilating agents that decrease systemic vascular resistance (SVR) and lower mean
arterial pressure (MAP) <50 mm Hg have been shown to improve surgical conditions.
– Bradycardia has been found to improve surgical conditions. Decreasing heart rate with a
short acting beta-blocking drug such as esmolol can provide better surgical conditions
than a vasodilator that decreases the mean arterial pressure.
– Controlled hypotension should be used with caution: 0.6% risk of ischemic organ failure.
• Antiemetic administration intraoperatively is recommended to reduce PONV and should be
chosen based on the suitability to each patient.
• Blood and secretions may be present in the airway and should be thoroughly cleared.
• Avoid coughing and straining which can lead to venous engorgement and bleeding.
• Laryngospasm can lead to negative pressure pulmonary edema.
• Ideally wait until airway reflexes have completely returned prior to extubation.
FOLLOW-UP
BED ACUITY
Ambulatory surgery or overnight hospital observation if significant blood loss or
comorbidities dictate
ANALGESIA
• Opioid analgesics may be needed (especially after remifentanil usage) in the early
• Non-opioid analgesics such as COX-2 selective NSAIDs
– Provide excellent analgesia without impairing platelet function or altering bleeding times
– Extreme discretion is necessary with the use of COX-2 selective drugs in patients at risk of
thrombotic complications.
• Non-selective NSAIDs should be avoided due to the risk of perioperative bleeding.
• Long-acting local anesthetic infiltration of the surgical field has not been found to improve
postoperative pain.
COMPLICATIONS
• Surgical failure of procedure
• General risks include bleeding, embolism, infection, anesthetic-related side effects, and
transfusion.
• Damage to adjacent structures:
– Brain: CSF leak, meningitis, headaches, hemorrhage
– Eye: Blindness, visual changes, double vision, nasolacrimal duct damage, extraorbital
muscle injury, intraorbital hemorrhage, watery eyes
– Nasal: Hemorrhage, anosmia, adhesions
– CV: Carotid artery damage leading to stroke or death
PROGNOSIS
• 80–90% rate of success of surgery
– Prognosis is improved in patients with recurrent acute or chronic infective sinusitis, and
those presenting with symptoms of facial pain and nasal blockage.
REFERENCES
1. Al-Mujaini A, Wali U, Alkhabori M. Functional endoscopic sinus surgery: Indications and
complications in the opthalmic field. OMJ. 2009;24:70–80.
2. Bajaj Y, Gadapelli C, Reddy TN. Functional endoscopic sinus surgery: Review of 266
patients. Internet J Otorhinolaryngol. 2007;6(1).
3. Baker AR, Baker AB. Anaesthesia for endoscopic sinus surgery. Acta Anaesthesiol Scand.
2010;54(7):795–803.
4. Tirelli G, Bigarini S, Russolo M, et al. Total intravenous anesthesia in endoscopic sinus:
Nasal surgery. Acta Otorhinolaryngol Ital. 2004;24(3):137–144. (C)
5. Yoo HS, Han JH. Comparison of surgical condition in endoscopic sinus surgery using
remifentanil combined with propofol, sevoflurane, or desflurane. Korean J Anesthesiol.
2010;59(6):377–382. (C)
Controlled hypotension
CLINICAL PEARLS
• Minimally invasive technique with a low risk of major complications (CSF leak most
common).
• The goal of the procedure is to restore sinus ventilation and normal mucociliary drainage of
the sinuses.
• TIVA with propofol, remifentanil, and LMA have been shown to provide excellent operating
conditions in suitable patients.
• Minimizing conditions that may predispose the patient to increased bleeding perioperatively
is of great importance.
ENDOVASCULAR ANEURYSM REPAIR (EVAR)
Jared Feinman, MD
BASICS
DESCRIPTION
General
• Endovascular aortic repair (EVAR) is a minimally invasive technique that was initially
introduced in the early 1990s for patients with poor health status that were considered
“unfit" for open aortic repair.
• EVAR is now widely used in elective cases and is garnering potential for ruptured abdominal
aortic aneurysm (rAAA) repair.
• Large vascular sheaths are introduced into the femoral arteries, through which guidewires,
catheters, and stent grafts are then passed.
• Fluoroscopy is utilized to perform a pre-intervention angiogram (to confirm preoperative CT
measurements) and subsequently guide stent deployment.
• The stent graft is advanced to the level of the aneurysm, carefully positioned at the top and
bottom of the defect, and opened. Opening occurs by removal of the sheath, allowing radial
forces of self-expanding stents and active fixation using hooks or barbs that attach to the
artery wall to hold the graft firmly in place (against normal aortic intima proximal and
distal to the aneurysm). This creates “new walls” in the aorta through which blood flows
and “excludes” the aneurysm, which will eventually thrombose around the stent graft.
• Anatomic criteria for successful EVAR:
– Femoral or external iliac arteries are sheath insertion points, and must be >7 mm in
diameter (tortuosity, calcifications, stenotic disease may also complicate sheath insertion).
– Proximal aortic neck diameter should be 18–28 mm. Additionally, there should be at least
15 mm of non-aneurysmal artery to allow successful proximal fixation of the stent.
Presence of mural calcifications, thrombus, and angulation are secondary considerations.
– Common iliac artery is the usual distal attachment site, and should be 8–20 mm in
diameter. Additionally, there should be at least 20 mm of non-aneurysmal artery to allow
successful stent fixation.
• Advantages of EVAR over open repair:
– Avoids a large abdominal incision that can be associated with increased bleeding and the
need for transfusion, significant postoperative pain with resultant pulmonary dysfunction,
inflammation, and third-spacing. There is also less potential for injury to surrounding
structures.
– Reduced hospital stays and ICU admissions
– Avoids aortic cross-clamping and unclamping which can be associated with significant
hemodynamic shifts, distal ischemia, and renal injury
– Allows for anesthetic choice: Monitored anesthesia care (MAC), general anesthesia (GA),
or neuraxial blocks
– Hypothermia is less likely.
– Associated with reduced 30-day postoperative morbidity and mortality in elective repair,
rAAA repair, elderly patients, and high-risk patients compared to open procedures.
• Disadvantages of EVAR over open repair:
– Not suitable for 20–50% of AAA repairs
– Annual surveillance CT angiograms are required to assess graft positioning and endoleak.
– Pre-procedural imaging is required to assess the anatomic criteria; thus, it may not be
suitable in a hemodynamically unstable rAAA.
– Increased cost for stents and annual CT scans. However, this may be offset by reduced
hospital stay and morbidity (i.e., renal injury).
– Increased need for re-interventions (endoleaks, device failure, access site hematomas and
infection, aneurysmal remodeling)
– Long-term survival benefit versus open AAA repair may not be sustained (studies have
shown equivalent all-cause mortality at 2- and 5-year follow-up).
Position
• Supine
• Prep from nipples to knees in anticipation of immediate conversion to open surgery
Incision
Bilateral, small femoral arteriotomy at the level of the groin
Approximate Time
1–3 hours
EBL Expected
250 mL
Hospital Stay
• 2–3 days (vs. 5–10 days for open repair)
• 10 days for rAAA
• Stent-equipped balloon catheter
• Fluoroscopy, IV contrast dye
• Capability to convert to open repair
EPIDEMIOLOGY
Prevalence
50,000 AAA repairs are performed annually; approximately 43% are EVAR.
Prevalence
Increases with age, male gender, smokers, hypertension, family history, connective tissue
disease
Morbidity
• Re-intervention is 20% (compared to 6% with open repair)
Mortality
• 30-day mortality for elective repair (compared to 4.6% for open); however, the trend toward
an early mortality advantage may be lost as early as 12 months, with no difference in all-
cause mortality at 5 years (DREAM trial).
• A benefit in overall or aneurysm-related mortality may not exist over medical management
in patients unfit for open surgery.
• Patient population with significant comorbidities
• Cardiac complications are the most common, significant perioperative complication, and
cause of late mortality
• Nephrotoxicity from IV contrast dye; particularly in patients with pre-existing renal
dysfunction. Consider renoprotective measures.
• Prepare to convert to an open repair “electively” or emergently.
SYMPTOMS
• Expansion can present with pain.
• Pulsating sensations in abdomen, chest, lower back, or scrotum
• Rupture presents with severe, sudden, or persistent pain in the abdomen or back; clammy
skin, shock, nausea, vomiting
History
• Often found incidentally on imaging for other complaints
• Careful assessment of comorbidities; patients are “vasculopaths,” and disease of the cerebral,
myocardial, renal, and peripheral vasculature may also be present.
Signs/Physical Exam
• Palpable abdominal mass
• Abdominal bruits may be noted.
MEDICATIONS
• Beta-blockers lower the number of pulsations and strength of contractility against the
aneurysmal wall. Outcome studies have shown a reduction in cardiac and overall morbidity
and mortality (DECREASE study), but there may be an increase in stroke risk (POISE study).
• Anticoagulants (clopidogrel, heparin, aspirin, warfarin)
Labs/Studies
• Electrolytes, creatinine
• PT/PTT, INR
• Hemoglobin
• Ultrasound of the aneurysm to assess for size and the presence of free peritoneal fluid
• CT scan provides 100% sensitivity in detection and also allows for preoperative anatomic
planning, including consideration for EVAR.
TREATMENT
Premedications
• Perioperative beta-blockers should be titrated to heart rate and balanced against drops in
blood pressure or increased peak inspiratory pressures in reactive airway disease.
Introduction to, and initiation of, therapy should also be considered.
• Statins should be continued perioperatively. Introduction to, and initiation of, therapy
should also be considered. Studies have suggested that patients started on statins prior to
major vascular surgery may have reduced hospital length of stay, postoperative
complications, overall cost, incidence of renal complications, and mortality. However,
guidelines do not exist as to drug selection, dosing, minimal treatment period, or other
criteria at this time.
• Blood consent for potential transfusion (especially if converted to open repair)
INTRAOPERATIVE CARE
• GA with ETT for pulmonary disease, Parkinson’s, chronic back pain, rAAA
• Monitored anesthesia care
• Regional (epidural, CSE) T12 level; need to inquire about anticoagulation medications, may
need preoperative PT/PTT/INR. Not contraindicated by usual intraoperative heparinization.
Follow ASRA guidelines for removal. If insertion is traumatic, the case may need to be
delayed.
Monitors
• Arterial line (beat-to-beat blood pressure monitoring, ACT, labs): Consider preoperative
placement if there is a potential for HD instability during induction.
• 2 large-bore IVs (14–18 g) for rapid resuscitation in case of rupture or emergent conversion
to open repair
• Central line access not usually necessary unless left ventricular dysfunction or poor IV access
• Foley catheter (allows adequate hydration with IV contrast dye)
Slow, controlled induction; avoid coughing, bucking, HD instability that may cause rupture or
exacerbate ischemia or COPD.
Maintenance
• Heat loss can result from significant exposure during prepping and draping.
• Stent deployment needs to take place during apnea (if GA, hold ventilation; if MAC/regional
it requires patient to be able to follow commands).
• Low HR reduces movement interference of the image (systolic beats cause aortic wall
distension).
• Marked hypotension may indicate retroperitoneal or intra-abdominal bleeding.
• Heparinization may require repeat dosing and monitoring of ACTs with a goal of 200–250.
Reversal with protamine may be required and should be discussed with the surgeon.
• Stent deployment can result in brief ischemia distal to the graft.
• Diligent assessment of UOP: Consider renoprotective measures against contrast-induced
nephrotoxicity, particularly in patients with baseline renal insufficiency. These include
sodium bicarbonate, mannitol, adequate IV fluid hydration, and statins.
• Avoid coughing and bucking
• Avoid hypertension. Consider antihypertensive drip such as diltiazem, nitroglycerin,
nitroprusside, and/or esmolol.
• Postoperative neurologic exam to assess for cerebral and peripheral ischemia
FOLLOW-UP
BED ACUITY
• Telemetry or ICU
• No flexion at groin for several hours after removal of large arterial sheaths
• Antiplatelet therapy (clopidogrel, aspirin), statins, and beta-blockers may need to be started
or continued postoperatively.
ANALGESIA
• Pain is typically mild; local anesthetic infiltration, NSAIDs, and PO opioids are often
sufficient.
• Epidural catheters should be removed using ASRA guidelines, and only after documenting
normal coagulation status.
COMPLICATIONS
• Rate of secondary intervention following EVAR is 10–15% per year, most commonly for
endoleak.
• Endoleak: Extravasation of blood outside of the stent graft and into the aneurismal sac (seen
in 20–30% of all EVARs during early postoperative period)
– Type I: Leak at proximal or distal graft attachment site (<5% of all leaks, and 80% heal
spontaneously by 6 months)
– Type II: Flow to and from the aneurysm sac by patent branch vessels (20–30% of all leaks,
about 50% of these heal spontaneously)
– Type III: Junctional leak due to overlapping device components
– Type IV: Increased porosity of graft fabric, heals spontaneously over time
• Endotension: In 5% of EVARs, the aneurysm continues to grow despite the absence of any
leak. Etiology of endotension remains unclear, but patients may require eventual open
repair.
• Stent graft device issues: Fracture of metallic components (stents, hooks, or barbs), tears in
the fabric component, inadequate proximal or distal seal zone, thrombus or calcification
that limits stent purchase, or migration may require revision.
• Acute dissection or rupture (1–1.5% per year after EVAR) requires emergent open repair or
EVAR revision.
• Embolization of atheromatous or thrombotic debris causing ischemia or stroke
• Retroperitoneal hemorrhage
• Postoperative delirium in the elderly
• Adverse cardiac events (ischemia, infarct, arrhythmias, CHF, hypertension, hypotension)
• Renal injury from IV contrast (∼50–80 mL of dye used for intraoperative angiograms)
and/or deployment of the stent over the renal arteries
• Postoperative fever and leukocytosis are common.
• Access site infection or hematoma
REFERENCES
1. Greenhalgh RM, Powell JT. Endovascular repair of abdominal aortic aneurysm. N Engl J
Med 2008;358(5):494–501.
2. Eliason JL, Upchurch GR. Endovascular abdominal aortic aneurysm repair. Circulation
2008;117:1738–1744.
3. DREAM Study Group. Long-term outcome of endovascular repair of abdominal aortic
aneurysm. N Engl J Med. 2010;362:1881–1889.
4. Bakker EJ, van de Luijtgaarden KM, van Lier F, et al. General anaesthesia is associated with
adverse cardiac outcome after endovascular aneurysm repair. Eur J Vasc Endovasc Surg.
2012.
5. Hyhlik-Durr A, Bischoff MS, Hakimi M. Technical aspects of EVAR for infrarenal AAA. J
Cardiovasc Surg. 2012;53(1 Suppl 1):111–118.
ADDITIONAL READING
• DECREASE study
• EUROSTAR study
• Abdominal aortic aneurysm (open repair)
CODES
ICD9
441.9 Aortic aneurysm of unspecified site without mention of rupture
ICD10
I71.9 Aortic aneurysm of unspecified site, without rupture
CLINICAL PEARLS
• Minimally invasive procedure with reduced 30-day morbidity and mortality compared to
open repair; however, the survival benefit is lost as early as 12 months.
• Beta-blockers and statins should be continued perioperatively; some evidence to suggest that
initiation of therapy confers a survival benefit.
• Acute dissection or rupture requires emergent conversion to an open repair.
• There is some evidence showing that general anesthesia is associated with an increased risk
of cardiac events compared to local/regional techniques.
EPIDURAL
Sharon L. Lin, MD
Jane C. Ahn, MD
BASICS
DESCRIPTION
• A technique for accessing the epidural space in order to deliver medications. Epidurals are
placed perioperatively for analgesia, surgical anesthesia, and in laboring patients. Pain
physicians also perform the procedure for diagnostic and therapeutic purposes.
• Epidurally administered medications are delivered close to their intended site of action, as
opposed to the intravenous route. This allows the anaesthetist to deliver smaller doses, with
the benefit of reduced side effects. Furthermore, medications within the epidural space
serve in an “extended release” capacity.
• Epidural kits: Accessing the epidural space requires the use of a hollow bore needle (varies
in length, diameter, and sharp edge). Single shots can be performed with a 19 G Crawford
epidural needle; continuous catheters can be placed with a styletted Tuohy epidural needle
that is usually 16–18 G and 8–10 cm in length. Syringes are available in glass or plastic.
• Identification of the epidural space relies on tactile sensation. Unlike IVs where blood return
confirms correct location or intrathecal/spinal blocks where CSF return confirms location,
epidural placement relies on a slight change in resistance to injection.
– Loss of resistance technique utilizes fluid or air; chronic pain physicians often utilize
radiographic imaging to assist with correct placement. No difference in block success has
been identified between air and saline for localization of the epidural space. Air may be
associated with a patchy block, or rarely pneumocephalus or subcutaneous emphysema.
• Indwelling catheters allow for medication delivery either as repeat boluses or continuous
infusions. Stiff, plastic catheters facilitate easy insertion; however, paresthesias and
intravascular catheter insertion may be more frequent. Flexible wired catheters may result
in a slightly more difficult insertion, but may reduce the likelihood of puncturing
intravascular or intrathecal spaces. Patient-controlled epidural analgesia (PCEA) allows for
continuous infusion with patient-initiated bolus dosing and has been associated with overall
lower drug usage and higher patient satisfaction.
• Depth of insertion <4 cm may increase the risk of catheter dislodgement by patient
movement whereas insertion >6 cm increases the risk of migration into the subdural or
intrathecal space or knot development.
• Medications commonly used include local anesthetics, opioids, vasopressors (epinephrine,
phenylephrine), and clonidine. All medications need to be preservative-free to avoid
undesired effects (i.e., transient neurologic symptoms).
• Local anesthetics produce differential blockade; nerve fibers have different sensitivities due
to their location in the spinal cord, diameter, and the presence or absence of myelin.
Sympathetic nerve fibers are blocked first, and are usually followed by pain, touch, and
motor blockade. Large, myelinated nerve fibers are more sensitive to local anesthetic
blockade compared to smaller, unmyelinated fibers.
– Concentration: Affects block density
– Volume: Influences spread and the number of segments blocked (taller patients require
larger volumes).
– Dermatomal distribution: Approximately 1–2 mL of local anesthetic is required to block
each anatomic segment. Generally half of the volume spreads cranially and half spreads
caudally; however, spread may be greater cranially.
• Opioids: Effective as a sole or adjuvant analgesic agent when administered epidurally. They
do not generally cause hypotension. Choice is often based upon availability, institution, and
pharmacokinetics (lipid solubility, duration of action, onset, and safety profile).
– Lipid solubility: Lipophilic opioids (fentanyl, sufentanil) have effects at the spinal cord and
systemically (secondary to vascular absorption). Hydrophilic opioids (morphine) have
effects primarily at the spinal cord.
– Onset and duration of action: Lipophilic opioids provide rapid onset of analgesia and
reduced respiratory depression due to rapid clearance from CSF. Hydrophilic opioids
produce a delayed but longer duration of analgesia along with a higher incidence of side
effects due to cephalic or supraspinal spread.
• Vasoconstrictors: Epinephrine enhances anesthetic depth and duration by decreasing the
rate of vascular absorption of local anesthetic. It is also an indicator of inadvertent
intravascular injection. Phenylephrine is not as effective as epinephrine.
• Bicarbonate increases the pH of the local anesthetic solution and the proportion of drug in
its un-ionized form (capable of intraneuronal diffusion to access its site of action); thus it
shorten the block onset time. Usual dose is 1 mL per 10 mL of local anesthetic.
• Clonidine: Prolongs and intensifies epidural local anesthetic effects via agonism of alpha-2
receptors on primary afferents, interneurons, and descending noradrenergic pathways found
in the spinal dorsal horn. Side effects include sedation, dry mouth, and dose-dependent
hypotension and bradycardia.
• Dexmedetomidine: Analgesic effect via alpha-2 receptor agonism at the spinal cord. Rapid
diffusion into CSF with epidural effects seen in 5–20 minutes.
• Ketamine: Safety in epidural space is not established. Racemic mixtures are associated with
neurotoxicity, but the preservative-free S(+) enantiomer may be safe.
• Steroids: The optimal dose, site of injection, and concurrent use of local anesthetics have not
been established in randomized controlled trials. Epidural steroid injections appear to
benefit patients with radicular pain and disc herniation, but only on a short-term basis.
• Dermatomes: Catheter incision-congruent epidural analgesia is associated with superior
analgesia, decreased morbidity, and minimal side effects such as lower extremity motor
block and urinary retention.
• Pressure changes in the pleural cavity are transmitted to the paravertebral space, then to the
epidural space. Deep inspiration will increase the negative epidural pressure, while
coughing will produce positive pressure.
ANATOMY
• The anterior border of the epidural space is comprised of the posterior aspect of the
vertebral body that is covered by the posterior longitudinal ligament. The posterior border
is formed by the ligamentum flavum.
• Epidural space communicates freely with paravertebral spaces and root sleeves; it contains
blood vessels, anterior and posterior spinal nerve roots, lymphatics, fat, and the filum
terminale. Epidural fat is loose and allows injected fluid to diffuse through it. Unilateral
blocks can result from segmentation by tissue.
• When performing a lumbar epidural, the needle passes through skin, subcutaneous fat,
supraspinous ligament, interspinous ligament, and ligamentum flavum. Thoracic epidural
placement via paramedian approach bypasses the supraspinous and interspinous ligaments.
• Epidural hematomas may be secondary to traumatic neuraxial block, anticoagulants, or
spontaneous bleeding from a spinal arteriovenous malformation. Patients present with
sudden, severe back pain with a radicular component. Neurologic deficits may progress over
hours to days.
• Epidural abscess is an infection with inflammatory granular tissue or pus in the epidural
space; there is a potential for rapid neurologic impairment due to spinal cord compression.
• Nerve damage: Permanent neurologic injury is rare. Techniques to avoid nerve injury
include minimal sedation during placement, discontinuing advancement if a paresthesia is
encountered, and insertion below the spinal cord when possible (L1 in adults, L3 in infants
and children).
• Postdural puncture headache is likely from a low-pressure CSF leak that is worsened by
standing or straining, but relieved by lying supine. It develops in approximately 50–70% of
patients after accidental dural puncture with an epidural needle. The sitting position
increases CSF hydrostatic pressure and may increase inadvertent dural puncture.
• Medication issues: Local anesthetics can cause hypotension and bradycardia, motor block,
nausea and vomiting, toxicity, and urinary retention. Opioids can cause nausea, vomiting,
pruritus, constipation, systemic absorption, delayed respiratory depression requiring
frequent monitoring or continuous pulse oximetry, and urinary retention with potential
delayed discharge.
• Total spinal: Inadvertent introduction of local anesthetics into the intracranial subarachnoid
space may result from unintentional dural puncture during placement, catheter migration,
or subdural spread.
• Adhesive arachnoiditis is associated with 2-chloroprocaine.
• Epidural catheter breakage can occur intrathecally, intravascularly, or subcutaneously.
• Failed epidural or placement of nonfunctioning epidural catheter ranges from 6% to 25%.
Unilateral block is more common when catheter insertion is >5 cm into the epidural space
or when the epidural needle is aimed towards a unilateral nerve root during insertion.
• Indications: Intraoperative and postoperative pain relief for lower limb, pelvic, lower/upper
abdominal, and thoracic surgery as well as nonsurgical pain
• Contraindications (absolute): Patient refusal, bleeding diathesis/coagulopathy, infection at
the insertion site, and proven local anesthetic allergy
• Contraindications (relative): Bacteremia, increased intracranial pressure, hypovolemic
shock, pre-existing neurologic injury or disease, severe valvular cardiac disease, previous
back surgery at the site of blockade, and certain thromboprophylaxis regimens
• Surgical anesthesia: Epidural anesthesia may also be utilized as a primary anesthetic with or
without MAC. With any epidural placement, preparation for airway management and a
difficult airway is necessary due to potential complications such as failed epidural, high or
total spinal, or local anesthetic systemic toxicity. Blockade to the mid-thoracic level does
not significantly change tidal volume, vital capacity, and minute ventilation in patients with
adequate lung function. Patients with severe chronic lung disease who are dependent on
accessory muscle function may be at higher risk of respiratory distress.
– In contrast to spinal analgesia, epidural analgesia requires a longer onset, has a longer
duration of action after single bolus injections, and increased medication dose is utilized
compared to spinals. Appropriate level of insertion is more important as compared to
spinal medications where the level of anesthesia may be adjusted significantly using the
effect of gravity.
• Postoperative analgesia: Catheters may be placed preoperatively or postoperatively.
Preoperative placement can allow for easier positioning and improved pain control on
emergence. Benefits of epidural analgesia include decreased postoperative pulmonary
complications, lower incidence of deep venous thrombosis, attenuation of stress response to
surgery, reduced intraoperative blood loss, reduced mortality, and facilitation of earlier
return of GI motility via attenuation of spinal reflex inhibition of the GI tract.
• T4–8 catheter insertion: Thoracotomy, video-assisted thoracic surgery (VATS), radical
mastectomy, thymectomy, post-traumatic rib fractures. Results in improved ventilation with
consequent decreases in postoperative pulmonary complications (hypoxia/atelectasis,
infection).
• T6–8 catheter insertion: Whipple procedure, gastrectomy, duodenectomy, esophagectomy,
hepatic resection
• T7–10 catheter insertion: General abdominal surgery, cystoprostatectomy, nephrectomy
• T8–11 catheter insertion: Abdominal aneurysm repair, colorectal surgery, radical
prostatectomy, total abdominal hysterectomy
• L1–L4 catheter insertion: Femoral-popliteal bypass, knee surgery, other lower extremity
surgery
• Epidural blood patch is effective in 50–70% of patients with postdural puncture headaches.
After accessing the epidural space, approximately 20 mL of freshly drawn blood is slowly
injected into the epidural space after obtaining the blood using sterile technique.
• Blockade of cardiac sympathetic fibers by thoracic epidural anesthesia leads to dilation of
normal and stenotic coronary arteries.
• Labor epidurals: Benefits include avoidance of hyperventilation, decreased circulating
catecholamines, uterine relaxation, and patient comfort. Neuraxial blocks are the preferred
anesthetic technique in parturients as it avoids instrumenting a potentially difficult airway
and allows the mother to remain awake during their baby’s birth. Early labor epidural
placement is advantageous in high-risk patients as it may be used for surgical anesthesia in
the event of an emergency Cesarean section. There is a higher incidence of unintended
epidural vein cannulation due to epidural venous engorgement.
• Higher incidence of unintended epidural vein cannulation is reported in pregnant patients
due to epidural venous engorgement.
Intervertebral foramina decrease in size with increasing age, resulting in higher block levels
for similar epidural doses of local anesthetic. Additionally, a decrease in adipose tissue within
the epidural space may also decrease dose requirements.
The distance from the skin to the epidural space is approximately 1 mm/kg between 6
months and 10 years of age. Usual volumes of injectate range from 0.5–1 mL/kg (up to 20
mL).
REFERENCES
1. Ellis H. The anatomy of the epidural space. Anaesth Intens Care Med. 2009;10(11):533–
535.
2. Fischer B. Techniques of epidural block. Anaesth Intens Care Med. 2009;10(11):552–556.
3. Saberski LR, Kondamuri S, Osinubi OY. Identification of the epidural space: Is loss of
resistance to air a safe technique? A review of the complications related to the use of air.
Reg Anesth. 1997;22(1):3–15.
4. Tiso RL, Thomas PS, Macadaeg K, et al. Epidural catheter direction and local anesthetic
dose. Reg Anesth. 1993;18:308–311.
5. Visser WA, Lee RA, Gielen MJ. Factors affecting the distribution of neural blockade by
local anesthetics in epidural anesthesia and a comparison of lumbar versus thoracic
epidural anesthesia. Anesth Analg. 2008;107(2):708–721.
6. Waurick R, Aken HV. Update in thoracic epidural anaesthesia. Best Pract Res Clinic
Aneaesthesiol. 2005;19(2):201–213.
• Total spinal
• Combined spinal epidural
• Epidural hematoma
• Epidural abscess
CLINICAL PEARLS
• Adjuvant drugs such as opioids added to the local anesthetic solution will improve the
sensory blockade, improve pain scores, and allow a lower concentration of local anesthetic
to be used.
• Case reports of complications associated with the use of air for the loss of resistance
technique include pneumocephalus, venous air embolism, subcutaneous emphysema, and
spinal cord and nerve root compression. Inadequate anesthesia (“patchy block”) has also
been reported with air. The use of saline may reduce the incidence of these complications;
however, there is no definite consensus.
• Continuous epidural analgesia may significantly benefit the patient, but only if there is an
acute pain service or physicians immediately available to troubleshoot and provide boluses
of epidural catheters when needed.
• If PCEA is not available, an IV PCA should be ordered to supplement epidural analgesia and
provide increased patient satisfaction.
• The distance from the skin to the epidural space is 4–6 cm in the majority of the population
(~80%). It is generally recommended that the epidural catheter be inserted 5 cm into the
epidural space.
EPIDURAL ABSCESS
Sharon L. Lin, MD
Jane C. Ahn, MD
BASICS
DESCRIPTION
• A collection of pus or inflammatory granular tissue in the epidural space with the potential
for rapid, irreversible neurologic impairment and death. Requires prompt diagnosis and
intervention.
• Epidural abscess associated with epidural catheter insertion is fortunately a rare occurrence.
However, due to the lack of available information, clear guidelines for diagnosis, treatment,
and prevention have not been established in anesthesiology. Extrapolation of infection
reduction from other scenarios (surgical site infection) and case reports have been utilized
to better understand and describe this complication.
• Potential routes of infection include iatrogenic inoculation or contamination, seeding from
the bloodstream, or extension from a nearby infected structure.
• Among obstetrical patients, infection is the most common cause of neuraxial injury.
EPIDEMIOLOGY
Prevalence
• Variable due to low rate of reporting, technical skills of the provider, and other
epidemiologic issues
• Spinal epidural abscess: 0.2–2 in 10,000 people admitted to hospital
• Rare after obstetrical epidural anesthesia
Morbidity/Mortality
• Delayed recognition (presence of neurologic deficit) may lead to permanent neurologic
injury, sepsis, and death.
• Mortality ranges from 6% to 32%; usually due to sepsis.
• Coexisting risk factors have been shown to be present in up to 80% of reported cases.
• Most common risk factors: IV drug use, infection elsewhere in the body, degenerative joint
disease, trauma, alcoholism, placement of stimulators or catheters, and neurosurgical
procedures
• Transient bacteremia and hematogenous spread of infection
• Diagnostic and therapeutic spinal interventions (epidural steroid injections)
• Immunocompromised patients
• Malignancy
• Longer duration of epidural catheterization (possible increased risk after >4 days; however,
studies with mean duration of catheter up to 6 days did not show increased risk)
• Age 30 years and older (peak incidence in 60s and 70s)
• Morbid obesity
• Males
• Penetrating injury to the spine or osteomyelitis
• Skin infection or abscess
• Caudal anesthesia
• Poor aseptic technique, performing neuraxial block without surgical mask and hat, or
traumatic insertion
• Pus or inflammatory granular tissue collections can result in spinal cord dysfunction
secondary to inflammation, as well as venous thrombosis, thrombophlebitis, edema, and
ischemia secondary to compression of the spinal arteries.
• Most epidural abscesses lie posteriorly because the dura mater is adherent to the vertebral
column anteriorly. Abscesses can extend easily over several vertebral segments because
there are no anatomic barriers in the posterior epidural space.
• Potential mechanisms for inoculation include exogenous and endogenous sources: Iatrogenic
contamination, the bloodstream, or infection from a nearby source.
• Epidural placement by anaesthetists is an opportunity for introduction of skin flora or other
contaminants. Staphylococcus aureus is the most common infective organism. Additional
bacteria, particularly Staphylococcus epidermidis, reside in large numbers in the deeper
recesses of hair follicles and are often difficult to eradicate by antiseptic skin preparations.
– Inappropriate sterile technique or a break in sterility
– Prolonged catheterization
– Traumatic catheter insertion may be associated with breaks in sterile technique and
subsequent need for manipulation.
– Blood in the epidural space provides a nidus for infection.
– Immunocompromised patients (diabetics, chronic steroid therapy, malignancy)
– Infection elsewhere: Inflammation at the epidural entry point occurs at a higher frequency
when there is an infected wound elsewhere. However, it is not a contraindication to
epidural insertion.
– Lack of sterile dressing on an indwelling epidural catheter entry point
• Labor epidurals: Increased risk in obstetric patients has been associated with catheters being
placed outside of the OR (delivery suite), the use of a surgical mask by the anaesthetist, and
lack of prophylactic antibiotics.
• Bloodstream: Gross or silent bacteremia. In 30–40% of cases, there is no identifiable source
and silent bacteremia is believed to be the culprit.
• Direct extension: Vertebral osteomyelitis or psoas muscle abscess
• Injectate: Racemic bupivacaine is bacteriostatic.
• Common bacteria
– Gram-positive cocci: S. aureus comprises 50–66% of all cases; of those, 15–40% are caused
by MRSA (particularly in patients with implantable spinal or vascular devices); S.
epidermis
– Gram-negative bacilli: Escherichia coli, Haemophilus influenzae
– Atypical organisms and fungi: Pseudomonas and Mycobacterium tuberculosis are most
commonly isolated from IV drug users and patients with tuberculous spondylitis.
• Severe and untreated cases can result in coma and cerebral edema.
• Aseptic technique: Wear mask, wash hands in alcohol or full surgical scrub after removing
hand jewelry. Prep widely with chlorhexidine in alcohol twice, drape the patient’s back, and
use powder-free sterile gloves without touching any unsterile area.
• Chlorhexidine is superior to povidone-iodine before epidural catheterization and lowers the
incidence of positive bacteriologic cultures.
• Use a bacterial filter during continuous epidural infusion.
• Limit disconnection and reconnection of neuraxial delivery systems.
• Accidentally disconnected catheters should be removed.
• Limit the duration of epidural catheterization.
• Daily evaluation of indwelling catheters for signs and symptoms of infection (fever, WBC
elevation, erythema or tenderness over epidural insertion site).
• Monitor neurologic function.
• Evidence for prevention of epidural abscess is sparse. Extrapolation from other fields,
indirect evidence, logic, and commonsense are utilized; case reports may be the only
“evidence.”
• Diagnosis may be difficult initially due to nonspecific signs or when neurologic signs or
symptoms have not manifested.
• Back pain with percussion or palpation of the spine, progressing to paralysis
• Erythema, induration or tenderness over epidural insertion site
• Neurologic changes can include meningeal signs, headache, paresthesias, difficulty standing,
and sphincter incontinence.
• Laboratory analysis shows leukocytosis (↑WBC) with a left shift, elevated erythrocyte
sedimentation rate, and elevated C-reactive protein.
• Blood cultures may be positive.
• Perform culture of epidural catheter tip or CSF analysis to determine viral, bacterial, or
fungal etiology.
• Imaging studies: X-ray may be abnormal if epidural abscess is secondary to spinal
osteomyelitis; however, plain x-ray images are neither sensitive nor specific.
• CT without contrast is not sufficiently sensitive to soft tissue densities in the spinal canal.
• Gadolinium-enhanced MRI is the most sensitive and specific imaging modality. Images
demonstrate linear enhancement that surrounds non-enhancing purulent or necrotic matter.
• CT myelography may be performed if an MRI is contraindicated; consider sending the CSF
for gram stain and culture.
• Neurosurgery consultation
• Infectious disease specialist consultation
• Herniation of intervertebral disc
• Vertebral osteomyelitis or discitis
• Meningitis
• Metastatic tumor
• Spinal cord injury
• Low back pain
• Transient neurologic symptoms
• Epidural hemorrhage
• Perinephric abscess
TREATMENT
• Some case reports indicate percutaneous drainage of abscess using fluoroscopic guidance or
CT-guided aspiration of abscess may be effective.
• Surgical intervention: Decompression within the first 24 hours with laminectomy,
hemilaminectomy, or interlaminar fenestration is associated with improved prognosis.
• Administer antibiotics: Empirical antimicrobial therapy should include a first-line anti-
staphylococcal agent (vancomycin) plus coverage for aerobic Gram-negative bacilli
(cephalosporin or fluoroquinolone). Once cultures return, antibiotic therapy should be
tailored.
• Prompt removal of in situ catheter if epidural abscess is suspected.
• Lumbar puncture is not recommended as it may induce meningitis if the needle traverses the
epidural abscess.
FOLLOW-UP
• Long-term antimicrobial therapy is often required for 4–6 weeks; 6–8 weeks for patients
with contiguous osteomyelitis.
• Complete recovery with full neurologic function is likely if neurologic symptoms are present
for <24 hours before initiation of therapy.
• Final neurologic outcome is assessed at least 1 year after treatment since some patients may
continue to regain neurologic function.
CLOSED CLAIMS DATA
• Epidural abscess comprised 4.5% (4/89) of neuraxial anesthesia claims in obstetrical
anesthesia (All Claims, n = 368).
• Epidural abscess comprised 4% (4/93) of all neuraxial block claims associated with steroid
injection (All Claims, n = 93).
– Claims resulting in payment: 43%
– Payment range: $2,000–$1,812,500
REFERENCES
1. Pradilla G, Ardila GP, Hsu W, et al. Epidural abscesses of the CNS. Lancet Neurol.
2009;8:292–300.
2. American Society of Anesthesiologists. Practice advisory for the prevention, diagnosis and
management of infectious complications associated with neuraxial techniques.
3. Borum SE, McLeskey CH, Williamson JB, et al. Epidural abscess after obstetric epidural
analgesia. Anesthesiology. 1995;82:1523–1526.
4. Mamourian AC, Dickman CA, Drayer BP, et al. Spinal epidural abscess: Three cases
following spinal epidural injection demonstrated with magnetic resonance imaging.
5. Darouiche R. Spinal epidural abscess. N Engl J Med. 2006;355:2012–2020.
ADDITIONAL READING
• Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: A meta-analysis of 915
patients. Neurosurg Rev. 2000;23:175–204.
• Sendi P, Bregenzer T, Zimmerli W. Spinal epidural abscess in clinical practice. QJ Med.
2008;101:1–12.
CODES
ICD9
324.9 Intracranial and intraspinal abscess of unspecified site
ICD10
G06.2 Extradural and subdural abscess, unspecified
CLINICAL PEARLS
• Prevent bacterial contamination by adhering to strict aseptic technique, and wearing sterile
gloves, mask, and hat.
• Initial clinical presentation of an epidural abscess, however, can be nonspecific. Fever and
tenderness over the epidural site may be the only symptoms.
• A large meta-analysis divided clinical manifestations into 4 stages (N = 915). However,
there appeared to be high inter-individual variability along with time to presentation (hours
to days).
– Stage 1: Back pain (71%) and fever (66%)
– Stage 2: Radicular pain (20%)
– Stage 3: Muscle weakness (26%), sphincter incontinence (24%), and sensory deficits
(13%)
– Stage 4: Paralysis (31%) and quadriplegia (3%) below level of infection
EPIDURAL HEMATOMA (SPINAL)
Caroline Fosnot, DO, MS
BASICS
DESCRIPTION
• Accumulation of blood in the epidural space, resulting in compression or ischemia of the
spinal cord. This can have devastating neurologic consequences.
• Hematomas remain a potential risk for a number of neuraxial procedures including:
– Epidural or spinal anesthesia
– Lumbar drain placement
– Diagnostic lumbar puncture
– Spinal cord stimulator insertion
– Epidural or transforaminal steroid injections
• It may also occur spontaneously or secondary to surgical trauma.
EPIDEMIOLOGY
Prevalence
• Incidence of spontaneous epidural hematomas is unknown.
• Epidural hematoma in a patient on fibrinolytic or thrombolytic therapy is estimated at
<1%.
• Occurrence of an epidural hematoma in association with neuraxial procedures is rare. Given
the infrequent occurrence, incidence is estimated:
– Epidural ∼1:150,000
– Labor epidurals ∼1:175,000
– Spinal <1:220,000
Morbidity/ Mortality
Spinal cord compression and/or ischemia can result in permanent nerve damage, cauda
equina syndrome, and/or paraplegia if left untreated.
• Pharmacologic agents:
– Anticoagulation agents: Warfarin, heparin, enoxaparin, dalteparin
– Fibrinolytic agents: Tissue plasminogen activator, streptokinase, urokinase
– Antiplatelet agents: Clopidogrel, ticlopidine
• Bleeding disorders:
– Hereditary: Von Willebrand disease, hemophilia A, hemophilia B
– Acquired: Uremia, preeclampsia, hepatic failure, leukemia, lymphoma, idiopathic
thrombocytopenia purpura, hypothermia, disseminated intravascular coagulopathy
• Traumatic neuraxial procedure
• Cavernous angioma or arteriovenous malformation (AVM)
• Anatomy of the spinal cord: The spinal cord extends to the first lumbar vertebrae (L1) in
adults (L3 in children). It is surrounded by 3 meninges (inner to outer): Pia, arachnoid, and
dura mater. The CSF accumulates between the pia and arachnoid meninges.
• Epidural space: The epidural space is a potential space bound anteriorly by the dura mater
and posteriorly by the ligamentum flavum. The epidural space normally contains tissue, fat,
and the epidural venous plexus.
– Expansion of the epidural space can occur with the introduction of local anesthetics,
blood, or pus.
• Injury of the epidural venous plexus can result in accumulation of blood within the epidural
space. Traumatic neuraxial procedures, particularly in the setting of abnormal coagulation,
may lead to compression and/or ischemia of the spinal cord.
• Neurologic deficits typically develop within 4–6 hours of the neuraxial procedure; in rare
instances, symptoms may develop 4–7 days after a procedure.
• Avoid neuraxial blocks in patients with bleeding diathesis:
– Thrombocytopenia
– Coagulopathy
• Avoid neuraxial procedures in the presence of anticoagulation agents. Guidelines outlined
by American Society for Regional Anesthesia (ASRA) (1):
– Unfractionated heparin (UFH)
SQ: No contraindications if total daily dose <100,000 U; check platelets and PTT if on
SQ dose >3 days
IV: Discontinue 4 hours; check PTT
– Warfarin: Discontinue 4–5 days; INR <1.5
– Low molecular weight heparin (LMWH) (enoxaparin and dalteparin):
Prophylactic dosing (enoxaparin 0.5 mg/kg/day; dalteparin 2,500–5,000 U/day):
Discontinue 12 hours
Treatment dosing (enoxaparin 1 mg/kg b.i.d. or 1.5 mg/kg/day; dalteparin 120
U/kg/day): Discontinue 24 hours
Remove catheter 2 hours before LMWH doses
– Clopidogrel: Discontinue 7 days prior
– Ticlodipine: Discontinue 14 days prior
– NSAIDS/Aspirin: No contraindication
– Herbal/OTC medications: No contraindications
• Severe back pain localized to site of the neuraxial procedure
• Radicular pain in appropriate dermatome distribution
• Sensory or motor deficits
• Depressed reflexes
• Bladder or bowel incontinence
• Reduced anal sphincter tone
• Coagulation studies: PT, PTT, INR
• CBC: Identify infection (WBCs), thrombocytopenia
• CT scan: Hyperdense fluid collection impinging on spinal cord
• MRI scan: Fluid collection compressing spinal cord
• Myelography: Illustrates a space-occupying lesion; not the first choice for an acute workup
• Disk herniation
• Local neuritis
TREATMENT
• Orthopedic or neurosurgical consult

– Decompression within 8–12 hours is associated with improved neurologic outcomes.
• Cases with minimal neurologic compromise may be managed conservatively with serial
neurologic exams.
FOLLOW-UP
• Physical therapy and/or neurologic rehabilitation for deficits

• Patient education about risk of epidural hematoma with future neuraxial procedures
CLOSED CLAIMS DATA
• As of 1992, there were 16 cases of spinal cord injury associated with epidural hematomas
(2)
– Systemic anticoagulation: 13/16
Preoperative heparin: 3/16
Intraoperative heparin: 13/16
Postoperative heparin: 5/16
– Neuraxial procedure: 13/16
Epidural: 11/16
Subarachnoid: 2/16
– Delay in diagnosis: 10/16
Sensory and motor deficits inappropriately attributed to local anesthetic
– Payment: 9/16
Median payment: $447,381
REFERENCES
1. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving
antithrombotic or thrombolytic therapy. Reg Anesth Pain Med. 2010;35(1):64–101.
2. Cheney FW, Domino KB, Caplan RA, et al. Nerve injury associated with anesthesia: A
closed claims analysis. Anesthesiology. 1999;90(4):1062–1069.
ADDITIONAL READING
• American Society of Regional Anesthesia Guidelines on Thromboprophylaxis
• Epidural
CODES
ICD9
432.0 Nontraumatic extradural hemorrhage
ICD10
• S06.4X9A Epidural hemorrhage w LOC of unsp duration, init
• S06.4X9D Epidural hemorrhage w LOC of unsp duration, subs
• S06.4X9S Epidural hemorrhage w LOC of unsp duration, sequela
CLINICAL PEARLS
• Surgical patients often present with anticoagulation for coexisting embolic disease (cardiac,
cerebral, peripheral vascular) and/or perioperative thromboprophylaxis.
• Neuraxial procedures and catheter removal should occur in the presence of minimal
anticoagulation agents.
• ASRA has established guidelines for neuraxial procedures in the presence of anticoagulation
agents.
• Patients at increased risk of epidural hematoma formation should be monitored closely with
serial neurologic exams.
• Severe back pain and worsening neurologic symptoms may signify an expanding epidural
hematoma.
• Prompt diagnosis and treatment improve neurologic outcomes.
EPIDURAL STEROID INJECTION
Eric S. Hsu, MD
BASICS
DESCRIPTION
• Epidural steroid injection (ESI) is performed to administer long-acting corticosteroids,
preservative-free local anesthetics, and normal saline into the epidural space to provide
symptomatic pain relief. It has the benefit of:
– Delivering medications in close proximity to the inflamed nerve
– Minimizing systemic side effects of steroids
• Pain relief from ESI is most likely the result of reducing inflammation and is often part of a
multimodal approach that also incorporates functional restoration.
• Prostaglandins (particularly prostaglandin E2) and leukotrienes contribute to inflammation,
sensitization, and pain at spinal nerve roots (1)[A].
– Phospholipase A2 (PLA2) is the rate-limiting enzyme in the conversion of arachidonic acid
to prostaglandins and leukotrienes.
• Steroids function to decrease inflammation in the epidural space by inhibiting the action of
PLA2. Additionally, steroids may also:
– Prevent and/or diminish ectopic neural discharge from neuromas
– Interfere with nociception by blockade of unmyelinated C-fibers but not A-beta fibers
– Reduce capillary permeability
• Steroids utilized include:
– Methylprednisolone acetate (MPA, Depo-Medrol): 80–120 mg
– Triamcinolone acetonide: 80 mg
• Dilute local anesthetics may also be administered to offer temporary analgesia without
demonstration of any specific level of sensory or motor blockade.
– Lidocaine has the advantage of providing a quick onset.
– Bupivacaine has the advantage of providing a longer duration.
• Normal saline is utilized to dilute the local anesthetic or provide a “flushing” agent that
dilutes the chemical or immunologic agents that promote inflammation and pain.
• There is no standard volume or composition in ESI. Typical volume of medication solution is
3–9 mL for interlaminar ESI and 10 mL or more for caudal ESI.
ANATOMY
• Epidural injections can be performed at the cervical, thoracic, lumbar, or caudal level.
• Both interlaminar and transforaminal approaches can be utilized and are based upon the
physician’s preference.
• Interlaminar ESI (ILESI), also termed translaminar ESI, provides diffuse coverage of the
posterior epidural space.
– Epidural needle is utilized.
– Technique is similar to perioperative epidural placement with the palpation of landmarks,
a midline (or paramedian) approach that begins at the skin, and then through
subcutaneous tissue, paraspinal muscles, supraspinous ligament, interspinous ligament,
and finally loss of resistance at the ligamentum flavum.
– Radiography is utilized in the anteroposterior and lateral positions to aid in advancement
and confirmation of epidural spread of contrast.
• Transforaminal ESI (TFESI) distributes injectate around the nerve root sleeve as well as into
the epidural space.
– It may be more precise and effective when the pathogenesis is from a specific nerve root.
– The goal is to identify and inject medications at the level of the intervertebral foramen
that lodges the specific affected spinal nerve root.
– A spinal needle is advanced to the inferolateral margin of the pars interarticularis utilizing
C-arm fluoroscopy; oblique view.
– The lateral view is then used to guide the needle toward the anterior and superior aspect
of the foramen to avoid the exiting nerve root.
– If a paresthesia is noticed by the patient during needle placement, the needle should be
withdrawn slightly, and the position confirmed with radiographic contrast in both
anteroposterior and lateral views.
• Caudal ESI (CESI) is an ILESI approach that uses the landmarks of the sacral hiatus and
enters through sacrococcygeal ligaments into the sacral canal and epidural space.
• Fluoroscopic guidance is utilized to facilitate location and optimal positioning. A test dose of
contrast medium confirms the flow along the target nerve and rules out intrathecal and
intravascular injections.
– 17% of cases of ILESI without radiography can be subdural or superficial to ligament
flavum.
– 35% of CESI without radiography result in intravascular injection (despite negative heme
on aspiration) or failure to reach the epidural space.
– Injectate of ESI may not reach the target level or interface even with correct needle
placement in the epidural space.
– It is possible to thread a catheter from the caudal space to higher lumbar levels to ensure
that medications reach appropriate levels.
• Radicular pain is a sharp, lancinating, radiating pain, often shooting from the low back
down to the lower limbs in a dermatomal distribution. It is the result of mechanical and
inflammatory irritation.
– Inflammation and nerve root edema have been demonstrated on radiographic imaging,
surgical findings, and histologic examination.
– Clinical manifestations of nerve root inflammation include some or all of the following:
Radicular pain, dermatomal hypesthesia, weakness of muscle groups innervated by the
involved nerve root(s), diminished deep tendon reflexes, and positive straight or reverse
leg-raising tests.
– Mechanical compression alone usually causes only motor deficits and altered sensation but
does not necessarily cause pain.
– Chronic inflammation can result in edema, Wallerian degeneration, and fibrotic changes
to the neural tissues.
• Animal models have demonstrated inflammatory mediators in herniated disc material, such
as PLA2, interleukins, tumor necrosis factor-α, and nitric oxide. Animal models
demonstrated:
– Motor weakness, demyelination of nerve roots, and decreased withdrawal thresholds with
administration of PLA2 in lumbar nerve roots.
– Thermal hyperalgesia and motor weakness with ligation of spinal nerve roots.
– A reduction of thermal hyperalgesia lasting 3–4 weeks following ESI.
• Complications of ESI include medication effects and needle trauma.
– Corticosteroids are capable of suppressing the hypothalamic–pituitary–adrenal (HPA) axis
and plasma cortisol level for up to 3 weeks after a single epidural injection of 80 mg
methylprednisolone. Diabetic patients can also see a transient increase in glucose levels.
Additionally, epidural steroids have been associated with the development of osteoporosis
and arachnoiditis (intrathecal injection). Certain steroid formulations contain benzyl
alcohol which is potentially toxic to neural tissue (arachnoiditis, meningitis).
– Local anesthetics: Hypotension from sympathetic efferent blockade has been reported in
up to 2.5% of lumbar ESIs. Allergic reactions are rare.
– Contrast dye reactions often occur within a few minutes after injection. Those with a
history may be considered for pretreatment with antihistamines, corticosteroids.
– Neurologic injuries from cord compression (hematoma or abscess), direct injection into
the spinal cord
– Bleeding from vascular injury by the needle
– Vasospasm of the artery of Adamkiewicz has been seen with TFESI.
– Dural injuries: Puncture may be linked to headaches.
– Infectious complications: Epidural abscesses and meningitis
– Radiation: Stochastic effects of fluoroscopy
• Studies that convincingly define specific indications for ESI are lacking (2)[B].
• Potential indications for ESI may include:
– Herniated disc: The gel-like material (nucleus pulposus) within the disc can bulge or
rupture through a weak area in the surrounding wall (annulus). Irritation, pain, and
swelling occur when this material extrudes and comes into contact with a spinal nerve.
– Degenerative disc: A breakdown or aging of the intervertebral disc can cause collapse of
the disc space, tears in the annulus, and growth of bone spurs.
– Sciatica: Pain that travels along the sciatic nerve in the buttocks and down the legs. It is
usually caused by compression of the 5th lumbar or 1st sacral spinal nerve.
– Spinal stenosis: A narrowing of the spinal canal and nerve root canal that can cause back
and leg pain, especially when walking. This is typically the result of impaired vascular
flow to the nerve root with resultant irritation, edema, and dysfunction.
– Spondylolysis: A weakness or fracture of the par interarticularis between the upper and
lower facets of a vertebra (spondylolisthesis) can compress nerve roots and cause pain.
– Compression fractures with radicular pain
– Degenerative scoliosis
– Facet or nerve root cyst with radicular pain
– Postherpetic neuralgia
– Diabetic neuropathy
• Efficacy and outcomes:
– There is fair evidence that ESI is moderately effective for short-term (but not long-term)
symptom relief of sciatica or prolapsed lumbar disc with radiculopathy (3)[C].
– Most studies have reported that optimal outcome results from a series of 1–3 ESIs by
interlaminar, caudal, or transforaminal approach.
– Symptoms <3 months have a positive response rate of 90%; <6 months it reduces to
70%; >1 year further reduction to 50%.
– Studies suggest that no more than 3 ESIs should be performed in the absence of clinical
benefit.
– Local and systemic infections
– Pregnancy
– Bleeding disorders
– Poorly controlled comorbidities such as diabetes, congestive heart failure, renal disease
– Acute spinal cord compression
– Allergic reactions to contrast, corticosteroid, local anesthetic
• Procedure:
– Performed in a sterile procedure room
– Intravenous access for cervical spine procedures is usually attained prior to the procedure;
not routinely placed for lumbar procedures.
– Mild or no sedation may be administered; patient should be able to communicate with the
physician.
– Positioning is often prone, but can also be performed in the sitting or lateral position.
– Appropriate postoperative recovery room monitoring to assess for hemodynamic change
and sedation
• Pain relief is seen in several stages:
– Immediate pain relief is from the local anesthetic.
– Maximal relief may take up to 7 days after ESI.
– Benefit from ESI may last weeks to months depending on original pathology and therapy
(4)[C].
REFERENCES
1. DePalma MJ, Slipman CW. Evidence-informed management of chronic low back pain with
epidural steroid injections. Spine J. 2008;8(1):45–55.
2. Friedrich JM, Harrast MA. Lumbar epidural steroid injections: Indications,
contraindications, risks, and benefits. Curr Sports Med Rep. 2010;9(1):43–49.
3. Chou R, Atlas SJ, Stanos SP, et al. Nonsurgical interventional therapies for low back pain:
A review of the evidence for an American Pain Society clinical practice guideline. Spine.
2009;34(10):1078–1093.
4. Armon C, Argoff CE, Samuels J, et al. Assessment: Use of epidural steroid injections to treat
radicular lumbosacral pain. Report of the Therapeutics and Technology Assessment
Subcommittee of the American Academy of Neurology. Neurology. 2007;68(10):723–729.
ADDITIONAL READING
• Dagenais S, Tricco AC, Haldeman S. Synthesis of recommendations for the assessment and
management of low back pain from recent clinical practice guidelines. Spine J.
2010;10(6):514–529.
• Manchikanti L, Boswell MV, Singh V, et al. Comprehensive evidence-based guidelines for
interventional techniques in the management of chronic spinal pain. Pain Physician.
2009;12(4):699–802.
• Rathmell JP. A 50-year-old man with chronic low back pain. JAMA. 2008;299(17):2066–
2077.
• Epidurals
CLINICAL PEARLS
• ESI is indicated for reducing the inflammatory response and radicular pain over the
extremity that is associated with acute disc herniation, degenerative disc disease, spinal
stenosis, spondylolysis, compression fractures, and postherpetic neuralgia.
• ESI has been shown to be moderately effective for short-term (but not long-term) symptom
relief of sciatica or prolapsed lumbar disc with radiculopathy.
• ESI is commonly incorporated as part of the comprehensive approach in the management of
degenerative disc disease and spinal stenosis. It is recommended in a series of up to 3
treatments so clinical efficacy may outlast the half-lives and presumed duration of either
local anesthetics or steroids.
• Both fluoroscopic guidance and test dose of local anesthetic are crucial in transforaminal
ESI.
EPIGLOTTITIS
Brian Gierl, MD
BASICS
DESCRIPTION
Epiglottitis describes cellulitis of the epiglottis and aryepiglottic folds that may result in
extrathoracic airway compromise and require emergent intubation. The condition is more
appropriately termed supraglottitis.
EPIDEMIOLOGY
Prevalence
• Pediatric: 0.7 per 100,000 persons annually in the US (1,2)
– Most common age is 3–7 years, although case reports of epiglottitis in infants exist.
– Rate reflects 10-fold decrease since Haemophilus influenzae type B (HiB) vaccine was
introduced in 1988.
• Adult: 1–2 per 100,000 persons annually
– Incidence unchanged across several decades
Morbidity
No long-term sequelae (1)
Mortality
• Pediatric: Rare
• Adult: 0.9% of all cases; mostly secondary to airway compromise and cardiorespiratory
collapse, often after discharge with a diagnosis of laryngitis
• Etiology
– Haemophilus influenza type B; remains the classic etiology in children although up to 10%
of children presenting with epiglottitis have a history of HiB vaccination (3).
– Group A β-hemolytic streptococci
– Staphylococci
– Pneumococci
– Candida albicans viruses in children and adults
• Risk factors
– Male:Female ratio of 3:2
– Pediatric: Risk increased without HiB vaccine
– Adult: Risk increased with tobacco abuse
– Uncommon in the immunocompromised patient
• General prevention (3,4)
– Pediatric HiB vaccination
• Cellulitis of the epiglottis and aryepiglottic folds with possible epiglottic abscess results in
edema and airway obstruction that may lead to cardiorespiratory arrest.
– The swollen epiglottis acts as an extrathoracic obstruction, limiting airway inflow velocity
(similar to obstructive sleep apnea or vocal cord dysfunction). Expiratory flow (both peak
expiratory flow [PEF] and maximum expiratory flow [MEF] rates) and lung volumes are
not affected.
– Tachypnea further increases inflow velocity and worsens the degree of obstruction,
limiting tidal volumes and worsening shortness of breath.
• Associated conditions
– Concomitant infections, such as otitis media, cervical adenitis, pneumonia, and meningitis,
occur in 50% of pediatric patients.
• Once the diagnosis is suspected, the patient must be accompanied by a physician capable of
providing an emergency airway and should remain seated (the supine position worsens this
extrathoracic variable airway obstruction).
• Intubate in the OR with personnel and instruments available to obtain a surgical airway.
– Rigid bronchoscope
– Tracheotomy kit
– Cricothyrotomy kit
• Pediatric: Adrenergic outflow in the form of agitation or crying can cause tracheal collapse
and can lead to clinical deterioration with an already compromised airway.
– Avoid racemic epinephrine (the chosen therapy for laryngotracheobronchitis [croup]).
Significant airway deterioration has been attributed to further agitation from
administration (5).
SYMPTOMS
• Fever, odynophagia, dysphagia, muffled “hot potato” voice, stridor
– Shortness of breath, tachypnea, tachycardia, and rapid progression are associated with a
more serious clinical course and warrant aggressive treatment.
– Laryngotracheobronchitis presents with fever, hoarseness, and stridor, without
odynophagia or dysphagia.
History
Abrupt onset with symptoms developing over 6–24 hours. This is in contrast to
laryngotracheobronchitis, in which symptoms develop over days, typically after an upper
respiratory infection.
Signs/Physical Exam
• Definitive diagnosis is the direct visualization of a red, swollen epiglottis either under
flexible or direct laryngoscopy.
• Patients assume the tripod position, leaning forward with arms on their knees and neck
extended to maximize airway diameter.
• Stridor, respiratory distress, and drooling are late signs. Inspiratory stridor indicates
significant airway narrowing. Progression to biphasic stridor is an even more ominous sign
of impending airway collapse.
• Delayed capillary filling is common due to dehydration secondary to odynophagia and
drooling.
• Adults frequently have tenderness to palpation over the hyoid bone.
Labs/Studies
• Lateral neck radiograph obtained with hyperextension during inspiration will reveal a
round, thickened epiglottis (“thumb sign”), loss of vallecula air space, and thickening of the
aryepiglottic folds.
• Direct fiberoptic visualization of an inflamed epiglottis and aryepiglottic folds confirms the
diagnosis.
• Leukocytosis with left shift and neutrophil predominance is common and indicates a
bacterial etiology.
• Obtain blood cultures after securing the airway and before initiating broad-spectrum
antibiotic therapy (allows the antibiotic regiment to be tailored to the offending organism).
• Differential diagnosis:
– Pediatric:
Laryngotracheobronchitis
Bacterial tracheitis
Diphtheria
Pertussis
Tonsillitis
Retropharyngeal abscess
Foreign body obstruction
Allergic reaction
– Adult:
Laryngotracheobronchitis
Mononucleosis
Diphtheria
Pertussis
Tonsillitis
Laryngeal mass
Allergic reaction
TREATMENT
Premedications
• Avoid depression of respiratory drive in any person with airway compromise.
• Pediatric:
– Maintain parental contact and avoid anxiety-provoking procedures such as phlebotomy.
– Heliox may be used in a cooperative, older child to reduce inspired gas density, increase
carbon dioxide diffusivity by 3.5 times, and increase flow rate by 1.8 times through the
narrowed airway.
INTRAOPERATIVE CARE
Pediatric patients without IV access should have an inhalation induction followed by
placement of IV access and intubation.
Monitors
• Pediatric:
– Pre-oxygenate and induce anesthesia via an inhalation induction in the upright position
while minimizing crying and airway compromise (if IV access exists prior to induction,
irrespective of the route of induction, spontaneous ventilation should be preserved at all
times, if possible. The use of lidocaine IV 1 mg/kg may be administered to decrease
laryngospasm).
– A decreased minute ventilation from airway obstruction will slow inhalation induction.
– Establish IV access after an adequate depth of anesthesia is achieved and initiate volume
resuscitation.
– Avoid any neuromuscular blockade prior to securing the airway.
– Consider placing a laryngoscope blade into the vallecula to lift the base of the swollen
epiglottis and relieve the obstruction. If the glottis aperture is difficult to visualize,
consider compressing the chest to expel a glottic bubble.
– Place a styletted endotracheal tube under direct vision; choose an ETT 0.5 mm smaller
than would otherwise be chosen for the patient.
– Have a physician who is competent in the performance of a surgical airway present until
the airway is secured.
• Adult (2):
– Airway intervention is not frequently required.
– Consider heliox administration.
– Pre-oxygenate and perform awake fiberoptic intubation if required.
Maintenance
Prevent accidental extubation by appropriately securing the endotracheal tube.
• Extubate only after pharyngeal pyrexia has resolved, typically within 24–48 hours.
– Evaluate for the presence of an air leak around the endotracheal tube.
– Consider examination of supraglottic structures via fiberoptic bronchoscopy.
– Consider extubation in the operating room.
• Prevent self-extubation with appropriate sedation and restraints.
FOLLOW-UP
BED ACUITY
Intensive care for intubated patient or any patient with diagnosed epiglottitis until their
condition improves
• Broad-spectrum antibiotics effective against β-lactamase producing Haemophilus influenzae
with good CSF penetration until blood culture results are available. Ceftriaxone and
ampicillin–sulbactam are common choices.
• The use of corticosteroids has not been shown to reduce length of ICU stay or hospital stay
(5).
COMPLICATIONS
• Pneumonia
• Otitis media
• Meningitis
• Pulmonary edema
REFERENCES
1. Shah RK, Stocks C. Epiglottitis in the United States: National trends, variances, prognosis,
and management. Laryngoscope. 2010;120:1256–1262.
2. Frantz TD, Rasgon BM, Quesenberry CP. Acute epiglottitis in adults. JAMA.
1994;272:1358–1360.
3. Shah RK, Roberson DW, Jones DT. Epiglottitis in the Haemophilus influenzae type B vaccine
era: Changing trends. Laryngoscope. 2004;114(3):557–560.
4. Guardani E, Bliss M, Harley E. Supraglottitis in the era following widespread immunization
against Haemophilus Influenzae type B: Evolving principles in diagnosis and management.
Laryngoscope. 2010;120:2183–2188.
5. Kissoon N, Mitchell I. Adverse effects of racemic epinephrine in epiglottitis. Pediatr Emerg
Care. 1985;1(3):143–144.
6. Madhotra D, Fenton JE, Makura ZCG, et al. Airway intervention in adult supraglottitis. Ir J
Med Sci. 2004;173(4):197–199.
• Tracheostomy
• Cricothyrotomy
• Laminar flow
CODES
ICD9
• 464.30 Acute epiglottitis without mention of obstruction
• 464.31 Acute epiglottitis with obstruction
• 476.0 Chronic laryngitis
ICD10
• J05.10 Acute epiglottitis without obstruction
• J05.11 Acute epiglottitis with obstruction
• J37.0 Chronic laryngitis
CLINICAL PEARLS
• Pediatrics:
– Children are more likely than adults to require intubation due to a smaller baseline airway
diameter.
– Consider heliox via facemask to improve airflow in a cooperative patient.
– Perform an inhalation induction in the child’s desired position while minimizing agitation
and maintaining spontaneous ventilation (even if an IV is present).
• Adults:
– Intubate adult patients with a rapid progression of moderate respiratory distress, stridor,
suprasternal retractions, a respiratory rate >30/min, perioral cyanosis, or an arterial
carbon dioxide >45 mm Hg over the prior 24 hours (4,6).
– Consider helium–oxygen inhalation therapy.
– Perform an awake fiberoptic intubation in adults with an endotracheal tube that is 0.5 mm
smaller.
ESOPHAGEAL INTUBATION
Michael Carter, MD, PHD
BASICS
DESCRIPTION
• Esophageal intubation may occur during attempted tracheal intubation due to the
anatomical proximity of the two structures. Possible consequences of inadvertent tube
placement or dislodgement into the esophagus during repositioning include:
– Injury to the esophagus
– Gastric insufflation and aspiration
– Hypoxia
– Cardiovascular collapse
• Intended “esophageal intubations” with orogastric tubes, nasogastric tubes, and esophageal
temperature probes can also cause esophageal injury and contribute to injury claims in
anesthesiology.
EPIDEMIOLOGY
Prevalence
• In non-operative emergency settings, esophageal intubation has been reported at rates from
1.3% to more than 5%, varying by study location.
• Actual incidence may be higher as many esophageal intubations are recognized immediately
and corrected without report.
Morbidity/Mortality
• Data from the American Society of Anesthesiologists (ASA) Closed Claims Project Database
indicated esophageal intubation as the cause of 13% of claims originating from a respiratory
damaging event and resulting in death or permanent brain damage.
• Previous analysis reported esophageal perforation as the result in 90% of all esophageal
injury claims.
• Esophageal perforation may result in infection, pneumomediastinum, pleuritis, or abscess
formation. Symptoms may progress to shock or death if untreated. Treatment is usually
surgical. If treated within 24 hours, complete recovery is expected. If treatment is delayed,
mortality up to 50% can be expected.
• Setting:
– First responders to trauma scene outside hospital
– Emergency rooms
– Hospital setting outside the OR (floor codes/emergency airway)
• Head repositioning
• Transport
• Age >60 years
• Female gender
• Anatomical anomalies (tracheoesophageal fistula, laryngeal mass)
• Esophageal damage: The normal trachea with its cartilaginous rings is held open for the
passage of endotracheal tubes (ETT). The esophagus collapses on itself, and passage of the
ETT (even without a stylette) can tear mucosa causing a perforation.
• Risk of aspiration increases. Attempts at ventilating after esophageal intubation will
insufflate the stomach. The increase in intragastric pressures significantly increases the
possibility of aspiration into the pulmonary tree.
• Hypoxemia resulting from ineffective oxygenation causes vasodilation, with increases in
heart rate and cardiac output as compensatory mechanisms to maximize perfusion.
• Cardiovascular collapse can result. Maximal vasodilation will cause hypotension with
resultant reductions in perfusion, precipitating shock, and cardiovascular collapse.
• Patient positioning: Obtain optimal sniffing position or other appropriate positioning as
indicated by body habitus and comorbidities.
• Appropriate monitors: Ensure that the pulse oximetry is on the patient prior to intubation.
Always have CO2 detection device available.
• Visualization of glottis at intubation: Try to visualize the ET tube passing through the vocal
cords.
• Have a video or optical intubating device available if a challenging airway is suspected.
• Follow the ASA Difficult Airway Algorithm in cases where a difficult airway is encountered,
rather than force a blind intubation.
• Lung auscultation lacks recognizable breath sounds bilaterally and in all fields.
• Stomach auscultation can reveal gurgling sounds while bag ventilation is attempted.
• Fiberoptic bronchoscopy remains the definitive gold standard to confirm tube placement.
Insertion through the ETT should demonstrate visible tracheal rings and muscular bands.
• Real-time ultrasound: The transverse view at the level of the thyroid may be used to detect
intubation of the esophagus. The limiting factor may be the experience of the sonograph
operator as this technique is not widely used yet.
• Esophageal detection devices (EDD) are attached to the ETT after intubation and apply
vacuum to the tube. Resistance indicates a collapsed lumen around the ETT, suggesting
esophageal intubation.
• CXR: Because the proximal airway overlies the esophagus, esophageal intubation may not be
distinguished from tracheal intubation. In addition to not necessarily being conclusive,
results are also slow to obtain. Thus, it is not recommended as a first choice to confirm
tracheal intubation. It is, however, useful for determining endotracheal position of the ETT
(distance from the carina) after confirmed tracheal intubation by other means.
• Chest and/or abdominal pain may be seen postoperatively secondary to injury from
esophageal intubation from ETT, orogastric tubes, nasogastric tubes, and temperature
probes.
MONITORS
• End-tidal CO2 tracing: May show no tracing or a reduced tracing that diminishes over time.
Bag-mask ventilation prior to intubation may result in stomach insufflation with a gas
mixture containing exhaled CO2. Also may be confounding in the setting of dead space
ventilation (cardiac arrest, pulmonary embolism).
• Pulse oximetry: After esophageal intubation normal oximetric values may be displayed if
pre-intubation oxygenation was sufficient. However, without pulmonary ventilation,
residual oxygen is taken up by pulmonary capillary blood flow and over time will be
exhausted. As the PaO2 begins to fall, the saturation, and thus the pulse oximeter, will begin
to decrease. The time to decrease depends on the residual capacity of the patient and
effectiveness of pre-oxygenation. Pulse oximetry may also be less reliable in states of low
cardiac output or cardiac arrest.
• Colorimetric end-tidal CO2 detectors are devices commonly used in settings outside of the
OR (e.g., emergency response teams, floor codes/emergency airways, etc.). They allow for
inline rapid detection of CO2 while ventilating the patient. They can give false-negatives in
the setting of cardiac collapse (code situation with reduced cardiac output) or false-positives
(gastric insufflation with mask ventilation).
It is critical to immediately recognize ETT misplacement in the esophagus. Esophageal
intubation often needs to be distinguished from other ETT malpositioning or the inability to
ventilate the lungs after intubation. The differential diagnosis includes:
• Pharyngeal intubation with the tip of the ETT at level of arytenoid cartilages or above
• Selective endobronchial intubation
• Herniation of the ETT cuff occluding the tip of the tube and preventing ventilation
• Severe bronchospasm causing inability to ventilate and decreased CO2 return
• Low cardiac output states and pulmonary embolism (conditions that may present with very
low ETCO2 readings)
TREATMENT
• Prompt diagnosis of the situation is critical.

• Suctioning through the ETT while it is still in the esophagus has been suggested.
• Removal of the ETT and replacement in the appropriate position must be performed
promptly. A change in airway management technique and/or provider is possibly indicated
at this time.
• Supportive measures for ventilation (bag-mask ventilation) and perfusion (pressors if
needed) must be provided prior to reintubation as needed. Consider administration of
additional anesthetic agents, as appropriate.
• Esophageal perforation requires surgical consultation and possible repair.
FOLLOW-UP
• Any repositioning or airway manipulation after tracheal intubation requires re-examination

and assessment of vital signs and monitors to ensure ETT is still in the trachea and not
displaced into the esophagus.
• After recognized intubation of the esophagus, patient must be monitored for chest or
abdominal pain as those are the first presenting symptoms of esophageal perforation. Fever,
tachycardia, dyspnea, and tachypnea are symptoms of progression after esophageal
perforation. Surgical consult should be obtained immediately if injury is suspected.
CLOSED CLAIMS DATA
• As mentioned above, an analysis of data from the ASA Closed Claims Project (years 1986–
2000) reported esophageal intubation to be responsible for 13% of events associated with
death or permanent brain damage.
• Analysis of previous claims (1961–1996) showed esophageal injuries to account for 18% of
airway injuries during anesthesia, with the highest mortality (19%) and the largest
monetary settlement (median payment $138,975) when compared to all other airway
injuries of the same claims period.
REFERENCES
1. Cheny FW, Posner KL, Lee LA, et al. Trends in anesthesia-related death and brain damage.
2. Domino KB, Posner KL, Caplan RA, et al. Airway injury during anesthesia. Anesthesiology.
1999;91:1703–1711.
3. Martin LD, Mhyre JM, Shanks AM, et al. 3,423 Emergency tracheal intubations at a
university hospital: Airway outcomes and complications. Anesthesiology. 2011;114:42–48.
• End-tidal carbon dioxide
CLINICAL PEARLS
• Confirmation of ETT placement should include physical exam as well as monitors; reliance
on only one method may delay diagnosis.
• Maintain a high index of suspicion if the airway was difficult with a poor view. Consider
visual confirmation (fiberoptic bronchoscope, video-assisted laryngoscopy) as quickly as
possible if you are unsure or the patient shows clinical signs of inappropriate ventilation
and oxygenation. DON’T wait for oxygen desaturation to verify.
• Notify the surgical team of any suspected complications and watch for possible esophageal
perforation.
• Be aware of other situations that may involve “esophageal intubations” in the perioperative
period and their associated risks. Positioning of the following devices may result in injury or
perforation, particularly in patients with esophageal hernias or diverticulitis:
– Esophageal temperature probe
– Orogastric or nasogastric tubes
– Transesophageal Doppler and transesophageal echocardiographic probes
• Although a rare occurrence, esophageal intubation while accessing the trachea for
intubation through a tracheostomy opening or a stoma has been described. It is a possibility
to consider in the case of an undiagnosed tracheoesophageal fistula through which the ETT,
even though correctly inserted through the tracheal opening, may proceed into the
esophagus.
EXTRACELLULAR FLUID
Venugopal S. Reddy, MD, EDIC, FFARCS
BASICS
DESCRIPTION
• In an average adult male, 60% of the body weight is water, and in an average adult female,
50% is water. Water is spread across 2 compartments and is in dynamic equilibrium with
one another:
– Intracellular compartment (ICC): 40% of total body weight, 66% of total body water (∼28
L in a 80 kg male). It is mainly comprised of potassium, proteins, and organic anions.
– Extracellular compartment: 20% of body weight, 33% of total body water (∼14 L in a 80
kg male). It is mainly comprised of sodium, chloride, and bicarbonate. This compartment
is further subdivided into:
Interstitial fluid (fluid lying between the cells or tissue fluid): 15% of total body weight,
24% of total body water (∼10 L in a 80 kg male)
Intravascular fluid (plasma): 5% of total body weight, 10% of total body water (∼4 L in
a 80 kg male)
Transcellular fluid (fluids lying outside the normal components such as CSF, mucus,
digestive juices): 2% of total body weight, 2–4% of total body water (∼1–2 L in a 80 kg
male).
• Movement of proteins, ions, and water between compartments. Although the composition
differs between the compartments, all of the body’s fluid compartments are in osmotic
equilibrium, except during transient changes.
– Intracellular←→Extracellular compartments: The cell membrane consists of a bilipid layer
membrane that is laden with protein receptors and ion transport channels that regulate
the movement of proteins and ions. Water can move freely.
– Interstitial←→Intravascular compartments: These 2 compartments within the extracellular
compartment are separated by a capillary endothelium that allows free passage of ions
(diffusion based) and water but not large protein molecules (red blood cells, platelets,
albumin, etc.).
• Extracellular fluid (ECF) volume is proportional to the total sodium content. It is comprised
of an:
– Intravascular fluid (IVF) compartment: This is the circulating volume. Approximately 35–
40% of plasma volume is comprised of red blood cells (hematocrit); another 7% is
comprised of proteins and lipids.
– Interstitial fluid (ISF) compartment: The space between the capillary and the cell;
represents the milieu in which the cells are bathed. The ISF is separated from the IVF
compartment by the capillary endothelium which allows free passage of ions, but not
large protein molecules. Because the ISF is in dynamic equilibrium with the ICC, it has a
different composition in different tissues and in different areas of the body.
• Extracellular versus intracellular fluid composition
– ECF mainly contains large amounts of sodium cation, chloride anion, and bicarbonate. In
addition, it also carries cell nutrients such as glucose, fatty acids, and amino acids. These
do not pass freely into the cells, but are carefully regulated based upon metabolic needs
and are often hormonally mediated (insulin, growth hormone, etc.).
– Intracellular fluid mainly contains potassium cation, followed by magnesium and
phosphate anion. The ionic concentrations are carefully regulated by ion channels and
ATP-dependent pumps.
• Intravascular versus interstitial fluid: The ionic composition is fairly similar; differences exist
mainly in the chloride and protein concentration.
• Homeostatic control of the extracellular compartment: There are several mechanisms that
detect deviations in total body water and osmolarity and maintain them within a narrow
range. Maintenance of total body water and osmolarity is carried out mainly by the kidneys.
• Osmotic receptors:
– Antidiuretic hormone (ADH): Also known as arginine vasopressin. Synthesized in the
supraoptic and paraventricular nuclei in the hypothalamus. ADH is the main determinant
of renal excretion of water.
– Renin–angiotensin–aldosterone: Juxtaglomerular cells in the glomerulus secrete renin.
Renin is responsible for the conversion of angiotensinogen to angiotensin I, and this in
turn is converted into angiotensin II.
– Atrial natriuretic peptide: Secreted by the cells in the cardiac atria in response to
distension of atria; opposes the effect of aldosterone and causes diuresis.
– Kidneys respond to the above-mentioned hormones to maintain homeostasis. Intrinsically,
they also maintain sodium balance, which ultimately determines the ECF volume.
• Starling’s law of capillary filtration represents the net fluid filtration at any point within a
systemic or pulmonary capillary. Q = Ka [(Pc – Pt) – s (Πc – Πt)], where:
– Q = Net flow of fluid; values >0 indicate flow out of the capillary and values <0
indicate flow into the capillary
– Ka = Capillary permeability
– Pc = Capillary hydrostatic pressure; dominant force at the arterial end of a capillary
– Pt = Interstitial hydrostatic pressure
– s = Staverman reflection coefficient for albumin, pulmonary lymph flow, interstitial space
geometry, and compliance
– Πc = Colloid oncotic pressure; dominant force at the venous end of the capillary
– Πt = Tissue oncotic pressure
• Increased capillary hydrostatic pressure (Pc), decreased colloid oncotic pressure (Πc), and
increased tissue oncotic pressure (Πt) would increase filtration of fluid from the
intravascular bed to the interstitial space causing interstitial edema. Increased interstitial
hydrostatic pressure (Pf) and a decreased tissue oncotic pressure (Πt) would decrease
filtration. It is also important to appreciate that an increased capillary permeability and a
decrease in pulmonary lymphatic flow tend to encourage edema formation.
• Variables that can be measured: The capillary hydrostatic pressure is clinically measured as
the pulmonary capillary wedge pressure (PCWP). The other variable that can be measured is
colloid oncotic pressure (Πc). What are not measured are interstitial pressures, capillary
permeability, and the Staverman reflection coefficient for albumin, pulmonary lymph flow,
interstitial space geometry, and compliance.
• At the arterial end of a vessel, the hydrostatic pressure is greater than the osmotic pressure,
so the net movement favors water and other solutes being passed into the tissue fluid. At the
venous end, the osmotic pressure is greater, so the net movement favors substances being
passed back into the capillary. This difference is created by the direction of the flow of
blood and the imbalance in solutes created by the net movement of water favoring the
tissue fluid.
Clinical disturbances in body fluid are often described based upon the ECF condition. A few
rules should also be considered: The 2 compartments are (almost) always in osmotic
equilibrium; the components of the ICC do not cross the cell membrane (water does); and
normal kidneys, hormone function, and thirst mechanisms will eventually reinstate
homeostasis.
• Hypo-osmotic expansion (excessive water intake): The primary disturbance is an increase in
free water that will distribute throughout both spaces (increase ECF and ICF volume). It
secondarily decreases the osmolality of both the ECF and ICF.
• Hypo-osmotic contraction (salt wasting by the kidneys): The primary insult is a decrease in
the ECF and ICF osmolality. Because water follows sodium, both ECF and ICF volume are
also decreased secondarily.
• Iso-osmotic expansion (isotonic crystalloid administration, congestive heart failure, renal
disease): There is an increase in total body volume and osmoles; therefore, there is no
change in the ECF or ICF osmolality, but the ECF and ICF volume increase. The interstitial
space provides a “cushion,” with resultant edema.
• Iso-osmotic contraction (hemorrhage, burns): The primary insult is a decrease in both total
body volume and osmoles; therefore, there is no change in ECF or ICF osmolality. The ECF
volume decreases primarily and can draw fluid from the interstitial and intracellular space
in order to maintain perfusion and circulation to tissues (this ability is limited).
• Hyperosmotic expansion (hypertonic saline, mannitol, hyperglycemia): The primary effect is
an increase in total body osmoles with the ECF >>> ICF. As a result, the ECF volume
increases from movement of water out of the ICC into the intravascular compartment.
• Hyperosmotic contraction (insensible losses such as sweating, respiratory track
evaporation): The primary insult is a loss of free water that will decrease both ECF and ICF
volume by approximately 1,400 mL (~7 times the original infused volume). The secondary
insult is an increase in osmolality, although there is no increase in total body osmoles.
• Third space loss: Early work on this topic (1960’s) suggested that during major surgery or
trauma there will be an internal redistribution of ECF that no longer participates in the
maintenance of hemodynamic status or urine output. This so-called “third space”
contributes to generalized tissue edema seen frequently after massive fluid loading. The
composition of third space losses is equivalent to the ECF and electrolyte composition plus a
small amount of protein. This loss could be replenished by infusion of crystalloids such as
lactated Ringer’s or normal saline. Third space loss depends on the severity of tissue
damage, duration of tissue damage, and hypotension.
• Normal saline and lactated Ringer’s have a similar osmolality to the ECF; therefore, water
distributes equally throughout the whole of ECF. Because ISF comprises 2/3rd of the ECF,
most crystalloids are distributed to the ISF resulting in interstitial edema.
• 5% dextrose is a hypo-osmolar solution with an osmolality around 270 Osm. With the
metabolism of glucose, there is a decrease in the plasma osmolality and water uniformly
distributes to all the compartments. Since the ICC is the largest, most of the water will enter
into the cell and cause cellular edema.
• Hypertonic saline: The osmolality is around 2,500 Osm compared to 290 Osm in the plasma.
An infusion of 200 mL of 7.5% hypertonic saline would quickly expand the intravascular
volume by a volume approximately 7 times the original infused volume. The mechanism by
which hypertonic solutions increase plasma volume expansion is secondary to shifting of
fluid mainly from the ICC (and to a smaller extent by the interstitial compartment). This
concept has been used in the early management of hypovolemic shock. Intravascular
volume increase lasts about 30–45 minutes. In order to prolong the effect of hypertonic
saline, some clinicians use hypertonic saline with dextran to extend its effect.
• Colloids: The addition of proteins with oncotic pressure (in an isotonic crystalloid solution)
results in an increased plasma oncotic pressure. Colloids are capable of expanding the
intravascular compartment by approximately 100–150%. A key benefit is the increase in
plasma volume without concomitant interstitial expansion.
• Hyperosmolar solutions: Mannitol and urea are therapeutically administered to draw water
out of the ICC. Its mechanism of action relies on its inability to cross cell membranes, thus
increasing the ECF osmolality preferentially. Mannitol is commonly administered for
neurosurgical cases and increased intracranial pressure. In the event of a disrupted blood–
brain barrier, the solution would be able to enter the cell and increase intracellular
osmolality.
EQUATIONS
Fluid distribution in an 80 kg male:
• Total body water = 80 × 0.6 = 48 L
• Intracellular water (ICC) = 80 × 0.4 = 32 L
• Extracellular water = 80 × 0.2 = 16 L
• Interstitial fluid = 80 × 0.15 = 12 L
• Plasma = 80 × 0.05 = 4 L
GRAPHS/FIGURES
See Table
See Table
REFERENCE
1. Brandstrup B. Fluid therapy for the surgical patient. Best Pract Res Clin Anesthesiol.
2006;20:265–283.
2. Shields CJ. Towards a new standard of perioperative fluid management. Ther Clin Risk
Manage. 2008;4:569–571.
3. Yeager MP, Spence BC. Perioperative fluid management: Current consensus and
controversies. Semin Dial. 2006;19:472–479.
CLINICAL PEARLS
• During homeostasis, all of the body’s fluid compartments are in osmotic equilibrium. During
transient changes, pathological or therapeutic, water moves based upon hydrostatic,
oncotic, and osmotic forces.
• Extracellular fluid (ECF) mainly comprises sodium, chloride, and bicarbonate ions. The ECF
volume is proportional to the total sodium content.
• The interstitial and intravascular compartments have similar ionic compositions; it varies
mainly in the chloride and protein concentrations.
EXTRACORPOREAL SHOCKWAVE LITHOTRIPSY (ESWL)
James J. Konvicka, MD
BASICS
DESCRIPTION
General
• Extracorporeal shockwave lithotripsy (ESWL) is a minimally invasive technique that was
initially introduced in 1980 to treat calculi that cannot pass through the urinary tract.
• It is the preferred technique by urologists for the treatment of renal stones, proximal stones,
and midurethral stones. Benefits of ESWL over open and endoscopic (cystoscopic)
techniques:
– Rates of cure are equivalent.
– Significant reduction in treatment costs
– Minimally invasive
• Methods to localize the stone:
– Fluoroscopy, biplanar or monoplanar, can be used to visualize radio-opaque stones, and
contrast dye can be injected into the ureter for radiolucent (uric acid) stones.
– Ultrasonography can provide images of all types of stones that are large enough, but air-
filled intestinal loops may limit visualization of ureteral stones.
• Prior to the ESWL, cystoscopy with stent placement is commonly performed to facilitate the
passage of stones through the ureters.
• Stones are pulverized in vivo into reduced size fragments that can be expelled by the body
spontaneously.
– There is little difference in the density of soft tissues; as a result, shockwaves move
through tissue with a minimal dissipation of energy.
– At the interface of the stone and fluid, there is a significant difference in density, along
with the concentration of the shockwaves in a focused area that provides a major
dissipation of energy.
– Fragmentation is due to this energy overcoming the tensile strength of the calculus.
– The process is repeated until the stone is pulverized into fragments that are ideally <1
mm, allowing them to pass spontaneously and painlessly.
• To avoid arrhythmias (R on T syndrome), shockwaves are synchronized and triggered by the
EKG to occur 20 milliseconds after the R wave during the refractory period for older
generation lithotriptors. Therefore, length of treatment was determined by heart rate.
Newer units have been developed to deliver lower energy and function independent of the
EKG.
Position
• Supine, lithotomy; lateral decubitus and prone may be considered depending upon the stone
location.
• A small, water-filled drum or a cushion with a silicone membrane is placed next to the
patient’s skin and functions as the coupling medium, thereby avoiding immersion-related
physiologic alterations. First-generation lithotriptors required the patient to be immersed in
water as the coupling medium.
Incision
Ureteroscopy through the urethra is performed. Otherwise, no skin incision is required.
Approximate Time
• Older lithotripters: 1,500–2,000 shocks that may be triggered by the EKG R wave.
• In general, typically 35–45 minutes
EBL Expected
Minimal
Hospital Stay
None; typically an outpatient procedure
• Lithotriptor: Has 4 basic components—an energy source, focusing device, coupling medium,
and stone localization system.
• Ureteroscope
• Fluoroscopy, ureteral contrast dye
• Ultrasound
EPIDEMIOLOGY
Prevalence
Annual incidence of urolithiasis is 16.4 per 10,000 in the US.
Prevalence
• 3 times more common in men than in women
• Peaks in the 3rd to 4th decade of life
Morbidity
1–4% develop stone fragment pileup in the ureter; risk increases for greater stone burdens
(10% for stone collections >2.0 cm2).
Mortality
Minimal
• Shock wave movement and impact through cutaneous tissue and viscera cause most of the
pain and discomfort during ESWL.
• Minimizing patient movement and respiratory excursion is necessary to maximize stone
damage, limit surrounding tissue damage, and decrease the length of the procedure.
SYMPTOMS
• Flank pain often mimicking appendicitis
• Renal insufficiency or renal failure
• Obstructed pyelonephritis or pyelitis
History
• Screening for contraindications
– Absolute contraindications:
Bleeding disorder or anticoagulation
Pregnancy
– Relative contraindications:
Large calcified aorta or renal artery aneurysms
Untreated urinary tract infections
Pacemaker or AICD
Neurostimulation implant
Morbid obesity
Signs/Physical Exam
Hematuria
MEDICATIONS
• Analgesics
• Antibiotics to treat infections if present
Labs/Studies
• Pregnancy test
• Urinalysis and urine culture
• KUB for radio-opaque stones
• CT scan for anatomic information
• Pacemakers and defibrillators: Pacemakers are often converted to demand mode pacing
because shock waves may be misinterpreted as a “sensed” signal and inhibit or trigger
activity. Defibrillators may misinterpret the shock wave as an arrhythmia and
inappropriately deliver a shock. Deactivation of either device should be in concordance with
either the company or in-house device clinic to ensure that it is properly performed as well
as appropriately “re-activated.”
Renal insufficiency may be present if there is obstruction.
TREATMENT
Premedications
• Topical application of local anesthetic cream to the skin area that contacts the shockwave
tube may decrease the need for IV analgesics.
• Anxiolytics and narcotics may be titrated to effect, as needed.
• In patients with pacemakers or defibrillators, discuss perioperative management.
• In patients receiving deep sedation or neuraxial blocks, discuss reasonable sedation goals
and the potential to convert to a general anesthetic.
• First choice is a fluoroquinolone or trimethoprim-sulfamethoxazole.
• Alternatives: Aminoglycosides, aztreonam, ampicillin, first- or second-generation
cephalosporin, or amoxicillin/clavulanate
INTRAOPERATIVE CARE
• General anesthesia with endotracheal tube (ETT): Has the potential benefit of decreasing
respiratory excursion of the diaphragm with inspiration and expiration as well as allowing
brief periods of apneic oxygenation
• General anesthesia with ETT and jet ventilator (jet adapter is attached to the ETT) may be
used to decrease movement, the number of shocks delivered, as well as OR and anesthesia
time. Drawbacks related to jet ventilation include:
– Risk for barotrauma and hypercarbia
– Inability to measure tidal volumes, FIO2
– Need for a total IV anesthesia technique (can actually increase anesthetic time and negate
the potential decreased procedure time)
• General anesthesia with laryngeal mask airway (LMA): Drawbacks include the potential for
stomach and bowel insufflation that can impair visualization by the surgeon. An LMA with a
port to place an orogastric tube may alleviate this problem. Additionally, spontaneous
breathing may move the stone in and out of the shockwave zone (both inspiration and
exhalation are active processes under general anesthesia).
• Deep sedation: Advantages include the avoidance of airway instrumentation and faster
recovery time. Drawbacks include difficulty with lying still, respiratory excursions that may
move the stone in and out of the focal zone, and limitations of sedation during stimulating
portions of the procedure (e.g., cystoscopy and stent placement).
• Neuraxial anesthesia (T6 level is required): Epidural fluid boluses may cause an air–tissue
interface in the epidural space; this can result in shockwaves causing damage in this area. A
spinal technique may avoid this complication. Drawbacks include difficulty lying still and
respiratory excursion moving the stone in and out of the focal zone. Additionally, the
dermatomal level that is required (T6) can cause motor blockade of respiratory accessory
muscles; patients with pulmonary disease may depend upon these muscles to maintain
adequate ventilation and oxygenation.
Monitors
• Prior to induction, the stone is usually localized and the patient is positioned. Prone and
lateral positioning are done after induction.
• Standard induction techniques
Maintenance
• General anesthesia is commonly maintained with volatile agents. When jet ventilation is
utilized, a total intravenous technique needs to be utilized.
• Ventilation
– Spontaneous respiration may allow the stone to move in and out of shockwave field. This
may prolong the treatment time.
– Paralysis and controlled ventilation will allow brief apneic oxygenation and controlled
respiratory excursion.
– A low heart rate may increase the treatment time in older lithotriptors that fire after the R
wave.
– Fluoroscopy requires radiation safety.
There are no specific issues with emergence for this procedure.
FOLLOW-UP
BED ACUITY
Recovery room followed by discharge home
ANALGESIA
• Pain is typically mild and described as soreness.
• Renal colic from stone fragment passage is not uncommon.
• Thin patients may have more pain because the converging shockwave is concentrated at the
point of skin penetration.
COMPLICATIONS
• Flank petechiae, hematuria, and passage of stone fragments with associated renal colic are
common.
• Perinephric hematoma
• Acute and chronic hypertension
• Bacteriuria and sepsis
• Less common complications may include pulmonary contusion, hemoptysis, pancreatitis,
splenic hematoma, elevated liver function tests (transient), and biliary colic with
inadvertent fragmentation of adjacent biliary stones.
PROGNOSIS
• Depending on stone size, composition, and location, cure rates are >90%; however, stones
may recur.
• ESWL has a similar rate of success compared to other stone removal techniques.
ADDITIONAL READING
• Lee C, Weiland D, Ryndin I, et al. Impact of type of anesthesia on efficacy of medstone STS
lithotripter. J Endourol. 2007;21(9):957–960.
• Ozcan S, Yilmaz E, Buyukkocak U, et al. Comparison of three analgesics for extracorporeal
shock wave lithotripsy. Scand J Urol Nephrol. 2002;36(4):281–285.
• Pearle MS, Calhoun EA, Curhan GC, et al. Urologic diseases in America project: Urolithiasis.
J Urol. 2005;173(3):848–857.
• Sorensen C, Chandhoke P, Moore M, et al. Comparison of intravenous sedation versus
general anesthesia on the efficacy of the Doli 50 lithotriptor. J Urol. 2002;168(1):35–37.
• Cystoscopy
CLINICAL PEARLS
• ESWLs are minimally invasive procedures that have reduced morbidity and mortality
compared to open stone removal.
• Older generation units may trigger off the R wave.
• General endotracheal anesthesia with paralysis may be requested by surgeon.
F-INSPIRATORY
Debra Domino Pulley, MD
BASICS
DESCRIPTION
• F-inspiratory (FI) is defined as the fractional percentage or relative concentration of a
specific gas in a mixture of inspired gases.
– Varies between 0 and 100%
– Commonly refers to oxygen (FIO2) but also applies to any gas that is inhaled by the
respiratory system such as nitrogen, nitrous oxide, and any volatile anesthetic gas
– Inspiratory gases → alveoli → pulmonary capillaries → tissues (brain, fat, muscle, etc.).
• FA is the fractional concentration of a gas in the alveoli.
• Partial pressure of a gas is the fractional amount of a gas times the barometric pressure. PA
is the partial pressure of a gas in the alveoli.
• Oxygen
– FIO2:
Room air oxygen fraction is 21% at sea level.
Intraoperatively, the fresh gas flows can be adjusted in relation to one another to attain
the desired FIO2. The anesthesia machine displays the FIO2 of the fresh gas flow.
– Circuit: The fresh gas flow mixes with the exhaled gases. An oxygen analyzer in the
breathing circuit thus measures the actual FIO2 that the patient receives.
– Alveoli: During inspiration, gases enter the body and travel to the lung.
Water vapor is added to the inhaled gas, and at the alveolar level, the gas is maximally
saturated. The partial pressure of water vapor at normal atmospheric pressures is 47 mm
Hg.
The partial pressure of oxygen in the alveoli cannot be easily measured, but it can be
calculated using the alveolar gas equation: PAO2 = [FIO2 × (Patm - PH2O)] -
[PaCO2/RQ]. This requires only an arterial blood gas to measure PaCO2. The A-a
gradient is the difference between partial pressure of oxygen in the alveoli and partial
pressure of oxygen in arterial blood.
– Alveolar capillary membrane: Gas flows down an area of high to low partial pressure to
attain equilibrium. Thus, oxygen moves from the alveoli to the pulmonary capillaries; at
the same time, CO2 flows from the pulmonary capillaries into the alveoli and is eliminated
with exhalation.
Blood. After crossing the alveolar and capillary membranes, oxygen binds with
hemoglobin and dissolves in the blood. The amount bound to hemoglobin is (1.36 × Hb
× SaO2)/100. At sea level, the amount dissolved is 0.0031 × PaO2. Blood oxygen
content is thus comprised of both values. Henry’s law states that the amount of dissolved
gas will be proportional to the partial pressure. In a hyperbaric chamber, 100% oxygen
is pressurized to 2 or 3 times the atmospheric pressure. Since the partial pressure
increases 2 to 3 times, the amount of dissolved oxygen in the blood also increases.
– Tissues: Oxygen is necessary at the cellular level for aerobic metabolism. An increase in
demand results in a hypoxic state that facilitates gas flow down a partial pressure
gradient. Additionally, changes in the metabolic environment (pH, etc.) cause a right shift
in the oxygen–hemoglobin saturation curve and facilitate unloading to the tissues.
• Volatile anesthetics
– Vaporizer dials are set to deliver a specific fraction of gas into the fresh gas flow. This
concentration can also be expressed as partial pressure: Pagent = FIagent × Patm.
– Circuit: The fresh gas flow, at the specific volatile agent fraction, mixes with the exhaled
gases. The gas analyzer in the breathing circuit allows a measure of the FIagent that is
actually being delivered to the patient.
– Alveoli: The partial pressure of the inhaled anesthetic at the alveoli is the fraction times
atmospheric pressure minus water vapor pressure.
The minimum alveolar concentration (MAC) is the lowest alveolar (absolute)
concentration to produce immobility to 50% of subjects at 1 atm (expressed as% atm).
MAC values are indirectly measured by the end-tidal concentration (FEagent); there is no
current method to measure the alveolar concentration. The lower the MAC, the more
potent the anesthetic. Nitrous oxide is one of the least potent anesthetics and has a MAC
greater than 100%. It would need to be delivered in a hyperbaric chamber to be a
complete anesthetic. When volatile agents are mixed, or more commonly when volatile
agents are utilized with nitrous oxide, MAC values are additive.
– FA/FI: As a volatile anesthetic is inhaled, the alveolar concentration (FA) will rise until it
reaches the inspired concentration (FI). The rate at which this occurs is determined by
several factors:
Inspired concentration (FIagent)
Alveolar ventilation
Opposing the increasing concentration of a gas is the uptake or absorption of the gas into
the blood and tissues. Uptake is the product of 3 factors: solubility, cardiac output, and
the difference (gradient) between mixed venous partial pressure and alveolar partial
pressure
– Tissues: The concentration of the inhaled anesthetic in a tissue is dependent upon the
partial pressure and tissue solubility. The partial pressure of inhaled gases in the brain will
determine the depth of anesthesia.
• Concentration effect: Increasing the inspired concentration of a gas results in an increased
alveolar concentration and also affects the rate of rise of FA/FI. This is due to a
concentrating effect and an augmented inflow effect.
• Second gas effect: Describes the concentration effect of one gas (nitrous oxide) upon
another. High concentrations of nitrous oxide are usually delivered. At the time of
induction, rapid uptake of nitrous from the alveoli into the blood occurs to obtain
equilibrium. This results in a decrease in alveolar volume and an increase in the
concentration of other gases present in the alveoli.
ANATOMY
• The alveolus is the terminal end of a series of branching tubes from the trachea. It is where
gas exchange occurs.
• Capillaries form a dense network in the walls of the alveoli.
– Capillary diameter is 10 microns.
– Red blood cell diameter is 6–8 microns.
• There is a very thin blood–gas barrier (<0.5 microns), and this includes a layer of
surfactant, alveolar epithelium, interstitium, capillary endothelium, and plasma
• Decreased FIO2 can result in hypoxemia, which is defined as an arterial PO2 <60 mm Hg.
Methods to increase the FIO2 include:
– Nasal cannula: There is an approximately 4% increase in FIO2 for each liter per minute
increase in flow. Thus, 2 L via NC is equivalent to approximately 29% FIO2.
– Simple mask: Covers the mouth and nose and decreases mixing with room air. With
exhalation, 1-way valves decrease rebreathing of carbon dioxide. It is suggested that at
least 4 L/min should be used to avoid rebreathing of carbon dioxide. An FIO2 of
approximately 40–50% can be delivered.
– Nonrebreather mask: In addition to covering the mouth and nose, the reservoir bag
contains approximately 1.5 L of oxygen. With inspiration, gas from the bag is
preferentially taken up. With exhalation, 1-way valves decrease rebreathing of carbon
dioxide. This allows for the delivery of an FIO2 of 60–90%.
– Trach collar: Used for patients with a tracheostomy; it is similar to a simple mask, except
it fits over the ostomy.
– At higher elevations, barometric pressure will decrease. The fractional component of
oxygen does not change, but the partial pressure will decrease.
– Hyperbaric oxygen treatment has been useful in situations when the delivery of oxygen to
tissues from hemoglobin is inadequate. Per Henry’s law, increasing the atmospheric
pressure will increase the amount of oxygen dissolved in the blood. These include
Profound anemia
Carbon monoxide poisoning
Failing skin grafts and flaps
Infections
Traumatic injury
Radiation necrosis
Non-healing wounds
• High FIO2 may cause
– “Absorption” atelectasis: Nitrogen is a relatively insoluble gas in blood, and thus serves as
an alveolar “filler” (prevents collapse of alveoli). Thus, in the absence of nitrogen, oxygen
absorption can result in complete absorption (into the pulmonary capillaries) of gas
contained in the alveoli (particularly in marginally ventilated alveoli).
– Acute lung injury from mild tracheobronchitis to diffuse alveolar damage
– Decrease in ventilation and accumulation of carbon dioxide in patients with COPD
– Retinopathy in the newborn
• Increasing FIO2 at higher levels of shunt will not (or only minimally) decrease the A-a
gradient
• In the perioperative setting, different compositions of gases enter the body. These include
oxygen, air (oxygen and nitrogen), nitrous oxide, helium, and volatile anesthetics such as
isoflurane, sevoflurane and desflurane.
• Significant morbidity and mortality (including hypoxic brain injury) can occur when
inadequate oxygen is delivered to a patient. Safety mechanisms have involved changes in
design to decrease the incidence of delivering a low oxygen mixture or the wrong gas to a
patient. They include:
– Multiple oxygen sources: Pipeline supply, cylinder supply, auxiliary oxygen supply
– Gas specific systems: Diameter indexed safety system, pin index system
– Oxygen supply and pressure alarms: Fail safe valve, pressure regulators
– Oxygen/nitrous oxide proportioning systems
– Inspired oxygen concentration monitor
• Exhausted CO2 absorbent can lead to inspired CO2 and a decreased FIO2.
• Treatment strategies when hypoxia occurs include:
– Increasing the inspired oxygen concentration prior to induction when apnea will occur
– Administering oxygen immediately after cessation of N2O to eliminate diffusion hypoxia.
• Different mechanisms of perioperative hypoxia can be distinguished by calculating the (A-
a)O2 gradient.
• Onset and emergence: Can be hastened by changing the concentration, increasing
ventilation, using an anesthetic that is less soluble, and increasing the fresh gas flow.
• Aerosolized drugs that are inhaled such as albuterol, prostacyclin, corticosteroids, and
racemic epinephrine are liquids and do not enter the bloodstream via gas exchange
EQUATIONS
• Dalton’s law of partial pressure – the total pressure of a mixture of gasses is equal to the sum
of the partial pressure of each gas
– PT = P1 + P2 + P3 +… + Pn
• PI = FI × Patm, where PI is the partial pressure of inspired gas, FI is the fraction of inspired
gas, and Patm is the atmospheric pressure.
• Alveolar gas equation – the partial pressure of oxygen in the alveoli
– PAO2 = [FIO2 × (Patm – PH2O)] – PaCO2/RQ
– Typically, Patm = 760 mm Hg, PH2O = 47 mm Hg, and RQ = 0.8
– PAO2 = (FIO2 × 713) – (PaCO2/0.8)
– A-a gradient – the difference between alveolar and arterial O2
– A-a gradient = PAO2 – PaO2
• Oxygen content of blood
– CaO2 = (1.36 × Hb × SaO2/100) + (0.0031 × PaO2)
GRAPHS/FIGURES
FIGURE 1. Rate of rise of anesthetic gas. There is an initial rapid rise, which slows with time as equilibrium between the
input and uptake from the alveoli occurs. Soluble anesthetics have greater uptake by the blood and thus take longer to
reach equilibrium. Conversely, poorly soluble inhaled agents quickly reach equilibrium.
REFERENCES
1. Yasuda N, Lockhart SH, Eger El II, et al. Comparison of kinetics of sevoflurane and
isoflurane in humans. Anesth Analg. 1991;72:316–324.
2. Yasuda N, Lockhart SH, Eger El II, et al. Kinetics of desflurane, isoflurane, and halothane in
humans. Anesthesiology. 1991;74:489–498.
3. Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy. NEJM. 1996;334:1642–1648.
4. Benoit Z, Wicky S, Fischer JF, et al. The effect of increased FIO2 before tracheal extubation
on postoperative atelectasis. Anesth Analg. 2002;95:1777–1781.
5. Edmark L, Auner M, Enlund M, et al. Oxygen concentration and characteristics of
progressive atelectasis formation during anaesthesia. Acta Anaesthesiol Scan. 2011;55:75–
81.
– Blood oxygen carrying capacity
– Supplemental oxygen
CLINICAL PEARLS
– Delivery of the inhaled anesthetic will be more rapid with increased concentration of
inhaled anesthetic, increased fresh gas flow, and increased alveolar ventilation.
– Emergence from anesthesia will be more rapid with lower solubility anesthetics, increased
alveolar ventilation, and increased fresh gas flow.
– High inspired concentration of oxygen before induction and during emergence can
increase atelectasis.
– Hypoxemia with normal A-a gradient is caused by alveolar hypoventilation.
– Hypoxemia with increased A-a gradient is caused by V/Q mismatch, shunt, and/or
impaired diffusion.
– Postanesthesia, hypoxemia occurs frequently and supplemental oxygen may be required.
FACET JOINT INJECTIONS, LUMBAR
BASICS
DESCRIPTION
• Facet joint disease, also known as zygapophysial arthropathy, is a common cause of back
pain.
• Lumbar facet arthropathy accounts for 15–40% of cases of chronic low back pain. The exact
prevalence is uncertain because most studies excluded patients with radicular symptoms or
prior back surgery.
Facet joints are a junction or pivot point between bony levels of the spine; movement (and
limits to motion) is the result of rotation around this joint (akin to railroad tracks).
• Cervicals: Joints in the upper cervical spine face backward, upward, and medial
(pneumonic: BUM), whereas the joints in the lower cervical spine face forward, downward,
and lateral (pneumonic: FDL). The atlanto-occipital joint is responsible for flexion–
extension; the atlanto-axial joint is responsible for rotation; and the joints from C2 to C7 are
responsible for smaller levels of flexion–extension, rotation, and lateral bending.
• Thoracic: Backward, upward, and lateral (pneumonic: BUL). The axis of rotation is at the
center of both the vertebral body and the disc. As such, the discs experience rotation torsion
but minimal shearing forces. Consequently, the upper thoracic vertebrae (T1–T10) offer
great rotational motion range (∼35° to the left or right) and are mainly constrained by
ligamentous attachments and the costal cage.
• Lumbar: Backward and medial; they face each other (pneumonic: BM). As a result of their
orientation, the axis of rotational motion is at the base of the spinous process. The disc
experiences greater shearing forces (the disc and vertebral body must slide past one another
in opposite directions) that severely limit rotation compared to the upper thoracics. Their
rotation is ∼5° to the left or right, whereas they are capable of forward and backward
bending. The upper lumbar facet joints are oriented more parallel to the sagittal plane,
whereas the lower lumbar facet joints are oriented more parallel to the coronal plane.
ANATOMY
• The paired facet joints join the vertebral arches of 2 adjacent vertebrae along the
posterolateral spine.
• They are true synovial joints with a synovial membrane, hyaline cartilage, and a fibrous
capsule containing 1–1.5 mL of synovial fluid.
• Posteriorly, the joint capsule is continuous with the multifidus muscle.
• Anteriorly, the capsule is continuous with the ligamentum flavum.
• The innervation of each facet joint comes from the medial branches of the dorsal ramus at
the same level and one level above the respective joint.
• Causes of facet joint pain include:
– Recurrent strain and low-grade trauma (responsible for most cases of facet joint pain)
– Lateral bending causes the greatest strain on the L1–2, L2–3, and L3–4 facet joint capsules.
– Forward flexion causes the greatest strain on the L4–5 and L5–S1 facet joint capsule
– Acute trauma
– Rapid deceleration injuries can result in dislocation.
• Predisposing factors to facet joint pain:
– Osteoarthritis
– Inflammatory arthritides
– Synovial impingement
– Synovial inflammation
– Synovial cysts in the facet joint
– Meniscoid entrapment
– Chondromalacia facetae
– Pseudogout
– Villonodular synovitis
– Infection
• Findings on history:
– Lumbar facet pain from any level may radiate into the groin.
– Pain from upper lumbar segments can radiate into the flank, hip, and upper lateral thigh.
– Pain from lower lumbar segments tends to radiate deeper into the thigh, usually laterally
or posteriorly.
– Facet joint pain rarely radiates below the knee, though pathologic changes in the joint
may cause foraminal stenosis resulting in radicular symptoms distinct from the joint pain
itself.
• Physical examination findings:
– Individual studies have shown findings of paraspinal tenderness or pain reproduction with
either forward flexion or extension–rotation on physical examination in patients with
block-confirmed facet pain.
– However, other studies have found that a positive response to diagnostic blocks is
associated with the absence of pain exacerbation with forward flexion or extension–
rotation.
• Diagnosis:
– A positive response to a diagnostic block is the standard for diagnosis. Medial branch
blocks and intraarticular injections are considered to be equally efficacious for diagnosis,
and there is no strong evidence of the superiority of one to the other.
– No set of history and physical examination findings has been found to be diagnostic for
facet joint pain.
– Degenerative changes can be seen on radiologic imaging but do not reliably correlate with
facet joint pain. CT and MRI findings have not been consistently shown to correspond
with response to diagnostic blocks.
• Spondylolysis is the result of weakness or stress fracture in the pars interarticularis that
connects the upper and the lower segments of the facet joints. It is most commonly seen at
the L4 and L5 level.
• Spondylolisthesis describes vertebra slipping out of the proper position onto the bone below
it. It can result from spondylolysis, congenital causes, or degeneration. In degenerative
spondylolisthesis, aging results in the discs losing water, which makes them less capable of
resisting vertebra movement. If the bone presses on a nerve, it manifests as pain.
• Conservative therapies for facet joint disease:
– Physical therapy
– Osteopathic manipulation
– Acupuncture
– NSAIDs and acetaminophen
– SNRI and tricyclic antidepressants
– Psychological counseling for coping skills
• Invasive therapies include intraarticular steroid injections, radiofrequency denervation,
cryodenervation, and phenol neurolysis.
• Intraarticular steroid injections have shown inconsistent outcomes. Conclusions of some
studies indicate that injections do not provide statistically significant benefit while others
have shown that they can provide intermediate-term relief (3–6 months). Complications are
rare but can include infections, spinal anesthesia, and postdural puncture headache.
• Radiofrequency ablation/denervation (RFA) has shown variable outcomes as well. Among
the confounding issues of those that failed to show benefit are suboptimal needle placement
and not selecting candidates through the use of diagnostic blocks. The most
methodologically well done studies have shown significant pain relief lasting from 6 months
to >1 year. Complications can include transient numbness, paresthesias, and neuritis.
• Techniques for needle placement and radiofrequency ablation are similar.
– Fluoroscopic guidance is utilized and sterile technique must be maintained. With the
patient prone, an AP view of the target joint is obtained.
– The L5 dorsal ramus can be approached from this view, the target point of which is the
junction of the sacral ala and the superior articular process.
– For lumbar levels cephalad to the sacral ala, the C-arm is rotated obliquely, approximately
15–20° until a clear view of the joint is obtained. This is sometimes referred to as the
“Scottie-dog” view. The target for needle placement is the junction of the superior
articular process and the transverse process. A 25-gauge needle is advanced into the joint,
until it contacts bone. Confirmation of needle position can be made with AP and lateral
views.
– A small amount of contrast is injected to confirm intraarticular spread. Then 0.5–1 mL of
injectate containing steroid, with or without local anesthetic, is injected into the joint.
While injecting contrast or steroid mixture, care should be taken to ensure that the
integrity of the joint capsule is not disrupted.
– For RFA, a 18- to 22-gauge radiofrequency cannula with a 10-mm active tip should be
used for each level. The target point for RFA is also the junction of the superior articular
process and the transverse process or sacral ala, depending on the level. However, since
the radiofrequency lesion extends radially from the electrode, the cannula should lie along
the lateral aspect of the superior articular process just above its junction with the
transverse process or sacral ala. This placement can be facilitated with a slight caudal tilt
of the C-arm prior to starting. After proper placement is confirmed with AP and lateral
imaging and test stimulation, ablation can commence.
• Other treatments that have been used include pulsed radiofrequency denervation,
cryodenervation, and phenol neurolysis.
• Surgical intervention: There is little evidence to support surgical intervention for chronic
lumbar facet arthropathy. Additionally, diagnostic facet blocks do not improve surgical
outcomes.
GRAPHS/FIGURES
REFERENCES
1. Cohen SP, Hurley RW. The ability of diagnostic spinal injections to predict surgical
outcomes. Anesth Analg. 2007;105:1756–1775.
2. Cohen SP, Raja SN. Pathogenesis, diagnosis, and treatment of lumbar zygapophysial (facet)
joint pain. Anesthesiology. 2007;106:591–614.
3. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy
for chronic lumbar zygapophysial joint pain. Spine. 2000;25:1270–1277.
4. Ianuzzi A, Little JS, Chiu JB, et al. Human lumbar facet joint capsule strains: I. During
physiological motions. Spine J. 2004;4:141–152.
5. van Kleef M, Barendse GA, Kessels A, et al. Randomized trial of radiofrequency lumbar
facet denervation for chronic low back pain. Spine. 1999;24:1937–1942.
ADDITIONAL READING
• Benzon HT, Rathmell JP, Wu CL, et al., eds. Raj’s practical management of pain, 4th ed.
Philadelphia, PA: Mosby/Elsevier, 2008.
• Raj PP, Lou L, Erdine S, et al., eds. Interventional pain management: Image-guided
procedures, 2nd ed. Philadelphia, PA: Saunders Elsevier, 2008.
• Rathmell JP. Atlas of image-guided intervention in regional anesthesia and pain medicine
and complications in regional anesthesia and pain medicine. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006.
• Epidural steroid injections
• Sacroiliac joint injections
CODES
ICD9
716.98 Arthropathy, unspecified, other specified sites
ICD10
M12.08 Chronic postrheumatic arthropathy [Jaccoud], vertebrae
CLINICAL PEARLS
• The lumbar facet joints are a common source of low back pain.
• Local anesthetic blocks are the only reliable method for diagnosing facet joint pain.
• Both conservative and invasive therapies are available to treat facet joint pain.
FAT EMBOLUS SYNDROME
Andrea Parsons, MD
BASICS
DESCRIPTION
• Fat embolus is the presence of fat droplets within the peripheral and lung microcirculation.
It most commonly occurs with long shaft bone (femur, tibia, radius, ulna, rib) or pelvic
fractures, but is also seen with joint arthroplasty, liposuction, and bone marrow transplants.
• Fat emboli syndrome (FES) is a rare and life-threatening consequence of fat emboli with a
classic triad of hypoxemia, delirium, and petechial rash that presents 24–72 hours after
fracture or surgical procedure.
• Early diagnosis and support of pulmonary and cardiac systems may improve prognosis.
EPIDEMIOLOGY
Incidence
• Epidemiologic values may underestimate true numbers since diagnosis lacks specific
laboratory tests or studies (1).
• Isolated fractures of any long bone (femur, tibia, radius, rib, etc.): 0.1% or 1 in 1,000
patients
• Multiple fractures of unilateral femur: 1.2%
• Bilateral femurs: up to 33%
• Liposuction: 19 in 100,000
Morbidity
• Mechanical obstruction can cause distal ischemia.
• Paradoxical embolus can result in a cerebral or myocardial ischemic event.
• Inflammatory response can result in hypoxia, heart failure, or cerebrovascular accident.
Mortality
• Large emboli can quickly progress to death despite adequate resuscitation.
• Fulminant FES: As high as 10–45% (2)
• Liposuction: 8.5% (3)
• Fat embolism most commonly occurs when endogenous fat is released from a tubular (long
shaft) bone or pelvic fracture into the circulation. Exogenous lipid emulsions injected into
the circulation can also cause fat embolism (1).
• Risk factors include:
– Long bone fractures (femur, tibia, radius, ulna, rib): Closed fractures have a higher
incidence than open fractures.
– Pelvic fractures: Closed fractures show higher incidence than open fractures.
– Orthopedic procedures (joint arthroplasty)
– Soft-tissue injuries
– Liposuction
– Bone marrow harvesting/transplant
– Bone tumor lysis
– Lipid infusions
• Fat embolus is distinct from fat embolus syndrome. Fat embolus describes the presence of fat
globules in systemic and pulmonary circulations and is often asymptomatic. On the other
hand, FES is a clinical consequence of fat embolus and manifests as a triad of:
– Pulmonary changes (shortness of breath, hypoxemia)
– Cerebral dysfunction (agitation, delirium, coma)
– Petechial rash (only in 20–50% of cases)
• The factors which predispose a patient to the development of this rare and life-threatening
syndrome remain unclear. Although fat emboli are present in several patients with long
bone fractures, only 1–3% develop FES. There is an increased incidence with multiple
fractures and bilateral injuries, suggesting the quantity of fractures may play a role.
• Pathophysiology involves inflammatory and mechanical manifestations:
– Inflammatory: In patients who develop FES, the breakdown of embolized fat into free fatty
acids has been linked to the development of acute respiratory distress syndrome (ARDS)
and cardiac dysfunction. Injury of vascular endothelium can lead to inflammatory
pathway activation via endothelin-1, fibrin, neutrophils, etc. Activation of this pathway
can result in pulmonary vasoconstriction (pulmonary hypertension), increased vascular
permeability (pulmonary edema), platelet aggregation (thrombocytopenia), and V/Q
mismatch (hypoxemia).
– Mechanical: Embolized fat travels to the right heart causing increased pulmonary artery
and right heart pressures. This can lead to right heart strain (increased central venous
pressure, jugular venous distension, peaked T waves) and decreased cardiac output
(increased wedge pressure, decreased MVO2, hypotension). Significant right ventricular
outflow tract obstruction can lead to right heart failure, cardiovascular collapse, and/or
death.
• Mechanical/traumatic etiologies: Occurs when bone marrow or adipose tissue is forced into
venules, which occurs with traumatic injury (fractures, liposuction, etc.). With bone
fractures, fat enters venules that are held open by osseous attachments.
• High intramedullary pressures: The reaming of the bone shaft, bone cement application, or
prosthetic placement can cause the extrusion of fat from the bone marrow into the
circulation.
• Nontraumatic: Occurs with lipid agglutination in critically ill patients receiving nutritional
fat emulsions.
• Paradoxical embolism: Fat can also pass from the right to left side of the heart through a
patent foramen ovale and may result in a cerebral or myocardial infarction. Patent foramen
ovale can be present in 20–30% of the general population.
• Early immobilization of bone fractures reduces the risk of FES. Operative reduction further
reduces the risk, as opposed to conservation measures (e.g., traction).
• Although still controversial, some evidence suggests that steroids given prophylactically in
the emergency department reduce the incidence of fat embolism.
• Surgical techniques to limit the increase in intraosseous pressures in cases involving bone
cement: Cleaning the bone to remove debris and marrow prior to bone cement placement,
creating a venting hole in the bone, and/or allowing the bone cement to become viscous
before applying.
DIAGNOSIS
• Clinical diagnosis: Guidelines for diagnosing fat embolism syndrome include one sign from
the major criteria category and 4 signs from the minor criteria category (4).
– Major criteria:
Petechiae in a vest distribution
Hypoxemia with PaO2 <60 mm Hg, FIO2 >0.4
Central nervous system depression disproportionate to hypoxemia
Pulmonary edema
– Minor criteria:
Tachycardia (heart rate >110 beats per minute)
Pyrexia (temperature >38.5°C)
Emboli visible in retina
Fat in urine
Fat in sputum
Unexplained drop in hematocrit or platelet count
Increasing erythrocyte sedimentation rate
• V/Q mismatch (ventilation/perfusion ratio).
– Low V/Q ratio (shunt) indicates impaired ventilation with respect to perfusion; can occur
with FES if pulmonary edema or ARDS is present (inflammatory).
– High V/Q ratio (dead space) indicates impaired perfusion with respect to ventilation; can
occur with FES as the fat emboli impair blood flow through the lung (mechanical).
• ECG: New right bundle-branch block or nonspecific T-wave changes.
• Thrombocytopenia can occur with the consumption of platelets. Anemia and low fibrinogen
levels can also be present.
• Transesophageal echocardiography can show evidence of emboli in the right ventricle, but it
is more useful to assess volume status and cardiac function if circulatory collapse is
imminent.
• A late laboratory marker of FES is serum lipase, which becomes elevated 3 to 5 days after
embolization and peaks at 5 to 8 days.
• Histology: Fat globules in vascular spaces
• Over time, chest radiography can show evolution of ARDS infiltrates.
• Thromboembolus
• Thrombotic thrombocytopenic purpura
• Bone cement implantation syndrome: Hypotension associated with the use of
polymethylmethacrylate or bone cement
TREATMENT
• Repair of orthopedic and soft-tissue injury should be performed promptly. Consider

continuous pulse-oximetry perioperatively in high-risk patients (long shaft bone fractures).
• The mainstay of treatment is supportive therapy. Use advanced cardiac life support (ACLS)
guidelines when necessary.
• Maintain oxygen saturation >90% in order to optimize tissue oxygenation. Administer
supplemental oxygen and consider intubation with mechanical ventilation if increased FiO2
and positive end-expiratory pressure (PEEP) is needed.
• Monitor hemodynamics closely to optimize tissue perfusion. Use fluids and vasopressors as
needed. Ephedrine, epinephrine, norepinephrine, and dobutamine can provide inotropic
support to a failing right heart.
• Treat anemia and coagulopathy appropriately.
FOLLOW-UP
• Close postoperative monitoring; pulse oximetry

• Patients may require mechanical ventilation or other support (i.e., continuous positive
airway pressure [CPAP], bilevel positive airway pressure [BiPAP]).
CLOSED CLAIMS DATA
• Femur fractures are the most frequent cause of lawsuits for orthopedic surgeons. In adults,
the most common complications include poor technique, infection, wrong-site surgery, fat
and/or pulmonary embolus, and delay in diagnosis or treatment.
– 32% of all claims involving femur fractures resulted in payments (n = 820).
– Payment average: $113,000
REFERENCES
1. Stein PD, Yaekoub AY, Matta F, et al. Fat embolism syndrome. Am J Med Sci.
2008;336(6):472–476.
2. Huber-Lang M, Brinkmann A, Straeter J, et al. An unusual case of early fulminant post-
traumatic fat embolism syndrome. Anaesthesia. 2005;60(11):1141–1143.
3. Grazer FM, DeJong RH. Fatal outcome from liposuction: Census survey of cosmetic
surgeons. Plast Reconstr Surg. 2000;105:436–446.
4. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br. 1974;56B:408–416.
ADDITIONAL READING
• American Academy of Orthopaedic Surgeons. Managing orthopaedic malpractice risk, 2nd
ed. 1999.
• Johnson MJ, Lucas GL. Fat embolism syndrome. Orthopedics. 1996;19:41–48.
• Bone marrow transplant
• Dead space
CODES
ICD9
958.1 Fat embolism
ICD10
• T79.1XXA Fat embolism (traumatic), initial encounter
• T79.1XXD Fat embolism (traumatic), subsequent encounter
• T79.1XXS Fat embolism (traumatic), sequela
CLINICAL PEARLS
• Fat embolus is distinct from fat embolus syndrome.
• The pathophysiology of FES is composed of mechanical obstruction, injury related to free
fatty acids, and endothelial injury causing activation of inflammatory pathways.
• The classic triad of pulmonary changes, cerebral dysfunction, and petechiae suggest FES.
However, it should be suspected in a trauma patient with V/Q mismatch, especially when
there is no other pulmonary injury (e.g., pulmonary contusions).
• Treatment is supportive including ACLS guidelines.
FEMORAL NERVE BLOCK
Angela T. Hsu, MD
BASICS
DESCRIPTION
• The femoral nerve consists of motor and sensory innervations to the anteromedial thigh and
medial leg.
• The femoral nerve block is a superficial regional block that is easy to perform and has a very
high success rate. When combined with a sciatic nerve block, almost complete anesthesia
and analgesia can be provided to the entire lower extremity below midthigh.
Local anesthetics bind to intracellular fast sodium channels and prevent nerve impulse
initiation and propagation.
ANATOMY
• The femoral nerve is formed from the dorsal divisions of the L2–L4 ventral rami, within the
psoas muscle.
• The femoral nerve emerges distally from the lateral border of the psoas muscle and descends
in the groove between the psoas and the iliacus muscles.
• Below the inguinal ligament, the femoral nerve is located lateral to the femoral artery and
deep to the fascia lata and fascia iliaca. It is separated from the femoral artery by a portion
of the psoas muscle which explains why a blind paravascular injection does not lead to local
anesthetic spread to the femoral nerve.
• The femoral nerve divides into anterior and posterior divisions.
– Anterior division: Medial cutaneous nerve, intermediate cutaneous nerve, and muscular
branches
Motor: Sartorius and pectineus muscles
Sensory: Anterior and medial thigh
– Posterior division: Saphenous nerve, muscular and articular branches
Motor: Quadriceps muscle (rectus femoris and vastus intermedius, lateralis, and
medialis)
Sensory: Medial aspect of the lower leg
– Functional innervation:
Dermatomal innervation: Skin of anteromedial thigh, knee, medial aspect of the lower
leg to medial malleolus
Myotomal innervation: Sartorius, pectineus, and quadriceps femoris muscles (rectus
femoris and vastus intermedius, lateralis, and medialis)
Osteotomal innervation: Anterior hip joint, anterior femur, and anteromedial knee joint
• Blocks of the lower extremity are gaining popularity with the advent of ultrasound
guidance.
• Femoral nerve block ± other lower extremity blocks can provide anesthesia for lower
extremity surgery when centroneuraxial blocks are contraindicated due to anticoagulation
or undesirable because of a sympathectomy.
• Even with anticoagulation, rarely is a femoral nerve block associated with significant
hematoma.
• Indications
– Analgesia:
Femoral neck or shaft fracture
Total hip arthroplasty
Total knee arthroplasty
Anterior cruciate ligament (ACL) repair
– Surgical anesthesia
Saphenous vein stripping
Knee arthroscopy
Femoropopliteal bypass surgery
Quadriceps muscle biopsy
Skin graft anterior thigh
• Contraindications (relative):
– Presence of prosthetic femoral artery graft
– Situations in which dense sensory blockade could mask the onset of compartment
syndrome
• Complications (rare):
– Hematoma
– Local infection
– Intraneural injection
– Fall risk if patient ambulates before block resolution
– Local anesthetic toxicity
Central nervous system: Tinnitus, confusion, metallic taste in the mouth
Cardiac: Tachycardia, hypertension, arrhythmia
• Medication selection:
– Choice of local anesthetic, concentration, ± epinephrine, and volume depends on whether
the block will be used for analgesia or surgical anesthesia. With ultrasound-guided blocks,
as little as 10 mL can be used.
Analgesia: 10–15 mL of 0.5% ropivacaine or 0.25% bupivacaine can last for 5–12 hours.
For longer coverage (12–30 hours), 15–30 mL may be used.
Surgical anesthesia: 15–20 mL of 1.5% mepivacaine with 1:400,000 epinephrine can last
for 3–4 hours. For longer cases, 15–20 mL of 0.5% ropivacaine with epinephrine or 0.5%
bupivacaine can last for 5–7 hours.
• Nerve stimulator technique:
– Patient position: Supine
– Equipment:
Standard monitors
Nearby resuscitative equipment
A 5 cm, 22 gauge insulated needle
Nerve stimulator set to deliver current at 1.0 mA, frequency 1 Hz, and pulse duration of
0.1 msec.
– Palpate the femoral artery along the inguinal crease. The femoral nerve usually lies 1–2
cm lateral to the artery; thus to maintain this spatial distance, the needle should be
inserted at the same angle as the patella. The needle can be inserted 1 cm above or below
the inguinal crease with a 30- to 45° cephalad tilt. Above the crease, the femoral nerve is
more compact and usually has not divided into its branches and for this reason may be a
more desirable approach.
– The needle is advanced until a twitch of the patella (quadriceps) is elicited. If the twitch is
maintained after turning down the nerve stimulator to 0.5 mA, a slow injection of local
anesthetic is started.
• Ultrasound technique:
– Patient position: Supine
– Equipment:
Standard monitors and nearby resuscitative equipment
A 5 cm, 22 gauge insulated needle
Ultrasound with linear probe and the transducer set at high frequency (8–15 Hz) to
locate the relatively superficial femoral nerve.
– With the ultrasound probe, first identify the femoral vessels, noting the vein is collapsible.
– From medial to lateral: Femoral vein → artery→nerve
– From superficial to deep: The fascia lata is first encountered, then the fascia iliaca, and
then the femoral nerve lying superficial to the iliopsoas muscle.
– The femoral nerve will often appear as a triangular or flat hyperechoic (white) structure.
Image, with permission, by Dr. Christine Chavez.
Out of plane needle technique:

Insert needle perpendicular to transducer from caudad to cephalad. In this case, only a
cross section of the needle shaft (small dot) is visible on ultrasound image. It is difficult
to track the location of the needle tip with this technique. Combining this technique
with a nerve stimulator is recommended. Aim for a patellar twitch in order to assess
correct needle tip depth.
– In plane needle technique:
The needle is inserted from lateral to medial in plane with the ultrasound beam. This
technique allows for visualization of the needle tip. Depending on the depth of the
nerve, a longer needle may be required.
Image, with permission, by Dr. Christine Chavez.
ADDITIONAL READING
• Murray JM, Derbyshire S, Shields MO. Lower limb blocks. Anaesthesia. 2010;65(1):57–66.
• Szucs S, Morau D, Iohom G. Femoral nerve blockade [Review]. Med Ultrason.
2010;12(2):139–44.
• ranco CD. Chap. 7, Regional Book. JHS Hospital of Cook County, 2009.
• Sciatic nerve block
CLINICAL PEARLS
• For nerve stimulator technique:
– Stimulation of the sartorius muscle (band of muscle from superior–lateral to inferior–
medial thigh) without a patellar twitch should not be accepted. The sartorius muscle is
innervated by anteromedial branches of the femoral nerve and one cannot be sure if the
branches lie within or outside the femoral nerve sheath. Withdraw the needle and redirect
laterally and slightly deeper.
– Local muscle stimulation of psoas or pectineus muscles means the needle is too deep.
Withdraw needle and redirect.
– Vascular puncture means the needle is too medial. Withdraw needle, hold pressure, and
then reinsert 1 cm laterally.
– If the needle is inserted and produces no twitches, reassess landmarks and work
progressively laterally from femoral artery. Reassess that the needle angle is parallel with
that of the patella.
– In obese patients, where the femoral artery is difficult to palpate and ultrasound is not
available, consider the use of a Doppler to localize the arterial pulsations.
• For ultrasound technique:
– Although ultrasound guidance has the potential to minimize complications, both
intravascular injection and intraneural injection have been reported despite its use. Be
vigilant for detecting signs of intravascular injection.
FETAL CARDIOVASCULAR PHYSIOLOGY
BASICS
DESCRIPTION
• Fetal circulation is primarily a series circuit as opposed to the parallel pulmonary and
systemic circuits of the infant and adult.
• In utero, the right ventricle (RV) is the primary systemic ventricle, with the left ventricle
(LV) acting mainly to pump comparatively “highly” oxygenated blood to the coronary
arteries and brain (1).
• This is created by a series of shunts:
– The ductus venosus (DV) shunts oxygenated blood from the umbilical vein (UV) into the
inferior vena cava (IVC), bypassing the liver.
– The ductus arteriosus (DA) shunts blood from the pulmonary arteries into the descending
aorta, bypassing the lungs, head, and upper extremities.
– The foramen ovale (FO) shunts blood from the right atrium (RA) into the left atrium,
bypassing the lungs.
• The low-resistance placenta acts as the gas exchange organ while the high-resistance
pulmonary circulation is mainly bypassed.
• In utero physiology is structured to maximize oxygen delivery to the brain and heart in the
comparatively hypoxic fetal environment.
• Simultaneously, maintenance of this fetal environment is dependent on this degree of
hypoxia.
– Hypoxia decreases nitric oxide production with resultant hypoxic pulmonary
vasoconstriction. The high pulmonary artery pressures lead to increased right heart
pressures that maintain the right-to-left shunt through the FO.
– Hypoxia also leads to increased circulating prostaglandins, which maintain the patency of
the DA and the DV.
• Delivery is marked by rapid and profound changes in this circulation that start the transition
to normal extrauterine circulation. These changes may take as long as several days to
complete.
ANATOMY
• Normal in utero circulation (1):
– Starting in the placenta, oxygenated blood is returned to the fetal circulation via the UV.
– The majority of this oxygenated blood is shunted around the liver through the DV into the
IVC and right atrium.
– 40% of the blood returning via the IVC crosses the FO into the left atrium LA.
– This blood enters the LV and is pumped into the ascending aorta. 70% of this blood flows
to the upper extremities and brain (relatively well-oxygenated), returning to the RA via
the superior vena cava (SVC).
– SVC blood return enters the RA and is preferentially directed across the tricuspid valve
into the RV. Only 10% of the blood returning into the SVC will cross the FO.
– Blood then travels into the PA, where 90% is shunted via the DA into the descending
aorta.
– About 40% of total cardiac output is then returned to the placenta via the umbilical
arteries (remaining flows to the lower extremities and organs).
• Normal transition to extrauterine life (2):
– Rapid changes in right and left heart pressures lead to decreased shunting.
With the clamping of the umbilical cord, the low-pressure placenta is removed from the
neonate’s circulation. The resultant increase in neonatal afterload increases pressure in
the left heart.
Simultaneously, as the neonate takes its first breath, circulating oxygen tensions increase
rapidly, leading to increased bradykinin and nitric oxide and decreased pulmonary
vascular resistance. Circulating prostaglandins, responsible for maintaining patency of
the DA in utero, fall rapidly.
– These changes in pressures lead to decreased flow across, and eventual closure of, the FO
and DA.
Functional closure of the FO is nearly immediate after birth, when the pressure change
“pushes" the septum primum against the septum secundum. Fusion of the septa occurs
within the first 3 months of life.
Closure of the DA usually occurs within the first 3 to 10 days of life.
• Intrauterine fetal hypoxia leads to a “diving reflex.”
– Heart rate slows to decrease myocardial oxygen demand.
– Blood is preferentially shunted to the brain, myocardium, and adrenals.
– Transient hypertension results; however, as hypoxia persists, cardiac output and
myocardial contractility fall, leading to hypotension.
– These changes may lead to a depressed neonate, hypoxia in the neonatal period, and
delayed transition (see below).
• Changes in the pulmonary circulation in utero can lead to delayed or incomplete transition
to a neonatal circulation.
– Maternal NSAID use can cause closure of the DA in utero; this causes increased pulmonary
blood flow and hypertrophy of the pulmonary vasculature. This hypertrophy can also be
seen with post-term gestation and chronic placental insufficiency.
– Congenital diaphragmatic hernia and pleural effusions lead to lung compression and
decreased size of the pulmonary vascular bed. This can lead to pulmonary hypertension in
the neonatal period.
• Dysfunctional transition to extrauterine circulation (3):
– Transient hypoxia is well-tolerated in the neonate. Prolonged hypoxia or acidosis,
however, can lead to impaired transition from fetal to neonatal physiology. This disorder
is called persistent fetal circulation or persistent pulmonary hypertension of the newborn
(PPHN).
Continued hypoxia maintains in utero levels of pulmonary vasoconstriction due to a lack
of bradykinin and NO production. High pulmonary vascular resistance leads to increased
flow across the DA, mechanically maintaining its patency.
High pulmonary artery pressures lead to high right heart pressures, which prevent
functional closure of the FO.
Hypoxia also leads to persistently elevated prostaglandin levels, further maintaining the
patency of the DA.
– PPHN, if untreated, can lead to persistent hypoxia, irreversible pulmonary hypertension,
and right heart failure.
– Treatment is aimed at correcting reversible causes of hypoxia and delivering supplemental
oxygen if necessary.
• Maintenance of fetal circulation: Fetal circulation, specifically patency of the DA, can be
maintained pharmacologically (with intravenous prostaglandin infusion), as a bridge to
surgery for congenital heart disorders featuring obstruction to outflow of oxygenated blood.
For example:
– Aortic stenosis
– Aortic atresia
– Hypoplastic left heart syndrome
– D-Transposition of the great arteries
GRAPHS/FIGURES
FIGURE 1. Fetal circulation. Numbers are percentage of combined left and right ventricular output reaching each point.
Ao—Ascending Aorta, PA—Pulmonary Artery, RV—Right Ventricle, LV—Left Ventricle, RA—Right Atrium, SVC—Superior
Vena Cava, LA—Left Atrium, IVC—Inferior Vena Cava. (Adapted from Ostheimer GW. Anaesthetists’ role in neonatal
resuscitation and care of the newborn. Can J Anaesth. 1993;40:R50–R63, with permission.)
REFERENCE
1. Ostheimer GW. Anaesthetists’ role in neonatal resuscitation and care of the newborn. Can J
Anaesth. 1993;40:R50–R63.
2. Lakshminrusimha S, Seinhorn RH. Pulmonary vascular biology during neonatal transition.
Clin Perinatol. 1999;26:601–619.
3. Wimmer JE. Neonatal resuscitation. Pediatr Rev. 1994;15:255–265.
• Fetal heart tracings
• Congenital diaphragmatic hernia
• Tetralogy of Fallot
CLINICAL PEARLS
• Fetal circulation exists primarily as a series circuit with the RV as the main systemic
ventricle and the LV mainly delivering blood to the brain and myocardium. This is possible
through 3 main shunts: the DV, DA, and FO.
• The neonate’s first breath causes an increase in oxygen tension and decreased pulmonary
vascular resistance while umbilical cord clamping causes increased systemic vascular
resistance. This leads to the functional closure of the DA and FO.
• Delayed transition to neonatal circulation can be caused by persistent hypoxia and acidosis
in the neonatal period or by structural anomalies in the heart or lungs, and can lead to a
persistent fetal circulation or PPHN (with resultant persistent hypoxia and right heart
failure). The mainstay in treatment of delayed transition is avoidance and correction of
hypoxia and acidosis by mechanical ventilation and supplemental oxygen.
• In certain congenital heart defects, patency of the DA can be maintained with prostaglandin
infusion as a bridge to surgery.
FETAL HEART TONES
BASICS
DESCRIPTION
• Electronic continuous fetal heart monitoring has become the mainstay of intrapartum
management of fetal well-being. The technique utilizes both changes in fetal heart rate and
timing of contractions to infer the intrapartum status of the neonate.
• The team-oriented approach in caring for the obstetric patient makes it imperative that the
anesthesia provider understands the terminology, appreciates the level of concern, and can
effectively communicate the tracings.
• Fetal heart rate (FHR) can be monitored externally by continuous Doppler ultrasound or
internally by fetal scalp electrode.
• Uterine contraction pattern can be monitored externally by tocodynamometry or internally
by intrauterine pressure transducer.
• A reassuring fetal heart rate tracing correlates more than 90% of the time with a 5-minute
Apgar score of 8 or higher. However, a nonreassuring fetal heart rate tracing carries a false-
positive rate as high as 50% (1)[A].
• Fetal heart rate pattern is the result of dynamic interplay between fetal sympathetic and
parasympathetic nervous systems.
• Fetal baroreceptors and chemoreceptors respond to asphyxia, acidosis, anemia, and/or
infection. The activity of these peripheral and central receptors mediates parasympathetic
and sympathetic tone, resulting in changes in the fetal heart tracing.
• These patterns are discussed in terms of 4 separate and interrelated parameters: Baseline,
variability, accelerations, and decelerations (2)[A].
– Baseline:
– The mean fetal heart rate in any 10-minute window.
– Normal is 110–160 beats per minute (BPM).
– Variability:
– Irregular fluctuations in both frequency and amplitude of fetal heart tracing measured
over a 10-minute period.
– Classified as absent (no fluctuation from baseline), minimal (<5 BPM from baseline),
moderate (6–25 BPM from baseline), or marked (>25 BPM from baseline).
– Moderate variability is considered normal.
– Accelerations:
– Visually apparent abrupt increases in fetal heart rate of at least 15 BPM lasting at least 15
seconds.
– For fetuses less than 32 weeks of gestation, an increase of at least 10 BPM for at least 10
seconds is sufficient to be considered as an acceleration.
– Presence is generally considered reassuring; however, absence is not necessarily abnormal.
– Decelerations:
– Visually apparent, abrupt decreases in fetal heart rate of at least 15 BPM lasting at least 15
seconds.
– Early deceleration: Gradual, symmetric decrease and return of fetal heart rate associated
with uterine contraction; the nadir of the deceleration occurs simultaneous with the peak
of the contraction (Figure 1).
FIGURE 1. Early deceleration. Gradual, symmetric decrease and return of FHR that occurs simultaneously with the peak of
uterine contraction.
– Late deceleration: Gradual, symmetric decrease and return of fetal heart rate associated
with uterine contraction; the nadir of the deceleration occurs after the peak of the
contraction (Figure 2).
FIGURE 2. Late deceleration. Gradual, symmetrical decrease and return of FHR that occurs after the beginning of a uterine
contraction.
– Variable deceleration: Abrupt, asymmetric decrease and return of the fetal heart rate. When
associated with uterine contractions, the onset, nadir, and duration vary with successive
contractions (Figure 3).
FIGURE 3. Variable deceleration. Abrupt, asymmetric decrease and return of FHR that lasts greater than 15 seconds and
less than 2 minutes.
• Baseline
– Fetal bradycardia is usually associated with fetal asphyxia and acidosis, especially when
FHR was previously normal. In rare situations, fetal bradycardia is caused by maternal or
fetal disease, including certain autoimmune disorders.
– Fetal tachycardia is most commonly secondary to maternal infection and/or fever (e.g.,
chorioamnionitis). Other causes of tachycardia include fetal anemia, hypovolemia, or
congenital heart disease.
• Variability
– Intact variability implies intact sympathetic and parasympathetic nervous systems and, by
extension, an intact central nervous system.
– Decreases in variability imply fetal CNS depression and can be caused by:
Fetal asphyxia and acidosis
Normal fetal sleep
Maternal medications (beta blockers, opioids, anxiolytics, magnesium, lithium)
Maternal general anesthesia
• Accelerations
– The presence of accelerations is a reassuring sign, further implying an intact CNS.
– Lack of accelerations, however, is a nonspecific sign that, by itself, is neither reassuring
nor nonreassuring.
• Decelerations
– Early decelerations are associated with fetal head compression within the birth canal. The
resulting increased fetal intracranial pressure leads to reflex bradycardia. It is not
considered worrisome and usually foretells imminent delivery.
– Late decelerations are associated with uteroplacental insufficiency.
Lack of sufficient oxygen transfer leads to fetal acidosis and hypoxia. Through
chemoreceptor activation, heart rate slows to maximize oxygen extraction and decrease
demand, and blood is shifted centrally to supply the most vital organs (brain, heart,
adrenals).
Always considered abnormal and a poor prognostic sign.
– Variable decelerations are associated with umbilical cord compression.
Compression of the umbilical artery removes the low-resistance placenta from the fetal
circulation, causing an abrupt increase in fetal systemic vascular resistance. This
activates fetal baroreceptors causing rapid reflex bradycardia.
Can become worrisome if they are prolonged or repetitive due to worsening fetal
oxygenation of acidosis.
• Sinusoidal heart rate tracing
– Specific pattern of fetal heart rate. Smooth sine-like waves with 3–5 cycles per minute
lasting 20 minutes or longer.
– Always considered profoundly abnormal.
– Associated with chronic fetal anemia (e.g., Rh isoimmunization), fetal or fetal-maternal
hemorrhage, or acute fetal asphyxia.
• There exists a 3-tiered FHR Classification System to aid in determining the presence of fetal
acidemia or the need to intervene (2)[A].
• Category I fetal heart tracings are normal (reassuring) and are indicative of fetal well-being.
It consists of all of the following:
– Baseline FHR 110–160 BPM
– Moderate variability
– No late or variable decelerations.
• Category II fetal heart tracings are of indeterminate significance. It consists of all tracings
that do not fall into Category I or Category III. It should be reassessed frequently.
• Category III fetal heart tracings are abnormal (nonreassuring) and are highly predictive of
fetal acidosis. It should be met with prompt intervention including correction of maternal
hypotension, oxygen therapy, maternal repositioning, etc. It may indicate the need for
urgent/emergent delivery. It consists of either of the following:
– Absent variability WITH
recurrent late decelerations, OR
recurrent variable decelerations, OR
fetal bradycardia
– Sinusoidal FHR pattern.
REFERENCES
1. Schifrin BS, Dame L. Fetal heart rate patterns. Prediction of Apgar score. JAMA. 1972;219:
1322–1325.
2. Macones GA, Hankins GD, Spong CY, et al. The 2008 National Institute of Child Health and
Human Development workshop report on electronic fetal monitoring: Update on
definitions, interpretation, and research guidelines. Obstet Gynecol. 2008;112:661–666.
3. Graham EM, Peterson SM, Christo DK, et al. Intrapartum electronic fetal heart rate
monitoring and the prevention of perinatal brain injury. Obstet Gynecol. 2006;108(3 Pt
1):656–666.
ADDITIONAL READING
• Perinatology.com. Intrapartum fetal heart rate monitoring. http://www.perinatology.com
• Uterine blood flow
• Cesarean section, emergent
CLINICAL PEARLS
• Normal fetal heart tracing correlates highly with a 5-minute Apgar score of 8 or higher;
however, an abnormal tracing can have a false-positive rate as high as 50%.
• Tracings are described by 4 components: Baseline, variability, accelerations, and
decelerations.
• Abnormal or absent variability can be associated with fetal CNS depression and/or fetal
asphyxia. However, studies have not conclusively demonstrated its effect on perinatal
mortality or pediatric neurologic morbidity (3).
• Late decelerations are the result of uteroplacental insufficiency and indicate periods of fetal
hypoxia. They are always abnormal.
• Fetal heart tracings are now classified into 3 categories: Category I tracings are normal and
indicative of fetal well-being, Category II tracings are indeterminate, and Category III
tracings are abnormal and require intervention.
FIBRINOGEN
Satoru Ogawa, MD
BASICS
DESCRIPTION
• Fibrinogen, or Factor I, is converted to fibrin by thrombin and is a critical component of the
coagulation system.
• Perioperatively, hypofibrinogenemia may be treated with purified human fibrinogen,
cryoprecipitate, or fresh frozen plasma.
• Normal plasma fibrinogen in adults is 1.5–3.5 g/L (150–350 mg/dL). Synthesis occurs in the
liver and is increased during an inflammatory state (infection, pregnancy, etc.).
• Physiological function: Fibrinogen is captured in the wound by activated platelets via
glycoprotein IIb/IIIa receptors. A fibrin monomer is formed after thrombin cleaves peptides
from fibrinogen. Thrombin also activates factor XIII, which cross-links fibrin monomers into
a mesh. Fibrin can catalyze plasmin activation by serving as binding sites (lysine residues)
for plasminogen and tissue plasminogen activator.
• Purified human fibrinogen (lyophilized) is currently indicated for acute bleeding episodes in
patients with congenital fibrinogen deficiency (e.g., afibrinogenemia, hypofibrinogenemia).
– Derived from pooled human plasma
– The concentrate is pasteurized (heat treated) at 60°C for 20 hours for virus inactivation.
– Can be stored between +2 to +8°C for 30 months
– Therapeutic target level is 1.0–1.5 g/L (or 100–150 mg/dL).
– In patients with congenital hypofibrinogenemia, the half-life is reported to be 78.7 ± 18.1
hours.
• Factor I deficiency: Presents as a combined bleeding disorder; it affects both platelets and
clotting
– Qualitative:
Dysfibrinogenemia results from defects to the factor I molecule. Patients rarely present
with bleeding; in fact, some are predisposed to forming clots. Typically does not require
any treatment such as cryoprecipitate, fresh frozen plasma, or purified fibrinogen.
Occasionally, patients may be on anticoagulants.
– Quantitative: Both conditions are inherited in an autosomal-dominant fashion and can
affect both males and females.
Afibrinogenemia is the complete absence of fibrinogen and is typically diagnosed in
newborns. It often presents as bleeding from the umbilical cord, genitourinary tract, or
CNS.
Hypofibrinogenemia is a low level of fibrinogen (<100 mg/dL). Symptoms can range
from mild, moderate, to severe bleeding.
• Increased fibrinogen levels:
– Stroke: Associated with an increased risk of fatal and non-fatal, first-time, and
hemorrhagic and ischemic strokes.
– Coronary artery disease: Patients have increased levels, particularly those with a history of
myocardial infarction.
– Independent risk factor. Some studies have suggested that increased levels of fibrinogen
exceed the effects of homocysteine, cholesterol, and other lipids in the pathogenesis of
myocardial and cerebral infarction.
– Mortality. A significant independent predictor of death from all causes in both men and
women. This is believed to be due to its ability to promote thromboses, the underlying
mechanisms for ischemia of myocardial infarction and stroke.
– Cancer, diabetes, hypertension: Increased levels have been associated with these disease
states.
– Inflammatory process: Fibrin may play a role in inflammatory processes such as the
development of rheumatoid arthritis.
– Modification of levels. Smoking cessation, exercise, and medications have been shown to
decrease levels.
• Complications of fibrinogen replacement:
– Purified fibrinogen:
In disseminated intravascular coagulation (DIC), it can potentially worsen coagulopathy
and organ dysfunction by forming fibrin in microcirculations.
Allergic reactions
The risks of pathogen transmission are considered to be low but possible for non-
enveloped virus including parvovirus B19 and hepatitis A.
Venous and arterial thromboembolic complications should be cautioned.
The safety of purified human fibrinogen concentrate during pregnancy or breastfeeding
has not been established in controlled clinical trials.
• Complications of cryoprecipitate and fresh frozen plasma replacement:
– Volume overload and decreased hematocrit
– Transfusion-related acute lung injury
– Thromboembolic risks with cryoprecipitate
– Infectious transmission
– Acute hemolytic transfusion reaction, nonhemolytic febrile, and allergic reactions
– Hypocalcemia
• Measuring fibrinogen:
– The Clauss method is used to measure the fibrinogen concentration (30–60 minutes turn-
around time). It may be falsely elevated after large amounts of hydroxyethyl starch
infusion.
– Thromboelastometry can be used to measure fibrin(ogen)-specific clot firmness using
cytochalasin D (FIBTEM value below 7 and 10 mm suggests plasma fibrinogen <150
mg/dL).
• “Acquired” hypofibrinogenemia:
– Major bleeding can be accompanied by decreased levels during trauma and surgery.
Assuming normal fibrinogen level at baseline, critical levels (1 g/L or 100 mg/dL) of
fibrinogen are reached after a loss of about 1.4 times the blood volume.
– Cell saver: Large amounts of shed blood processed in the cell salvage system can deplete
plasma coagulation factors, including fibrinogen.
– Disseminated DIC that is associated with severe sepsis and eclampsia.
• Purified fibrinogen replacement:
– No blood typing or thawing is necessary.
– Less likely to induce hemodilution and thrombocytopenia after infusion compared to fresh
frozen plasma (FFR).
• Following major obstetric hemorrhage, a work up should include an assessment of
fibrinogen levels.
• Fibrin sealant: Human plasma-derived fibrinogen is clinically used as a fibrin sealant
(Tisseel, Crosseal, Evicyl) for topical hemostasis.
EQUATIONS
• Dose (mg/kg body wt) = [target level (mg/dL) – measured level (mg/L)]/1.7 (mg/dL per
mg/kg body weight).
• To raise plasma fibrinogen from 99 to 150 mg/dL, the required dose is (150 – 99)/1.7 = 30
mg/kg.
• In case of bleeding and fibrinogen level is unknown, the recommended initial dose is 70
mg/kg.
GRAPHS/FIGURES
See Table
REFERENCE
1. Manco-Johnson MJ, Dimichele D, Castaman G, et al. Pharmacokinetics and safety of
fibrinogen concentrate. J Thromb Haemost. 2009;7:2064–2069.
2. Hiippala ST, Myllylä GJ, Vahtera EM. Hemostatic factors and replacement of major blood
loss with plasma-poor red cell concentrates. Anesth Analg. 1995;81:360–365.
3. Kruskal JB, Commerford PJ, Franks JJ, et al. Fibrin and fibrinogen-related antigens in
patients with stable and unstable coronary artery disease. NEJM. 1987;317(22):1361–
1365.
4. Nienaber U, Innerhofer P, Westermann I, et al. The impact of fresh frozen plasma vs
coagulation factor concentrates on morbidity and mortality in trauma-associated
haemorrhage and massive transfusion. Injury. 2011;42(7):697–701.
5. Alexopoulos D, Ambrose JA, Strump D, et al. Thrombosis-related markers in unstable
angina pectoris. J Am Coll Cardiol. 1991;17(4):866–871.
6. Zhang B, Zhang W, Li X, et al. Admission markers predict lacunar and non-lacunar stroke
in young patients. Thromb Res. 2011;128(1):14–17.
7. Bembenek J, Karlinski M, Kobayashi A, et al. Early stroke-related deep venous thrombosis:
Risk factors and influence on outcome. J Throm Thrombolysis. 2001;32(1):96–102.
8. Lowe G. Can haemostatic factors predict atherothrombosis? Intern Emerg Med.
2001;6(6):497–501.
• Cryoprecipitate
• D-dimer
• Transfusion related lung injury
CLINICAL PEARLS
• Fibrinogen replacement in congenital fibrinogen deficiency reduces bleeding episodes and
thromboembolic complications related to invasive procedures.
• Antifibrinolytics (-aminocaproic acid and tranexamic acid) may be useful in stabilizing
fibrin against a premature breakdown by plasmin. It is not recommended in cases of DIC.
• Coagulase-positive bacteria (e.g., Staphylococcus aureus) are able to convert fibrinogen to
fibrin as a defense mechanism, enabling abscess formation.
• Red blood cells can be split apart by fibrin strands as they flow through a forming clot.
These fragmented RBCs are called schistocytes and can result in a microangiopathic
hemolytic anemia.
• In acute respiratory distress syndrome, neutrophils create capillary leakage that allows
fibrinogen and proteins into the lung space and the creation of hyaline membranes.
• Estrogen increases the synthesis of fibrinogen among other factors and inhibits antithrombin
III.
• D-dimer is a measure of fibrin split products and may be a useful laboratory measurement to
rule out pulmonary embolism in low-risk patients. During fibrinolysis, activated plasmin
degrades the cross-linked fibrin, which releases fibrin degradation products and exposes the
D-dimer antigen, which is typically not present in the body except when the coagulation
system has been activated.
FLOW VOLUME LOOPS
BASICS
DESCRIPTION
• Spirometry measures lung volumes (y-axis) as a function of time (x-axis).
– Flow rates are determined from spirometry by measuring volume achieved over a given
time period (y/x values).
FIGURE 1. Spirometry and lung volumes.
• Flow volume loops are a graphic representation of inspiratory and expiratory air flow (y-
axis) as a function of lung volume (x-axis). It measures a complete respiratory cycle in a
clockwise manner from forced maximal expiration to maximal inspiration.
– Components of maximum air flow depend on volumes.
FIGURE 2. Normal flow volume loop.
– Volume (x-axis): Movement along the x-axis from left to right indicates decreasing lung
volumes.
– Expiration (positive y-axis): Curve moves from high to low lung volumes (left to right on
x-axis). There is a rapid rise to peak expiratory flow (PEF) followed by a linear fall as lung
volumes decrease, airways narrow, and resistance increases.
– Inspiration (negative y-axis): Curve moves from low to high lung volumes (right to left) in
a symmetrical saddle shape.
• Lung volumes (Figure 1): Measurements obtained with spirometry
– Tidal volume (TV): Volume of air measured with passive ventilation.
– Inspiratory reserve volume (IRV): Volume of air measured from end tidal volume
inspiration to maximal inspiration.
– Expiratory reserve volume (ERV): Volume of air measured from passive expiration to
maximal forced expiration.
– Residual volume (RV): Volume of air that remains in the lungs after maximal expiration;
unable to measure with spirometry.
• Lung capacities (Figure 1): Represents the sum of two or more lung volumes on spirometry.
– Functional vital capacity (FVC): Volume of air forcibly exhaled after maximal inspiration
(does not include RV).
FVC = IRV + TV + ERV
– Functional residual capacity (FRC): Volume of air present in the lungs at the end of
passive expiration.
FRC = ERV + RV
– Total lung capacity (TLC): Volume of air contained within the lungs following maximal
inspiratory effort.
TLC = FVC + RV
• Lung flows (Figure 2):
– PEF: Maximum rate of respiratory gas flow during expiration (peak of expiratory curve).
Following PEF, the slope of the expiratory curve is nearly linear. It is a function of airway
diameter, patient effort, and expiratory muscle strength
– Maximal expiratory flow at 50% FVC (MEF50): Flow value on the positive y-axis at the
midpoint of the x-axis.
– Maximal inspiratory flow at 50% FVC (MIF50): Flow value on the negative y-axis at the
midpoint of the x-axis.
– Under normal conditions, MEF50 is only slightly less than MIF50 (secondary to dynamic
compression resulting in reduced flow).
– Under pathophysiologic conditions, the discrepancy between the MEF50 and MIF50 can be
significant.
• Comparison of flow-volume curves performed during resting ventilation with those during
forced inspiration and expiration should demonstrate significant ventilatory reserves in
normal subjects (1)[B].
• Obstructive lung disease:
– Asthma, chronic bronchitis, bronchiectasis, COPD
FIGURE 3. Obstructive lung disease.
– Curves shift leftward on the x-axis secondary to hyperinflation. “Air trapping” results in
higher lung volumes and RV.
– PEF and MEF50 are significantly reduced, and MEF50 < MIF50.
– “Scalloping” of the expiratory loop (positive y-axis) indicates reduced expiratory flow at
all lung volumes (no longer linear).
– Since inspiratory flow (not expiratory flow) is primarily increased during exercise, patients
with obstructive disease experience increased end-expiratory lung volumes
(hyperinflation) with exertion. This may be in addition to hyperinflation present at
baseline.
• Restrictive lung disease:
– Fibrosis, scoliosis, obesity
FIGURE 4. Restrictive lung disease.
– Curves shift rightward on the x-axis secondary to a decreased TLC; all lungs volumes are
reduced.
– PEF, MEF50, and MIF50 are all reduced; flow reduction is congruent over the inspiratory
and expiratory loops and MEF50 ∼ MIF50. Additionally, PEF is not as diminished or
affected compared to obstructive disease.
• Fixed upper airway (extrathoracic) obstruction:
– Tracheal stenosis, goiters
FIGURE 5. Fixed extrathoracic obstruction.
– Volumes (x-axis) are not affected.

– Flow is decreased throughout the respiratory cycle at all lung volumes.
– Curves are flattened on both the inspiratory and expiratory curves, MEF50 ∼ MIF50.
• Variable (nonfixed) upper airway (extrathoracic) obstruction:
– Vocal cord dysfunction, obstructive sleep apnea, tracheomalacia
FIGURE 6. Variable extrathoracic obstruction.
– Volumes (x-axis) are not affected.

– Flow is decreased with inspiration but does not affect expiration (MEF50 > MIF50). PEF is
unchanged.
– The inspiratory curve is flattened.
– Insensitive test for upper airway obstruction: The tracheal lumen circumference must be
decreased to less than 8 mm (80% reduction in tracheal area) before abnormalities are
detected (2)[B].
• Variable (non-fixed) intrathoracic obstruction:
– Endobronchial tumors or bronchial compression by other malignancies (anterior
mediastinal masses)
FIGURE 7. Variable intrathoracic obstruction.
– Volumes (x-axis) are unchanged.

– Flow is decreased during expiration but does not affect inspiration (MEF50 < MIF50); PEF
is significantly reduced.
– The expiratory curve is markedly affected.
• Flow-volume loops can aid in the diagnosis and monitoring of the progression of chronic
lung diseases.
• Flow volume loops provide an alternative to advanced imaging modalities that are not
immediately available or feasible in the operative room and intensive care unit.
– Asthma, COPD exacerbations
– Endobronchial intubations
• Vocal cord dysfunction (Figure 6): Flow volume loops are commonly utilized to confirm the
diagnosis (3)[B].
• Anterior mediastinal mass (Figure 7): In addition to the clinical history and radiological
imaging, flow-volume loops provide a tool to measure the “functional” effects of a mass.
Abnormalities in the expiratory loop may be accentuated in the supine position and may
indicate the potential for complete airway obstruction with anesthetic induction and muscle
relaxation.
EQUATIONS
• FVC = IRV + TV + ERV; where FVC is forced vital capacity, IRV is inspiratory reserve
volume, TV is tidal volume, and ERV is expiratory reserve volume
• FRC = ERV + RV; where FRC is functional residual capacity, ERV is expiratory reserve
volume, and RV is residual volume
• TLC = FVC + RV; where TLC is total lung capacity, FVC is forced vital capacity, and RV is
residual volume
REFERENCE
1. Stoller JK. Spirometry: A key diagnostic test in pulmonary medicine. Cleve Clin J Med.
1992;59:75–78.
2. Dempsey JA, McKenzie DC, Haverkamp HC, et al. Update in the understanding of
respiratory limitations to exercise performance in fit, active adults. Chest. 2008;134:613–
622.
3. Deckert J, Deckert L. Vocal cord dysfunction. Am Fam Physician. 2010;81:156–159.
ADDITIONAL READING
• Gal TJ. Pulmonary function testing. In Miller’s anesthesia, 6th ed., chap. 26. 2004:1100–
1103.
• Stock MC. Respiratory function in anesthesia. In Barash PG, ed. Clinical anesthesia, 5th ed,
804–807.
• Philadelphia, PA: Lippincott Williams & Wilkins, 2006.
• Spirometry
• Anterior mediastinal mass
• Asthma
CLINICAL PEARLS
• Spirometry is the measurement of volume (y-axis) versus time (x-axis).
• Flow volume loops are plots of air flow (y-axis) as a function of lung volume (x-axis) during
FVC maneuvers obtained by spirometry. All determinants of air flow depend on lung
volumes.
• PEF, maximal expiratory flow at 50% vital capacity (MEF50), and maximal inspiratory flow
at 50% vital capacity (MIF50) are useful in describing dynamic airway obstruction. The
volumes and shape of flow-volume loops provide additional information.
• Flow-volume loops are instructive in the preoperative assessment (vocal cord dysfunction,
anterior mediastinal mass, chronic lung disease) and intraoperative and postoperative
evaluation (asthma exacerbation).
FRESH FROZEN PLASMA
Satoru Ogawa, MD
BASICS
DESCRIPTION
• Transfusion of fresh frozen plasma (FFP) is mainly indicated for the treatment of complex
coagulopathies in which multiple coagulation factors and inhibitors are depleted. Some
common indications include the following (1,2):
– Massive bleeding in trauma, cardiovascular surgery, or organ transplantation with
prolonged prothrombin time and/or activated partial thromboplastin time
– Active bleeding during or prior to invasive procedures/surgery in patients with congenital
or acquired factor deficiency when no alternative therapies (factor concentrates) are
available.
– Acute reversal of vitamin K antagonist therapy
– Disseminated intravascular coagulation
– Thrombotic thrombocytopenia purpura
• A cross matching is not required, but ABO compatibility should be considered before
transfusion (Table 1).
See Table
• Normal plasma volume is about 50 mL/kg or 3,500 mL in a 70-kg man.
• Normal coagulation factor levels are in the range of 50–150% (0.5–1.5 IU/mL).
• Plasma proteins exert an oncotic pressure of 25–30 mm Hg (60–70% derived from albumin).
Normal plasma albumin levels are 3.5–5.0 g/dL.
• Plasma preparation:
– Whole blood centrifuge: Donor whole blood is centrifuged and the top plasma fluid layer
is separated from red blood cells and platelets.
– Plasmapheresis donations: Allows for a single donor and reduces recipient exposure to
infection and HLA antibodies. It is an extracorporeal therapy technique that involves
removal of whole blood, sequestration of plasma via a cell separator, and return of
nonplasma components.
• Freezing:
– FFP is frozen within 8 hours of collection to –18°C to help prevent inactivation of labile
coagulation factors V and VIII.
– FP24 is the plasma that is frozen within 24 hours of phlebotomy (3). It is being used
increasingly as a substitute for FFP because it allows for selection for male-only donors in
an attempt to reduce the risk of transfusion-related acute lung injury (TRALI). It contains
slightly lower levels of factors V and VIII, but their replacements are not typically
indicated.
– Although they are technically different products, they are considered therapeutically
equivalent. Both are stored, thawed, and infused similarly.
• Storage:
– <–18°C: products can be stored for up to 12 months
– <–65°C: products can be stored up to 7 years
• Contents:
– 1 donor unit of FFP = 250 mL (∼220 mL plasma, ∼30 mL anticoagulant)
– In theory, 1 mL of plasma = 1 unit of coagulation factors; thus 1 plasma unit contains 220
units. Actual coagulation factors vary significantly among different plasma units. Freezing
and thawing may reduce factor levels.
– Contains coagulation factors, anticoagulant proteins, albumin, and immunoglobulins
– Devoid of red cells, leukocytes, and platelets. (The lack of leukocytes makes the risk of
CMV transmission a nonissue.)
• Thawed FFP
– After thawing, FFP contains near normal levels of many plasma proteins (procoagulant
and inhibitory components of the coagulation cascades, acute phase proteins,
immunoglobulins, and albumin), fats, carbohydrates, and minerals in circulation.
– Coagulation factors are reasonably well maintained with some decreases of factor V and
VIII in thawed plasma kept at 1–6°C for up to 5 days.
• ABO compatibility:
– Antigenic red blood cells are removed during processing; however, small amounts may
still be present in donor FFP. Additionally, ABO antigens may be present in the donor FFP.
To that extent, although ABO compatibility is preferred whenever possible, in
emergencies, it is not necessary.
– Type AB is considered the universal FFP donor, as it has no antibodies in the plasma to
Type A, B, AB or O erythrocytes (Table 1).
• Complications of FFP administration:
– TRALI is caused by anti-HLA antibodies present in donor plasma. It is the leading cause of
morbidity and mortality after plasma transfusion. Female donor units are more likely to
be associated with TRALI. In some countries, male donors are specifically chosen, with a
demonstrated decrease in incidence. More commonly, male donor FP24 is being utilized.
– Allergic reactions are the most common complication with a 1–3% incidence.
– Patients with IgA deficiency may develop an anaphylactic reaction when transfused with
IgA-containing blood products including FFP. IgA is a serum immunoglobulin and
antibody found at mucosal surfaces. IgA deficiency results from an intrinsic B cell defect.
– Fluid or circulatory overload can result from large volume administration, particularly in
patients with limited cardiovascular reserve.
• Infection transmission:
– The risks of viral transmission, particularly hepatitis C and human immunodeficiency
virus, have been significantly reduced by the nucleic acid testing of donor blood.
– Treatment of FFP with methylene blue or solvent-detergent further reduces virus
transmission risks.
– Prion disease transmission (Creutzfeldt-Jakob disease) should be reduced by avoiding
plasma collections from an endemic area.
– Hypocalcemia from citrate overload can occur with massive plasma transfusion.
• In adults, 1 unit of plasma increases most factors by ∼2.5%; 4 plasma units by ∼10%. A
10% increase in factor levels is typically necessary to make a significant change in
coagulation status. However, this will vary depending on the patient’s size and clotting
factor levels.
• Pediatric dosing: 10–15 mL/kg gives a 15–20% rise in factor levels.
• Little evidence exists to inform the best therapeutic plasma transfusion practice. Current
indications include the following (2,3):
– Abnormal coagulation screening tests in the face of bleeding or prophylactically in
nonbleeding subjects prior to invasive procedures or surgery.
– Microvascular bleeding in the presence of PT or PTT > 1.5 times normal. This is believed
to correspond to factor levels <30% of normal. However, the relationship among
coagulation tests, the extent of coagulopathy, and the need for FFP remains unclear.
– Urgent reversal of warfarin; consider vitamin K if time permits and prothrombin complex
concentrate if available.
– Massive transfusion may require coagulation factor replacement with FFP without waiting
for laboratory results. Abnormalities of PT/PTT are often seen after a rapid infusion >4
units of packed RBCs. The main advantage of “damage control resuscitation” with a fixed
ratio (1:1) transfusion of RBC and FFP is the prevention of severe dilution and early
correction of coagulopathy.
– Isolated factor deficiency (factors II, V, VII, IX, X, XI) replacement II, V, VII, IX, X, XI)
when specific component therapy is unavailable
– Hereditary antithrombin or protein C deficiency; however, purified lyophilized
antithrombin or protein C concentrate is available and preferable to FFP.
– Disseminated intravascular coagulation
– Plasmapheresis for thrombotic thrombocytopenic purpura
– Infants with protein-losing enteropathy
– Cell salvage processing can result in depletion of plasma fractions. FFP may be needed
after several units have been administered
• Plasma is not as viscous as packed RBCs and does not need to be diluted with crystalloid.
REFERENCES
1. Stanworth S, Brunskill SJ, Hyde CJ, et al. Appraisal of the evidence for the clinical use of
FFP and plasma fractions. Best Pract Res Clin Hematol. 2006;19:67–82.
2. ’Shaughnessy DF, Atterbury C, Bolton Maggs P, et al. Guidelines for the use of fresh-frozen
plasma, cryoprecipitate, and cryosupernatant. Br J Haematol. 2004;126:11–28.
3. Yim R. Fresh frozen plasma for transfusion: A review. Blood Bulletin. 2008;10:1–2.
• Transfusion-related lung injury
• Red blood cell transfusion
• Infectious risk of transfusion
CLINICAL PEARLS
• Critical levels (20–25%) of normal coagulation factors levels are reached after a loss of twice
the blood volume.
• Excessive crystalloid/colloid administration in a massive hemorrhage can result in dilutional
coagulopathy, which may be prevented by early administration of FFP.
• Adult dosing, in general, is recommended with 5–8 mL/kg. However, a dose up to 10–30
mL/kg may be necessary to keep coagulation factors above 50% of normal.
• Plasma-derived, virus-inactivated prothrombin complex concentrate is an alternative to FFP
in acute reversal of vitamin K antagonist therapy.
• Fresh frozen plasma administration is contraindicated for the augmentation of plasma
volume or albumin concentration due to its potential for immunological and infectious risks
as well as limited supply.
FUNCTIONAL RESIDUAL CAPACITY
BASICS
DESCRIPTION
• Functional residual capacity (FRC):
– Is equal to residual volume (RV) plus expiratory reserve volume (ERV)
– Is the volume of air in the lungs at the end of a normal exhalation or tidal volume (TV)
– Participates in alveolar gas exchange, not volume movement. TV serves as the functional
component of volume movement and gas exchange (“checking account" where most of the
activity takes place). Gas (oxygen, volatiles, nitrogen) from the TV readily diffuses into the
alveolar units that comprise the FRC (akin to a "volume of distribution").
– Functions as a “storage" or “reservoir" for O2 in the event of hypoxia or apnea ("overdraft
coverage").
– Corresponds to an intrapleural pressure of 0 cm H2O. The outward rib cage expansion and
inward lung recoil forces are balanced (“tug-of-war" tie).
• Factors that reduce FRC include: Compression of the thoracic wall, cephalad movement of
abdominal contents and diaphragm, and increased blood volume of the chest/abdomen.
FIGURE 1. Lung volumes. FRC is the sum of ERV and RV. IRV = inspiratory reserve volume, FRC = functional residual
capacity, VC = vital capacity, VT = tidal volume, ERV = expiratory reserve volume, RV = residual volume.
• FRC is comprised of the RV and ERV. Lung capacities are comprised of lung “volumes." The
lung volumes are measured parameters. FRC is approximately 35 mL/kg (~2,500 mL in a
healthy 70–kg male).
• The (inward) lung recoil force is referred to as transpulmonary pressure (Ptp). The (outward)
chest wall force is referred to as the transmural pressure (Ptm). At end expiration of a
normal TV, Ptp and Ptm are numerically equal but opposite in sign (positive and negative),
resulting in an equilibrium.
• FRC during a normal TV does not contribute to the minute ventilation (volume movement).
The open alveoli in the FRC, however, will equilibrate with the gas composition in the TV.
Thus, FRC functions as a reservoir, or a volume of distribution, in which O2, nitrogen,
volatiles, and CO2 diffuse to. Assuming normal blood perfusion to the alveolar units,
oxygenation, ventilation, and gas exchange with the blood take place. During periods of
apnea (no new oxygen in the TV), FRC becomes a valuable supply for oxygen. Hence, it
provides “overdraft coverage” and buffers alveolar gas tensions against abrupt alterations in
O2 and CO2 during the respiratory cycle.
– ERV during a forced vital capacity (FVC) can participate in volume exchange (open alveoli
can contribute to gas exchange).
– RV during a FVC cannot contribute to volume exchange (unable to empty the alveoli from
dynamic airway closure/collapse).
• The concept of FRC as a “reservoir” or “savings account” is utilized and harnessed when we
preoxygenate prior to anesthetic induction. In the event of apnea, the body will have 35
mL/kg of 100% O2 available (e.g., a 70-kg healthy male: 35 mL × 70 kg 2,500 mL × 1.0
FiO2 = 2,500 mL O2; body uses ∼ 250 mL O2/minute). This provides additional time
before desaturation in the event that ventilation, laryngoscopy, or fiberoptic bronchoscopy
are difficult or prolonged.
• Alveoli within the FRC need to be patent/open in order for gas to diffuse into, participate in
gas exchange, and function as an oxygen reservoir. Obstruction at any point during the
breathing cycle or atelectasis may lead to a venous admixture.
• In young healthy individuals, the majority of the alveoli in the FRC (RV + ERV) remain
open in the standing position (available for gas exchange and reservoir). This is because the
closing volume (CV) is less than FRC (CV <<< FRC).
– Closing volume is the volume at which dynamic compression of the airways begins.
– Alveoli do not have cartilaginous structures that hold them open but are instead
dependent upon proteins (elastin, collagen, trypsin) that surround the alveoli in the
parenchyma.
FIGURE 2. The proteins maintain a tight conformational structure that “pull" open the surrounding alveoli (tight coiling
effect in parenchyma pulls open the alveoli which are essentially potential spaces).
– When lung volumes reduce (forceful exhalations, FVC, or reductions in FRC), Ptm is
increased. When the volume falls below the CV, Ptm exceeds the ability of the
parenchymal proteins to keep alveoli open. Atelectasis and air trapping or auto-PEEP
occurs.
– Alveoli in Zone 4 (lung bases) are most affected during maximal exhalation. They have
low resting volumes from gravitational forces on blood (increased Ptm) and are vulnerable
to compression during active expiration.
– CV is affected by age, smoking, and disease states that affect the tight conformational
structure of these parenchymal proteins (reduced coiling). Thus, there is reduced alveolar
patency and increased closing at all lung volumes; gas exchange cannot occur and
shunting occurs. CV initially infringes upon ERV and proceeds into the TV.
– Closing capacity (CC) = CV +RV
• FRC is variable. Factors that affect the Ptp and Ptm can increase or reduce FRC. They include
the thoracic wall, abdominal wall, diaphragm, and blood volume within the
lung/abdominal cavities. Meanwhile, CV is not variable but based upon the “health” or
“tightness” of the surrounding parenchymal proteins.
• FRC cannot be measured with spirometry; RV cannot contribute to volume exchange during
a FVC and hence, cannot be directly measured
– Gas dilution techniques: Inhalation of a known concentration and volume of an inert
tracer gas, such as helium, is performed for 7–10 minutes in a closed circuit (allows for
equilibration). The final exhaled helium concentration is diluted in proportion to the
unknown volume of air in the patient’s chest (RV) and can be calculated.
– The nitrogen-washout technique (single-breath and multiple-breath techniques): In the
single-breath technique, the patient inhales 100% oxygen and exhales into a 1-way valve
with a nitrogen sampler; creates a curve of nitrogen versus expired volume. At the
beginning of exhalation, nitrogen concentration is 0 (dead space contribution that does
not participate in alveolar exchange). With continued exhalation, nitrogen concentration
starts increasing as alveolar volume is exhaled.
– Bedside ventilator-based FRC measurement techniques are available. There is evidence
that FRC measurement (combined with arterial oxygenation and respiratory compliance)
can help guide and assess therapy.
ANATOMY
• Lung units: Alveoli, pulmonary capillaries.
• Rib cage: Intercostal, sternocleidomastoid, and scalene muscles; xiphoid process, ribs.
• Abdominal contents: Fat, fluid, blood flow, pregnancy.
• Diaphragm: C3, C4, C5 bilateral innervations (affected with interscalene blocks).
• Factors that reduce lung expansion will reduce FRC and result in alveolar
collapse/atelectasis and air trapping. Atelectasis results in V/Q mismatch (shunting; blood
perfuses collapsed alveoli and are not oxygenated; gas exchange cannot occur). With
increased numbers of alveolar units being shunted, the F(A-a) gradient increases and
hypoxia results. Furthermore, airway compliance, O2 reservoirs, and mixed venous O2
reduce; peak and static airway pressures increase.
• Absorption atelectasis: Reductions in FRC also result in air trapping. Absorption of gas
behind the closed or intermittently closed airway leads to collapse/atelectasis [hence V/Q
mismatch, shunting, and increased F(A-a) gradient]. This may be exacerbated by a high
FiO2 from near complete uptake of oxygen in the alveoli. Room air and partial air mixtures
contain nitrogen which is inert and poorly dissolved in blood. As a result, nitrogen serves as
an alveolar “filler,” reducing complete collapse (like foam packaging in a box; if
compressed, less likely to be completely collapsed).
• The outward chest wall force (Ptp) and inward lung recoil (Ptm) determine the FRC (intrinsic
factors). However, they are altered by factors that affect the thoracic wall, abdominal wall,
diaphragm, and blood volume. These factors are variable, extrinsic, and often affected by
anesthesia and surgery. FRC is still the volume at the end of a normal TV, and Ptp + Ptm
continues to equal 0 mm Hg; however, lung volume at FRC will be re-established
• Thoracic wall: Reduction in diameter and cross-sectional area are seen with restrictive lung
diseases affecting the chest wall—scoliosis, muscle dystrophies (ALS, paraplegia, etc.), and
obesity (fat on the chest).
– Age affects chest wall compliance. Babies have very compliant thorax and lung (allows for
easy passage through birthing canal); FRC is small and roughly equal to RV. They also
have a low O2 reservoir and increased O2 consumption (∼ 6 mL O2/kg/minute, double
that of older children and adults) that results in rapid desaturation during apnea (1).
– Elderly have ossified thoraxes that become stiffer and increase outward forces and FRC
(3% per decade). CV, however, increases at a greater rate, leading to airway closure,
atelectasis, and V/Q shunting.
– Inspiratory muscle tone affects the intercostals, sternocleidomastoid, and scalene muscles
during GA and/or NMBD (reduces thoracic outward force, FRC) (2).
– Barrel chest, seen with emphysema, increases chest wall diameter, Ptm, TLC, and hence
FRC. It is a compensatory mechanism to reduce atelectasis in the face of an increased CV
from damaged parenchymal proteins that are unable to maintain patent alveoli.
• Abdominal wall: Obesity, pregnancy, ascites, abdominal and thoracic surgery, abdominal
retractors and packing, pneumoperitoneum, and supine and Trendelenburg position allow
for cephalad movement of abdominal contents. This results in external compression or
“invasion” into the lung cavity and an increase in Ptp (reduces FRC).
• Diaphragm: Intrinsic muscle tone is reduced with NMBD and anesthesia (IV and volatile),
reducing diaphragmatic excursion and lung expansion (reduced FRC). Bilateral diaphragm
paralysis (cervical quadriplegia, surgical injury, radiation) produces similar effects on FRC.
• Blood volume within lung/abdominal cavities as seen during surgery, congestive heart
failure (CHF), acute respiratory distress syndrome (ARDS), and fluid overload states reduce
lung expansion and hence FRC.
• CV, unlike FRC, has limited variability.
• An abnormal increase in FRC can result from obstructive airway diseases (asthma, reactive
airway disease, emphysema, chronic bronchitis) due to an increase in RV, at the expense of
ERV. The increased RV cannot contribute to the exhaled volume; gas exchange can occur in
alveoli that open with inhalation/increased lung volumes, despite closing with exhalation
(decreased lung volumes).
– High-altitude inhabitants compensate for low atmospheric O2 with increased FRC and lung
volumes in general. In this scenario, they increase the FRC compared to CV so that more
alveoli are open and can function in oxygen exchange. They have an increased work of
breathing at the higher lung volumes.
• Intraoperative shunt is greater in patients with pre-existing low PaO2, but the percentage
increase is larger in healthy subjects
• Reductions in FRC may be significant intraoperatively and perioperatively. Intraoperative
shunt is greater in patients with pre-existing low PaO2, but the overall percentage is larger
in healthy subjects.
• Supine position (0.8 L) and induction of general anesthesia (0.5 L) are not inconsequential
(1.3 L reduction; reduces lung volumes from 3.5 to 2.2 L, brings closer to, and may overlap
CV) (1)
• Although positive pressure ventilation reduces the effects of the diaphragm and abdominal
wall on FRC, it does not negate it entirely (3).
– Implementing large TV (10–12 mL/kg) and PEEP may increase FRC and gas exchange.
Opens atelectatic alveoli during inspiration (allows O2 and CO2 to be exchanged with
blood); consider pressure control ventilation or an increased inspiratory pause time
(increases time that alveoli are open during inspiration).
– PEEP preferentially affects upper lung zones; airway closure and reduced FRC
predominantly affect dependent lung zones. Higher PEEPs may improve airway patency in
dependent lung regions but can reduce cardiac output and pulmonary perfusion (V/Q
mismatching, dead space)
• 30° head-up tilt (not back up) allows gravity to bring the abdominal contents downward,
increase FRC, and reduce atelectatic units.
• High FiO2 that is often used perioperatively can result in absorption atelectasis in poorly
ventilated or “closed" alveoli.
• After intubation, early recruitment maneuvers (up to 40 cm H2O for 10 seconds) may reduce
atelectasis.
• Coughing during intubation, intraoperatively, or extubation reduces FRC. Avoid with
adequate induction and NMB medication dosage and time for onset. Consider recruitment
maneuvers prior to extubation.
• Postoperative reductions in FRC can cause hypoxemia, atelectasis, and pneumonia; different
etiology than intraoperative decreases. Results from absorption atelectasis (high O2 behind
closed airways), incisional pain, and reflex dysfunction of the diaphragm (local irritation,
bowel distension, pneumoperitoneum) after abdominal and thoracic surgeries
– Active lung expansion: Deep breathing exercise and coughing, incentive spirometry, CPAP.
Intensity and frequency of sessions are more important than form of therapy.
• Postoperative analgesia: Epidural analgesia may allow for deep breathing and diaphragmatic
excursion.
EQUATIONS
• FRC = RV + ERV; FRC = TLC – IRV – TV; where FRC is functional residual capacity, RV is
residual volume, ERV is expiratory reserve volume, TLC is total lung capacity, IRV is
inspiratory reserve volume, and TV is tidal volume.
• CC = CV + RV; where CC is closing capacity, CV is closing volume, and RV is residual
volume.
REFERENCES
1. on HF, Wahba WM, Craig DB. Airway closure, gas trapping, and the functional residual
capacity during anesthesia. Anesthesiology. 1972;36(6):533–539.
2. Laws AK. Effects of induction on anaesthesia and muscle paralysis on functional residual
capacity in the lungs. Can Anaesth Soc J. 1968;15(4):325–331.
3. Heinze H, Sedemund-Adib B, Heringlake M, et al. Changes in functional residual capacity
during weaning from mechanical ventilation: A pilot study. Anesth Analg.
2009;108(3):911–915.
ADDITIONAL READING
• Murray and Nadel’s Textbook of Respiratory Medicine, 5th ed. Saunders, 2010.
• Closing capacity
• Spirometry
• Ventilation and perfusion matching
CLINICAL PEARLS
• Functional residual capacity is comprised of the RV and ERV.
• FRC is affected by several perioperative factors (general anesthesia, supine positioning,
abdominal procedures, obesity, abdominal surgery, etc.) and can result in shunting.
GASTRECTOMY
Allen Alexander Holmes, MD, MS
BASICS
DESCRIPTION
General
• Gastrectomy describes the surgical excision of part (subtotal) or all (total) of the stomach.
The most common indication is for cancer, but emergent cases of gastric trauma or
uncontrollable bleeding ulcers do occur. Most bariatric procedures involve a functional
subtotal gastrectomy.
• Following incision, dissection involves separating the ligaments that connect the stomach to
the spleen and colon. A clamp is placed at the duodenum, which is then resected and
sutured close. Subsequently, the stomach is clamped and resected (partially or completely).
The anastomosis is performed usually via a Roux-en-Y jejunal limb.
– Esophagojejunostomy for total gastrectomy
– Gastrojejunostomy for subtotal gastrectomy
• For cancer, an associated limited “D1” or extensive “D2” lymphadenectomy is performed.
• A feeding jejunostomy tube (J-tube) is frequently placed for postoperative nutrition.
• Laparoscopy. Diagnostic evaluation may be performed prior to laparotomy. Resection may
also be performed but has been limited to patients requiring a distal gastrectomy (early
stage disease or palliation).
Position
• Supine
• Prep from nipples to pubis
Incision
• Midline laparotomy +/– lateral extension (“L” or Makuuchi incision) or bilateral subcostal
incision (Chevron incision)
• Laparoscopy via 3–5 small incisions for trochar insertion
Approximate Time
3–6 hours depending on the degree of lymphadenectomy and whether the anastomosis is
hand-sewn versus stapled
EBL Expected
• 100–200 mL for uncomplicated cases
• Higher with extended lymphadenectomy (especially involving the spleen or pancreas) and
total gastrectomy
• Bleeding ulcers or traumatic injuries can result in massive blood loss
Hospital Stay
7–14 days, primarily dependent on tolerance of oral feeding
Possible laparoscopic equipment
EPIDEMIOLOGY
Prevalence
In the US, there were 21,000 new cases of gastric cancer diagnosed in 2010.
Prevalence
• Helicobacter pylori infection is implicated in distal gastric cancer
• Gastric cancer patients have a mean age in their 70s
Morbidity
• Complication rate of 9% in subtotal gastrectomy and 13% for total gastrectomy
• Postoperative complications are increased if lymph node dissection is performed; they are
doubled if spleen or adjacent organs are removed.
Mortality
• In the US in 2010, there were 10,570 deaths due to gastric cancer. Increased occurrence in
Japan, Iceland, Chile, and Australia.
• Perioperative mortality is 1% in subtotal gastrectomy and 2% for total gastrectomy.
• Avoid excessive fluid administration; a positive fluid balance may affect postoperative
complications and mortality (particularly cardiac and pulmonary).
• If a total laparoscopic approach is attempted, there is a possibility to convert to an open
procedure. If a laparoscopic diagnostic exam is performed first, the case could be aborted on
short notice.
• An epidural catheter should be considered for adequate postoperative pain management.
SYMPTOMS
• Vague pain, nausea, indigestion, early satiety, and weight loss
• Melena for bleeding ulcers, leiomyosarcomas, and large adenocarcinomas
History
• Assessment of comorbidities
• Bowel prep for surgery
• Consumption of smoked, pickled, or salt-cured foods
Signs/Physical Exam
• Usually nonspecific
• Rarely, a palpable epigastric mass
MEDICATIONS
• Gastric cancer patients demonstrate improved survival with chemotherapy prior to surgery
(1). However, treatment can affect multiple organ systems:
• Myelosuppression
• 5-FU – Coronary vasospasm
• Anthracyclines – Cardiac toxicity
• Cisplatin – Nephrotoxicity
• Trastuzumab – Cardiac toxicity and pulmonary toxicity
• Ulcers. Acid reducing drugs including antacids, H2 blockers, and proton pump inhibitors
Labs/Studies
• CBC to evaluate bone marrow function
• Chemistry panel (electrolyte derangements after bowel prep)
• PT/PTT prior to epidural, especially in setting of recent chemotherapy
• Staging CT or PET scan
• Endoscopic exam
• Malignancy. Types:
• Adenocarcinoma (90–95%)
• Lymphoma
• Leiomyosarcoma
• GI stromal tumor
• Carcinoid
• Usual comorbidities of advanced age
• Ulcers refractory to medical therapy may be complicated by bleeding, perforation, or pyloric
obstruction.
TREATMENT
Premedications
• Benzodiazepines can be titrated for anxiety
• GI medications to decrease gastric volume and acid may be considered in patients at risk for
aspiration.
• Octreotide helps to minimize vasoactive compound release from carcinoid tumors
• Deep venous thrombosis (DVT) prophylaxis should be discussed with the surgeon.
Epidural catheter placement, including risks and benefits, should be discussed if planned.
• Bowel anaerobes (Bacteroides, etc.)
• 2nd or 3rd generation cephalosporin (cefotetan, cefoxitin, ceftriaxone)
• Ertapenem (advantage of one time dose for 24-hour coverage)
• Quinolone + metronidazole for β-lactam allergy
INTRAOPERATIVE CARE
• General anesthesia with endotracheal tube
• Epidural catheter for postoperative pain (mid-thoracic level) management
Monitors
• Arterial line for most cases to allow for beat-to-beat BP monitoring and frequent labs
• Central venous access if large bore peripheral access is unavailable
• Noninvasive hemodynamic monitors may be helpful in avoiding excessive fluid
administration.
Generally, a rapid sequence induction is indicated as patients can have poor gastric emptying.
Maintenance
• Volatile or IV balanced technique
• Muscle relaxation is usually needed to assist with surgical exposure.
• Narcotic or continuous epidural for pain management. Epidural infusions may be started
intraoperatively; however, the sympatholysis may compound hypovolemia/hemorrhage;
some practitioners wait until the period of blood loss has been completed to avoid this.
• Fluids. Administration should be tailored to maintain an effective circulatory volume while
avoiding interstitial fluid overload.
• A fully awake extubation is recommended to decrease the risk of aspiration.
• Carefully secure and protect any NG tube if present as it will be impossible to replace across
anastomosis without reopening.
POSTOPERATIVE CARE
BED ACUITY
• A monitored bed (telemetry versus ICU) is typical for total gastrectomy or any case
involving significant blood loss.
• A regular floor bed is possible for uncomplicated subtotal gastrectomy in otherwise healthy
patients.
ANALGESIA
• Epidural or PCA. In addition to providing improved pain relief in the first 72 hours after
surgery (2), epidural infusions are also associated with a decreased incidence of pulmonary
complications (3). DVT prophylaxis should be considered when planning catheter removal.
• Continuous bilateral transversus abdominis plane (TAP) blocks are an opioid-sparing
alternative to epidurals, although evidence is lacking (4).
COMPLICATIONS
• Anastomotic leak or failure
• Postoperative bleeding
• Any cancer patient is at increased risk of DVT and PE.
• Postoperative pneumonia
• Poor oral feeding tolerance
• Dumping syndrome – Result of poorly digested contents being dumped into small bowel.
Symptoms include cramps and nausea and can be immediate or delayed in onset.
PROGNOSIS
5-year survival for gastric cancer is 30–50% for stage II and 10–25% for stage III
REFERENCES
1. agner AD, Unverzagt S, Grothe W, et al. Chemotherapy for advanced gastriccancer.
Cochrane Database Syst Rev. 2010;(3):CD004064. [A]
2. erawatganon T, Charuluxanun S. Patientcontrolled intravenous opioid analgesia versus
continuous epidural analgesia for pain after intra-abdominal surgery. Cochrane Database
Syst Rev. 2005;(1):CD004088.[A]
3. Popping DM, Elia N, Marret E, et al. Protective effects of epidural analgesiaon pulmonary
complications after abdominal and thoracic surgery: A meta-analysis. ArchSurg.
2008;143(10):990–999; discussion 1000. [A]
4. Charlton S, Cyna AM, Middleton P, et al. Perioperative transversus abdominis plane (TAP)
blocks for analgesia after abdominal surgery. CochraneDatabase Syst Rev.
2010;12:CD007705. [B]
• Laparoscopy
CLINICAL PEARLS
• Communicate with the surgeon regarding the status of all NG tubes including esophageal
stethoscopes and thermometers prior to stapling.
• Compression of the right heart and concomitant hypotension is common as surgeons work at
the distal esophagus.
• Recent chemotherapy can cause multiorgan system derangements.
GASTROESOPHAGEAL REFLUX DISEASE (GERD)
Tara L. Paulose, MD
BASICS
DESCRIPTION
• Gastroesophageal reflux disease (GERD) describes the abnormal reflux of gastric contents
into the esophagus due to
– Incompetent or relaxed lower esophageal sphincter (LES) tone
– Increased intragastric pressures
• This can result in pulmonary aspiration during general anesthesia or sedation
EPIDEMIOLOGY
Incidence
• Documented gastric reflux in 20–40% of the population
Prevalence
No predilection for age or sex
Morbidity
• Discomfort
• Can lead to metaplasia (Barrett’s), low-grade dysplasia, high-grade dysplasia, and ultimately
adenocarcinoma.
• Barrett’s metaplasia increases the risk of adenocarcinoma by 30–60 times that of the general
population.
Mortality
Esophageal cancer is the 7th leading cause of cancer death worldwide; information is not
available on the number that results specifically from GERD.
• Pregnancy
• Obesity
• Delayed gastric emptying; diabetes, history of vagotomy
• Presence of a hiatal hernia
• Presence of intra-abdominal pathology; tumor
• Ingestion of offending foods and/or medications:
– Caffeine
– Alcohol
– Calcium channel blockers
– Nitrates
– Beta-blockers
– Progesterone hormone
PATHOPHYSIOLOGY
• Reflux of acidic stomach contents into the esophagus is pathological and can result from
factors that increase the barrier pressure; barrier pressure = intragastric pressure – lower
esophageal pressure. It can result from an
– Increased intragastric pressure
– Incompetent LES
– Excessive relaxation of the LES
• Repeat and chronic exposure to acidic contents can result in atypical cell development and
potentially adenocarcinoma of the esophagus.
The geriatric population often presents with atypical symptoms such as “anginal” pain and
develop esophagitis secondary to concomitant use of medications (e.g. NSAIDs) to treat
comorbid conditions.
Common in the pediatric population, particularly in the first year of life, characterized as the
complete absence of severely diminished LES tone.
This patient population carries an especially high-risk given the increase in abdominal
pressure secondary to uterine enlargement as well as the effects of progesterone of the LES.
• GERD can result in the passive reflux and aspiration of stomach contents into the lungs
during any anesthetic period where protective airway reflexes are blunted (including
sedation).
• Preoperatively, aim to neutralize and decrease the volume of gastric contents in order to
minimize the possibility of reflux and thereby, aspiration.
• Aim to minimize the risk of aspiration: Consider rapid sequence induction (RSI), avoid
insufflating the stomach during hand ventilation, and consider endotracheal devices over
supraglottic airways.
SYMPTOMS
• “Heartburn;” anginal symptoms in the absence of cardiac findings
• Regurgitation of actual gastric contents
• Metallic taste in mouth
• “Full” sensation in chest
• Cough
• Dysphagia
• Hoarseness of voice
History
• Focused questions regarding presence, frequency, and severity
• Exacerbation of symptoms while recumbent or bent over
• Presence of symptoms with an empty stomach
• History of sleeping with several pillows in the absence of cardiac history
• Confirmation of NPO status
• Review of comorbid conditions/factors that increase reflux/aspiration risk (e.g., diabetes,
hiatal hernia, ileus, protracted hospital stay, opioid use)
Signs/Physical Exam
• Typically unremarkable
• Dental erosion
• Wheezing; an uncommon finding
TREATMENT HISTORY
• Lifestyle modifications:
– Weight loss
– Avoidance of trigger foods/medications
– Time lapse between oral intake and recumbency
– Smaller, frequent meals
– Elevation of head of bed
• Nissen fundoplication is a surgical intervention that may be performed for persistent
symptoms despite adequate treatment trials
MEDICATIONS
• Antacids can immediately neutralize/increase the pH of gastric contents. Antacids are
inorganic salts that release anions upon dissolving in acidic gastric secretions; anions
combine and neutralize hydrochloric acid. Increasing the gastric fluid pH will inactivate
pepsin, which then has bile-chelating effects as well as stimulates gastrin release; this results
in enhanced motility and esophageal sphincter tone. Nonparticulates (sodium citrate, 0.3M)
are more commonly used because mixing is more complete and rapid than particulate
antacids and if aspirated, they cause less foreign body reactions. Chronic use can cause
urine alkalinization and result in urolithiasis.
• H2 receptor antagonists decrease the baseline parietal cell acid and volume secretion as well
as blunt the response to normal stimulus (e.g., food, histamine, insulin, caffeine). It is a
competitive antagonist of histamine and inverse agonist at H2 receptors of gastric parietal
cells. In turn, the reduced acid and volume inactivates pepsin and stimulates gastric release.
Chronic use can inhibit p450 enzymes and prolong the duration and concentration of
warfarin, lidocaine, and diazepam.
• Proton pump inhibitors irreversibly bind to and inhibit H+/K+ ATPase enzymes on parietal
cells; they inhibit the “proton pump” and gastric acidity. This is the terminal step of gastric
acid production and is irreversible; therefore, it is capable of inhibiting close to 100% of
gastric acid secretion (1)[B].
Labs/Studies
• Largely a symptom-based diagnosis
• Patients may have undergone an endoscopy, 24-hour esophageal pH monitoring, esophageal
manometry, chest radiograph/upper GI series, or gastric emptying study on an outpatient
basis. These tests are not typically ordered preoperatively.
• EKG or cardiac enzymes may have been ordered to rule out cardiac etiology.
• Esophagitis leading to Barrett’s esophagus
• Increased risk of esophageal adenocarcinoma
Generally speaking, there is no need to delay a case if appropriate airway technique and
induction is undertaken by an experienced operator.
TREATMENT
Premedications
• Antacids. Useful in urgent and emergent cases where immediate gastric acid reduction is
desired (e.g., Cesarean sections); ideally administered 15–20 minutes prior to induction.
Sodium citrate for adults: 10–30 mL PO q6h prn; pediatrics: 5–15 mL PO q6h. Can increase
gastric fluid volume with resultant stomach distention; this can possibly increase nausea,
emesis, and volume of aspirate should aspiration occur (can offset the desirable effects of
pH reduction).
• H2 receptor antagonists do not affect the pH of the fluid already in the stomach, only future
production. Onset of action is 20–30 minutes (ideally administered 60–90 minutes prior to
induction). Ranitidine 50 mg IV (dilute in 20 mL NS or D5W). Famotidine 20–40 mg IV.
• Proton pump inhibitors do not affect the pH of the fluid already present in the stomach, only
future production. Pantoprazole is available in IV formulation and 40 mg IV may be
administered.
• Promotility agents can be used to decrease the volume of gastric contents by increasing
gastric emptying; can also increase LES tone. Metoclopramide for adults: 10–15 mg IM or
IV; pediatrics 0.1–0.2 mg/kg IM or IV.
• Increased risk of aspiration during deep sedation and induction/emergence of anesthesia.
Deep sedation may not be an option; may have to consider lighter levels or general
endotracheal anesthesia.
• Patient will need to be fully awake with full recovery of protective airway reflexes prior to
extubation.
INTRAOPERATIVE CARE
• General anesthesia with a cuffed endotracheal tube.
• Deep sedation may impair upper airway reflexes; may need to consider lighter levels or no
sedation.
Monitors
• Preoxygenation
• Standard induction for low-risk patients (based on history)
• RSI for high-risk patients. A true rapid sequence involves administering the induction agent
and muscle relaxant in succession without assessing the ability to bag-mask ventilate the
patient; the endotracheal tube is placed as soon as muscle relaxation has set in. Cricoid
pressure (Sellick’s maneuver) is maintained prior to induction and until tracheal tube
placement is confirmed. A modified RSI involves minimal ventilation with an airway
pressure <20 cm H2O; cricoid pressure is maintained in the same manner.
• Induction in the “head-up” position; reverse Trendelenburg is preferred over “back up.”
Reverse Trendelenburg takes advantage of gravity and decreases passive reflux. The “back
up” position can increase intragastric pressures.
• Awake intubation in cases of severe GERD history or “potential full stomach” – this
technique aims to complete an endotracheal intubation in a patient whose airway reflexes
and esophageal sphincter tone remain intact as it is undertaken with only topicalization of
the airway to blunt reactivity, prior to induction of anesthesia.
• Cuffed endotracheal tube is the preferred airway device to decrease the entry of gastric
contents into the lungs. The ProSeal LMA may be considered for lower risk cases, since
despite it being a supraglottic airway, it also includes a channel through which the stomach
can be emptied (via suction).
Maintenance
Consider the placement of an orogastric tube to suction stomach contents and decrease
volume. May leave in place to allow for suctioning prior to extubation.
• Suctioning gastric contents prior to emergence
• Consider readministration of antacid, H2 blockers, or promotility agents prior to extubation.
• Standard criteria. Patient should be fully awake, muscle relaxation reversed, and capable of
protecting their airway.
• Elevated head of bed
POSTOPERATIVE CARE
BED ACUITY
• Dependent on surgical procedure and patient comorbidities.
• If aspiration is noted or suspected, the airway is unstable, or there are poor airway reflexes,
a higher level of care to an ICU or step-down unit may be warranted.
• Patients may present in the recovery room with chest pain secondary to reflux. Life-
threatening causes (cardiac, pulmonary) should be considered and ruled out, as appropriate,
despite the possibility of GERD.
• Gastroenterology consult if needed to assess severity of GERD and sequelae.
COMPLICATIONS
• Aspiration pneumonitis
• Postoperative chest pain
REFERENCES
1. JeskeHC. Preoperative administration of esomeprazole has no influence on frequency of
refluxes. J Clin Anesth.2008;20:191–195.
2. SchiemanC, GrondinSC. Paraesophageal hernia: Clinical presentation, evaluation,
andmanagement controversies. Thorac Surg Clin.2009;19:473–484.
3. RichterJE. The many manifestations of gastroesophageal reflux disease:Presentation,
evaluation, and treatment. Gastroenterol Clin NorthAm.2007;36:577–599.
4. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce
the risk of pulmonary aspiration: Application of healthy patients undergoing elective
procedures. A report by the American Society of Anesthesiologists Task Force on
Preoperative Fasting. Anesthesiology. 1999;90:896–905.
5. Cotton BR, Smith G. The lower esophageal sphincter and anaesthesia. Br Jour of Anes.
1984;56:37.
• Hardy JF. Large volume gastroesophageal reflux: A rationale for risk reduction in the
perioperative period. Can J Anesth. 1988;35:162–173.
• Pulmonary aspiration
• Hiatal hernia
CODES
ICD9
530.81 Esophageal reflux
ICD10
K21.9 Gastro-esophageal reflux disease without esophagitis
CLINICAL PEARLS
• GERD can place a patient at increased risk for aspiration and respiratory sequelae.
• A thorough history-taking, appropriate premedication, and tailored anesthetic plan are
paramount to patient safety.
GASTROINTESTINAL BLOOD FLOW
Megan M. Freestone-Bernd, MD
Mary E. McAlevy, MD
BASICS
DESCRIPTION
• The splanchnic circulation consists of the blood flow to the stomach, intestines, pancreas,
liver, and spleen.
• At rest, the splanchnic circulation receives 15–25% of the cardiac output; this is equivalent
to ~30 milliliters of blood per minute per 100 grams of tissue (30 mL/min/100 g) and can
reach 250 mL/min/100 g.
• Splanchnic circulation passes through the liver prior to entering the inferior vena cava and
back into the general circulation.
• Blood flow increases sequentially along the digestive tract as digestion occurs.
• Vasodilation of the splanchnic circulation increases to augment blood flow during digestion.
It is regulated by (1):
– Parasympathetic nervous system stimulation which increases glandular secretion of
gastrin, secretin, vasoactive intestinal peptide, and cholecystokinin.
– Possibly kallikrein and bradykinin (directly secreted by GI glands into the GI tract lumen)
– β-agonists
– Products of digestion such as fatty acids and glucose.
– Decreased oxygen concentration from an increased metabolic rate during digestion.
• Vasoconstriction of the splanchnic circulation is mediated by sympathetic nervous system
stimulation, α-agonists, vasopressin, angiotensin, and endothelin (1).
• Hepatic arterial buffer response (HABR) describes the ability of the body to protect the liver
during low-flow states by increasing hepatic arterial flow when portal venous blood flow is
decreased. It is hypothesized that the buildup of adenosine in low-flow states is responsible
for the vasodilation of the hepatic artery (1).
ANATOMY
• Celiac artery. Branches off the abdominal aorta and then divides into the gastric artery
which supplies the stomach. The gastric artery divides into the splenic artery which supplies
the spleen and pancreas.
• Superior mesenteric artery. Branches off the abdominal aorta and forms smaller arteries that
supply the small intestine and pancreas.
• Inferior mesenteric arteries. Branches off the abdominal aorta and forms smaller arteries
that supply the large intestine.
• Superior and inferior mesenteric arteries. Form arcading arterial branches that allow
multiple pathways for blood flow and decreases the risk of ischemia.
• Portal vein. Venous blood leaves the stomach, spleen, pancreas, and intestine through the
portal vein, which provides about 70% of the blood supply to the liver. The remainder of
the hepatic blood supply comes from the hepatic artery.
• Hepatic vein. Drains the liver (portal vein and hepatic artery) and empties into the inferior
vena cava.
• Acute circulatory failure
– Splanchnic blood flow may either be reduced proportionately or disproportionately, as
related to systemic perfusion. Oxygen supply to the liver does not decrease until more
than 30% of the total blood volume is lost due to HABR. Additionally, the decrease in
perfusion is variable; the celiac trunk may receive less blood flow than the superior
mesenteric, inferior mesenteric, and hepatic arteries (1).
– Patients with right ventricular failure are at increased risk of developing severe liver
dysfunction. There may be a 20-fold increase in either serum alanine or aspartate
aminotransferase. This is reversible and is usually seen in patients with documented
systolic BP <75 mm Hg for greater than 15 minutes (1).
• High sympathetic stimulation states such as shock, hemorrhage, or hypovolemia can result
in:
– Vasoconstriction of the splanchnic circulation. This may provide as much as 200–400 mL
of blood back into the general circulation (high capacitance).
– Decreased splanchnic blood flow, as described above.
• Hemodilution. Studies have shown that there is an overall increase in the blood flow to the
splanchnic circulation; this is believed to preserve oxygenation/tissue perfusion (1).
• Portal hypertension can occur from cirrhosis. It describes impaired blood outflow from the
portal bed and an increase in splanchnic blood flow. Eventually, the increased pressure in
the portal bed, combined with a lack of drainage, results in the formation of collateral
circulation to other areas of the general circulation. These collateral vein sites cause caput
medusa, hemorrhoids, and esophageal varices (2).
• Mesenteric occlusion activates visceral afferent sympathetic fibers secondary to ischemia of
the abdominal visceral organs, severe hypoxia, and the release of bradykinin and
prostaglandins. This results in a reflex increase in arterial BP, heart rate, and cardiac
contractility. The reflex is more profound with superior mesenteric artery occlusion than
with celiac artery occlusion.
• Pneumoperitoneum for laparoscopic surgical procedures may also cause decreased
splanchnic blood flow. At insufflation pressures of 12–15 mm Hg, the intra-abdominal
pressure is greater than normal portal circulation pressure. There is a reduction in cardiac
output and mesenteric vasoconstriction resulting in decreased organ perfusion and portal
venous flow (3).
• Cardiopulmonary bypass (CPB) causes a systemic inflammatory response that may lead to
increased GI permeability related to ischemia/reperfusion, and/or inflammation. During
CPB, GI blood flow does not change but mucosal blood flow may decrease by as much as
50%. Perioperative volume loading and early postoperative enteral nutrition may help
improve mucosal blood flow.
• Supraceliac aortic cross clamping. Aortic clamping results in vasodilation proximal to the
clamp (to decrease myocardial afterload) and vasoconstriction distally (to maintain
perfusion pressure). Supraceliac clamping can have profound hemodynamic changes as
compared to more distal clamping (e.g., infrarenal):
– Increased preload from vasoconstriction of the splanchnic vasculature and volume shifting
to the central circulation.
– Increased afterload from the mechanical clamp. With infrarenal clamping, vasodilation of
the splanchnic vasculature can help alleviate the increase in afterload.
– Increased myocardial work. This may be poorly tolerated in patients with poor LV
function due to increased myocardial work and oxygen consumption. Myocardial ischemia
and LV failure can result if not properly anticipated. Aggressive treatment may be
performed with vasodilators such as nitroprusside, nicardipine, and propofol.
REFERENCES
1. Jakob SM. Splanchnic blood flow in low-flow states. Anesth Analg. 2003;96:1129–1138.
2. Cichoż-Lach H, Celiński K, SŁomka M, et al. Pathophysiology of portal hypertension. J
Pharmacol. 2008;59, Suppl 2:231–238.
3. Sammour T, Mittal A, Loveday BPT, et al. Systematic review of oxidative stress associated
with pneumoperitoneum. Br J Surg. 2009;96:836–850.
ADDITIONAL READING
• Mitsuoka H, Kistler EB, Schmid-Schönbein GW: Generation of in vivo activating factors in
the ischemic intestine by pancreatic enzymes. Proc Natl Acad Sci. 2000;97:1772–1777.
• Abdominal aortic aneurysm, suprarenal
• Cirrhosis
• Laparoscopy
CLINICAL PEARLS
• Vasopressin and drugs that act as α-agonists will cause intestinal vasoconstriction.
• β-agonists will cause intestinal vasodilation.
• The HABR compensates during low venous blood flow to the liver by increasing hepatic
arterial blood flow.
• Splanchnic blood flow may be decreased due to pneumoperitoneum depending on the
insufflation pressure used, anesthetic technique, and patient positioning (3).
• Damage to the GI mucosa during CPB may be decreased by perioperative volume loading
(1).
GASTROSCHISIS
Joel Stockman, MD
Swati Patel, MD
BASICS
DESCRIPTION
General
• Gastroschisis presents as the evisceration of the gut through a 2–3 cm defect in the anterior
abdominal wall and lateral to the umbilicus; it usually occurs on the right. The abdominal
wall and covering (sac) are absent.
• The pathogenesis is poorly understood, but four mechanisms have been proposed:
– Teratogenic exposure during the 4th week of development can hinder embryonic
mesenchymal differentiation.
– Amniotic membrane rupture at the umbilical cord during physiologic herniation or later
secondary to delayed umbilical ring closure.
– Abnormal right umbilical vein leading to growth impairment and viability of the
mesenchyme, resulting in a skin defect and rupture.
– Intrauterine occlusion of the omphalomesenteric artery leading to ischemia and atrophy of
the abdominal muscles (1).
• Management includes surgical correction involving either of two modes of closure (2).
– Staged silo repair with delayed closure (spring-loaded versus stitched). Spring-loaded silo
can be placed at the bedside, without the need for general anesthesia, whereas the
stitched silo requires placement in the operating room. Delayed closure in the operating
room occurs once abdominal contents are successfully reduced (2–7 days).
– Primary closure can lead to ventilatory compromise, impede venous return, or cause
aortocaval compression secondary to increased intra-abdominal pressure from direct
compression (abdominal compartment syndrome).
Position
Supine
Incision
Midline closure of present defect
Approximate Time
Dependent on the size of the defect; ∼2 hours
EBL Expected
Dependent on the extent of adhesions
Hospital Stay
Approximately 45 days (2)
Ventilator with pressure control (PC) capability and spirometry
EPIDEMIOLOGY
Incidence
• Approximately 4/10,000 births
• Increased risk associated with decreasing maternal age; greatest in women <20 years of age
(1).
Prevalence
The male to female ratio is 1.5:1.
Morbidity
• Infants with gastroschisis experience significant delays in starting and reaching full feeding
support and may require prolonged total parenteral nutrition (TPN) support (3)[C].
– Extensive intestinal resection may result in short-gut syndrome.
– Constriction of mesentery may cause intestinal atresia and decreased absorptive capacity
of the gut.
– Closed loop obstruction from volvulus or malrotation of the midgut.
Mortality
Current survival appears to be >85%. Postponed surgical management and the develop of
abdominal compartment syndrome are associated with a worsened prognosis (4)[C].
• Fluid and heat loss are a primary focus. It can be minimized by using a warm, moist, sterile
saline-soaked gauze or plastic bowel bag as well as ensuring a neutral thermal environment.
• Extruded bowel is susceptible to infection, so broad spectrum antibiotics should be started.
• Ventilatory compromise may be present prior to repair secondary to prematurity, decreased
FRC from impaired diaphragm excursion during reduction in extruded bowel, and during
primary closure.
• Additionally a primary closure can present as an “abdominal compartment syndrome” and
care must be taken to prevent this devastating complication.
SYMPTOMS
• Acid–base status should be closely monitored; respiratory compromise can occur secondary
to the defect
• Gastroesophageal reflux is not uncommon.
History
• Defect is typically identified on the prenatal ultrasound.
• Malabsorption and intestinal fixation (secondary to chronic exposure to amniotic fluid) may
accompany the abnormality.
• Non-GI abnormalities are uncommon.
• Need for preoperative intubation is dependent on respiratory and acid–base status and
degree of prematurity.
Signs/Physical Exam
• Defect typically to the right of the umbilicus and measures <5 cm
• Intestine may show varying degrees of inflammation and edema. This is dependent on the
magnitude of ischemic injury caused by mesenteric compression and amniotic fluid
exposure (implications include fluid losses and increased bleeding).
• Observe for obvious signs of hypovolemia.
MEDICATIONS
• Broad spectrum antibiotics
• Histamine-2 (H2) receptor blockade
• TPN
Labs/Studies
• CBC
• Electrolytes
• Type and screen; depending on starting hematocrit and comorbidities, consider
crossmatching 10–20 cc/kg.
• Arterial blood gas (ABG)
• CXR
• Echocardiogram
• Rare, but may be related to prematurity.
• Cardiac anomalies (most commonly PDA, ASD, VSD) present in ∼4% of infants (5)[C].
TREATMENT
Premedications
Not anticipated
• Need for continued postoperative intubation
• Transfusion unlikely secondary to repair, but if comorbidities increase likelihood, risks of
transfusions should be discussed.
Broad spectrum antibiotics are used to prevent peritoneal cavity contamination.
INTRAOPERATIVE CARE
• General anesthesia for primary closure
• Sedation can be administered in the neonatal intensive care unit (NICU) in intubated
patients (ketamine and/or fentanyl, midazolam) for abdominal reduction via a silo device
• Neuraxial technique (epidural or caudal catheter) has been described for aiding with
reduction of extruded bowel; it may also allow for early extubation in patients with small
defects. May not be necessary for patients who will remain intubated and sedated for
several days postoperatively.
Monitors
• Standard ASA monitors with a pulse oximeter above and below the diaphragm to assess
lower extremity perfusion with abdominal closure.
• Consider arterial line for serial ABGs to assess potential abdominal compartment syndrome.
• Foley catheter for fluid resuscitation assessment.
• Surgical (tunneled) central line placement may be considered for future prolonged TPN
administration. Additionally, it allows for monitoring of central venous pressures that may
guide fluid management and assure adequate venous return once the abdomen is closed.
• If no central access will be placed, adequate IV access (at minimum, one well running IV)
must be established prior to the start of surgery.
• Umbilical arterial line or venous line may be placed in the NICU to aid with BP monitoring
and volume resuscitation. However, they may need to be removed during abdominal closure
if it is in the surgical field. Preoperative discussion with surgeons is warranted.
• Decompression of the stomach with suctioning via an orogastric or nasogastric (NG) tube
may decrease the risk of aspiration. Additionally, decreasing bowel distention can increase
the likelihood of successful abdominal closure.
• Rapid sequence IV induction is indicated. Care with (or avoidance of, if possible) bag mask
ventilation if possible. Drugs should be tailored to the patient’s underlying conditions; those
without significant comorbidities and who are adequately volume resuscitated may tolerate
a propofol induction. Alternatively, etomidate or ketamine and/or narcotics may be
appropriate when cardiac anomalies are present. Rocuronium or succinylcholine may be
used (potential risk factors for succinylcholine must be considered prior to use).
• Age/size appropriate ETT should be placed; the leak should not prevent the ability to
adequately ventilate the patient once the bowel is reduced and the abdomen is closed.
Appropriate leak will depend on the size of the defect and underlying lung disease (20–30
mm Hg may be required). A low profile cuffed ETT may be considered to allow for dynamic
changes in ventilatory pressures required but care must be taken to maintain the leak below
30 mm Hg (pressure at which mucosa may be prone to ischemia).
Maintenance
• Fresh gas. Avoid nitrous oxide as it can distend bowel. The oxygen-air mixture should be
titrated to maintain the SpO2 in the mid-90s to decrease the risk of retinopathy of
prematurity.
• MAC. Unlike infants who have a higher MAC requirement than adults, neonates have a
decreased (up to 25% less) MAC requirement.
• Opioid technique with judicious use of volatile anesthetics (to avoid hypotension) is
indicated. High dose narcotics, such as fentanyl (5–15 μg/kg) can be titrated as tolerated for
intraoperative maintenance, especially when extubation is not planned.
• Muscle relaxation facilitates closure of the abdomen.
• Ventilation parameters. Monitor peak inspiratory pressures (PIP) and tidal volumes (TV)
throughout abdominal closure. An increase in PIPs or a decrease in TVs or SpO2% may
mean abdominal closure will not be tolerated. Maximum allowable PIP is dependent on
underlying lung disease, degree of prematurity, and need to avoid barotrauma; but in
general, pressures >25 mm Hg should be avoided. Additionally, high frequency oscillatory
ventilation may be required if conventional ventilation is inadequate. Serial ABGs may
guide management.
– Fluid requirements will be high. Up to 10–200 mL/kg/hr may be required during primary
closure and is dependent on the level of bowel exposure.
– Use isotonic fluids or colloid (albumin) for volume resuscitation.
– Warm all fluids and maintain body temperature with forced air warmer and radiant
heater. Additionally, room should be warmed to (70–72°F) prior to start of case.
– Run TPN or dextrose containing IV fluids (usually D10) at ½ maintenance to avoid
intraoperative hyperglycemia. Blood sugar should be monitored closely.
• Intra-abdominal pressure monitoring via intragastric (NG tube) or intravesicle catheter
(Foley) can guide surgeons on whether abdominal closure can be tolerated; should be
maintained <20 mm Hg. Decreased preload secondary to compression of the inferior vena
cava or decreased urine output secondary to diminished renal blood flow can provide
further evidence of increased intra-abdominal pressure.
• Postoperative ventilation is common in most neonates for 24–48 hours, especially for larger
defects.
• Immediate postoperative extubation may be considered for small defects. Also consider the
size of the patient, associated defects, hemodynamic stability, and intraoperative events.
POSTOPERATIVE CARE
BED ACUITY
NICU. Postoperative ventilation is common in most neonates for 24–48 hours.
ANALGESIA
• Ketamine and/or opioid for staged NICU closure
• Opioid +/– benzodiazepine following primary closure
• Epidural/caudal catheters may be appropriate (institution dependent)
COMPLICATIONS
• Infection – GI (necrotizing enterocolitis), ventilatory, wound, etc.
• Prolonged postoperative ileus
• Abdominal compartment syndrome, which may impede splanchnic blood flow, resulting in
intestinal ischemia or necrosis.
• Hepatotoxicity secondary to prolonged parenteral nutrition.
• Hypertension secondary to decreased renal perfusion.
PROGNOSIS
Long-term bowel complications are not uncommon (e.g., malrotation, volvulus, small bowel
obstruction, gastroesophageal reflux) (2,3).
REFERENCES
1. Feldkamp et al. Development of gastroschisis: Review of hypotheses, a novel hypothesis,
and implications for research. Am J Med Genet Part A. 2007;143:639–652.
2. Banyard D, Ramones T, Phillips SE, et al. Method to our madness: An 18-year retrospective
analysis on gastroschisis closure. J Pediatr Surg. 2010;45(3):579–584.
3. Kitchanan S, Patole SK, Muller R, et al. Neonatal outcome of gastroschisis and exomphalos:
A 10-year review. J. Paediatr Child Health. 2000;36:428–430.
4. Tasai MH, Huang HR, Chu SM, et al. Clinical features of newborns with gastroschsis and
outcomes of different initial interventions: Primary closure versus staged repair. Pediatr
Neonatol. 2010;51(6):320–325.
5. Kunz LH, Gilbert WM, Towner DR. Increased incidence of cardiac anomalies in pregnancies
complicated by gastroschisis. Am J Obstet Gynecol. 2005;193:1248–1252.
• Omphalocele
CODES
ICD9
756.73 Gastroschisis
ICD10
Q79.3 Gastroschisis
CLINICAL PEARLS
• Unlike omphaloceles, gastroschisis is usually an isolated defect.
• Fluid resuscitation is a key element of anesthetic management, as the exposed bowel has the
potential for significant insensible fluid losses.
• Careful monitoring for changes in respiratory function during closure is mandated.
GERIATRIC PHYSIOLOGY
Stephen Dechter, DO
Bruce Vrooman, MD
BASICS
DESCRIPTION
• Aging correlates with a physiologic decline and increase in prevalence of disease.
• Care of geriatric patients is growing in number and need and will continue to do so; it is
important for the anesthesia provider to understand the accompanying
physiology/pathophysiology that results with age.
• Neurologic system
– Cerebral blood flow (CBF) and volume decrease due to a combination of reduced cerebral
metabolism and cerebral vascular changes including atherosclerosis, decreased vessel wall
compliance, and vessel narrowing.
– Short-term memory, learning, and information processing decrease.
– Temperature regulation is impaired; there is decreased autonomic vasomotor control and
sensitivity to changes.
• Cardiovascular system
– Systolic blood pressure (SBP) and diastolic blood pressure (DBP) increase due to decreased
atrial and vessel elasticity (1)[A]; there is a resultant widened pulse pressure.
– Atrial contraction becomes increasingly important due to impaired diastolic filling (2)[A].
– Resting and maximum heart rate (HR) decrease due to a reduction in beta-adrenergic
responsiveness and cardiac contractility; the general rule is maximum HR = 220–age.
– Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume
(LVESV), and stroke volume increase due to myocardial structural changes (contractility,
hypertrophy, and enlargement).
– Resting and exercise cardiac output (CO) remain normal due to Frank–Starling
mechanisms (2)[A].
– Valves thicken and calcify
– Maximal oxygen consumption (VO2) decreases due to loss of body muscle mass, vascular
structural changes, and gas exchange systems (3)[A].
– Baroreflexes become impaired due to reduced arterial compliance leading to impaired
mechanical transduction of arterial pressure changes and reduced cardio-vagal neural
outflow.
• Pulmonary system
– Oxygen gas exchange is impaired due to increased ventilation/perfusion imbalances; lower
PaO2 baseline values and normal SpO2% are seen.
– Carbon dioxide excretion is normal
– Hypercapnic and hypoxic respiratory responses are impaired; there is also a reduced
ability to handle congestive heart failure (CHF), infection, and obstruction.
– Total lung capacity (TLC) is normal (4)[A]; residual volume (RV) can increase by 50%;
vital capacity (VC) can decrease by 50–75% due to decreased chest wall compliance
combined with air trapping.
– Functional residual capacity (FRC) increases due to stiffer, ossified thoraxes by ~3% per
decade (decreased compliance, increased outward forces. Closing volume (CV), however,
decreases to a greater extent and leads to airway closure, atelectasis, and V/Q shunting.
– FEV1 decreases by 20–40 mL/year; forced vital capacity (FVC) decreases in males
>females; results in increased breathing energy expenditure (up to 20%) due to changes
in small peripheral airways and reduced chest wall compliance.
– Respiratory muscle strength, cough, and ciliary function decrease.
• Hepatic system
– Hepatic mass and blood flow decrease due to cell loss and reduction in the number of
mitochondria with a compensatory increase in hepatocyte and mitochondrial size to
preserve function.
– Drug metabolism decreases
• GI system
– Esophageal function and emptying decrease
– Gastric motility, acid secretions, and absorption decrease (calcium, iron, zinc, folic acid,
B12)
– Colonic muscle contraction and rectal perception decrease
• Renal system
– Renal mass, tubular mass, renal blood flow, creatinine clearance, and glomerular filtration
rate decrease (1% per year after age 30) due to atrophy of afferent and efferent arterioles,
generalized sclerosis, and comorbid disease (primary renal failure, atherosclerosis).
– Drug clearance decreases
– Sodium, potassium, hydrogen ion concentration, and vascular volume usually have no
change.
• Immunologic system
– Risk of infection increases due to impaired immune function secondary to decreased
functional competence of NK cells, granulocytes, macrophages, impaired phagocytosis and
chemotaxis-impaired cytokine production, T and B cell deficits, and increased number of
autoantibodies.
• Endocrine system
– Insulin resistance increases; insulin secretion becomes impaired; FBS and cortisol remain
normal.
– Thyroid hormone regulation decreases; T4 stays normal.
– Testosterone, estrogen, and growth hormone decrease.
• Musculoskeletal system
– Muscle mass, strength, and power decrease
– Bone mineral density decreases
– The increase in weight and decrease in body water/lean body mass lead to an increase in
body fat%. Fat-soluble drugs (fentanyl, benzodiazepines) have an increased volume of
distribution (VD). Water-soluble drugs (ethanol, digoxin, gentamicin) have a decreased VD
(5)[A].
• Integumentary system
– Connective tissue elasticity, moisture, and skin sensation decrease.
– Collagen cross-linking increases and causes tissue fragility. This increases the risk of
pressure ulcers and skin breakdown.
ANATOMY
• Brain weight: 15% decrease
• Blood volume contraction: 20–30%
• Liver volume: 24% decrease
• Renal mass: 20% decrease
• Neurologic diseases
– Cerebrovascular accident (CVA) risk doubles each decade after age 55 (10-year probability
of CVA in men is 5.9% at age 55, 13.7% at age 70, and 22.3% at age 80).
– Dementias may be the result of genetic, autoimmune, infectious, vascular, or traumatic
brain/neuronal damage. 10% of those aged 65 and older and 20% of those aged 80 and
over have some form of dementia.
– Increased incidence of glaucoma, cataracts, macular degeneration, and presbyopia. 4% of
those aged 65 years and 16% of those aged 85 have visual impairment.
– Hearing loss may cause social isolation and contribute to paranoid ideation. 20% of those
aged 50 and 90% of those aged 80 have hearing loss.
• Cardiovascular diseases
– Hypertension (HTN) is often treated with antihypertensives. These drugs can have side
effects including orthostasis, urinary frequency, dehydration, and fatigue. Prevalence is
44% at age 40 and 65% at age 70.
– Arrhythmias. Treatment with antiarrhythmic medications, anticoagulation, and
implantable pacemakers (5)[A]. Prevalence is 2% at age 60 and 10% at age 80.
– Coronary artery disease (CAD) from plaque/cholesterol buildup can decrease coronary
blood flow. Symptoms include substernal chest pain (33%), dyspnea (20%), weakness,
malaise, worsening CHF, syncope, arrhythmia, or confusion. Prevalence is 20% at age 55
and 30% at age 75.
– CHF symptoms include dyspnea and chest pain. Treatments with digoxin and diuretics
have anesthetic implications. Prevalence is 22% at age 60 and 70% at age 80.
– Valvular disease from thickened and calcified valve tissue may develop. Symptoms range
from asymptomatic to dyspnea to fatigue. Treatment includes anticoagulation and
valvular replacement. Prevalence is 40% at age 75–85 for mild disease and 13% for severe
disease.
• Pulmonary diseases
– Obstructive sleep apnea (OSA) from blockage of the soft palate during sleep can result in
increased work of the diaphragm/lungs and brief apneic episodes. Symptoms include
fatigue, snoring, headaches, and HTN. Prevalence of sleep-disordered breathing is up to
30% in the elderly.
– Chronic obstructive pulmonary disease (COPD) may result from years of smoking.
Prevalence is 20–40% in those aged >65.
– Respiratory failure from coexisting disease (pneumonia, left ventricular failure) is more
likely. Increased work of breathing on top of their baseline may increase.
– Extubation may be delayed due to decreased ventilatory responses to hypoxia and
hypercarbia, maximal breathing capacity, VC, cough strength, and clearance of secretions,
as well as increased air trapping and V/Q mismatch.
• Immunologic diseases
– Cancer increases with age due to uninhibited cell growth with tumor formation and/or
distant metastasis. Symptoms include weight loss, fever, chills, night sweats, and new
onset back pain. Prevalence is 1% at age 50 and 4% at age 85.
– Infectious response may be impaired.
• Endocrine diseases
– Diabetes is associated with large and small vessel disease. Prevalence is 10% at age 50 and
20% over age 75.
• Musculoskeletal diseases
– Osteoarthritis increases presentation to the OR for joint replacements. Prevalence
increases from 27% at age 70 to 44% at age 80.
– Osteoporosis may result in an increased incidence of fractures. Prevalence in women over
50 is 4% and 44% at 80.
• Neurologic relevance. Postoperative cognitive dysfunction (POCD) is common in the elderly.
At 3 months after surgery, the incidence of POCD was 9.9% in patients >60 years old
versus 2.8% for the control group.
• Cardiac relevance. Increased risk of arrhythmias, HTN, hypotension; induction time can be
affected (inhalational agents can have an increased onset, and intravenous agents a
decreased onset time).
• Pulmonary relevance. Increased risk of pulmonary edema, pneumonia, aspiration (impaired
cough and mucociliary clearance).
• Hepatic relevance. Impaired metabolism requires a decreased dosage of induction agents
(e.g., propofol and inhalational agents); results in prolonged effects of opioids,
benzodiazepines, local anesthetics, and neuromuscular blocking drugs.
• Renal relevance. Low muscle mass decreases serum creatinine values. A “normal” value may
be abnormal. Drug excretion may be impaired resulting in prolonged half-life (t1/2); fluid
balance may be impaired.
• GI relevance. Increased risk of aspiration due to impaired gastric emptying and esophageal
motility.
• Musculoskeletal relevance. Weakness, prolonged recovery, poor mobility, increased risk of
DVT, pneumonia, and decubitus ulcers.
See Table
REFERENCE
1. Franklin SS, Gustin W 4th, Wong ND, et al. Hemodynamic patterns of age-related changes
in blood pressure. The Framingham Heart Study. Circulation. 1997;96(1):308–315.
2. Lakatta EG, Levy D. Arterial and cardiac aging: Major shareholders in cardiovascular
disease enterprises. Circulation. 2003;107(2):346–354.
3. Fleg JL, Lakatta EG. Role of muscle loss in the age-associated reduction in VO2 Max. J Appl
Physiol. 1988;65(3):1147–1151.
4. Janssens JP, Pache JC, Nicod LP. Physiological changes in respiratory function associated
with aging. Eur Respir J. 1999;13(1):197–204.
5. Mangoni AA, Jackson SHD. Age-related changes in pharmacokinetics and
pharmacodynamics: Basic principles and practical applications. Br J Clin Pharm.
2004;57(1):6–14.
6. Qaseem A, Snow V, Shekelle P. Pharmacologic treatment of low bone density or
osteoporosis to prevent fractures: A clinical practice guideline from the American College
of Physicians. Ann Intern Med. 2008;149(6):404–415.
ADDITIONAL READING
• Abass IB. The biology and physiology of aging. West J Med. 1990;153(6):641–645.
• Kitzman DW, Diastolic heart failure in the elderly. Heart Fail Rev. 2002;7(1):17–27.
• U.S. Census Bureau. http://www.census.gov/
• Respiratory physiology
CLINICAL PEARLS
• Increased perioperative mortality is due to multisystem changes related to aging.
• Caution is warranted with induction agents and medications due to impaired metabolism
(renal, pulmonary, cardiac, hematologic, hepatic) that can lead to overdose and death.
• Monitor body temperature carefully due to impaired thermoregulation.
• Careful monitoring of fluid balance, electrolytes, and oxygen saturation is necessary.
• Caution with use of NSAIDs (renal failure, GI side effects) and opioids (pulmonary
depression, sedation, AMS).
GESTATIONAL DIABETES
Peter Drocton, MD
Mark Zakowski, MD
BASICS
DESCRIPTION
• Diabetes mellitus (DM) is a common metabolic disorder.
– Type 1 DM is primarily characterized by insulin deficiency.
– Type 2 DM is primarily characterized by insulin resistance.
• Gestational diabetes mellitus (GDM) implies that the first occurrence is during pregnancy
and brought on by the hormonal changes of pregnancy.
• Pregestational DM occurs before pregnancy
• Good glycemic control has been shown to reduce perinatal complications; 60–95 mg/dL has
been used as a target range.
EPIDEMIOLOGY
Prevalence
Gestational diabetes has an ∼7% incidence; it is increased among certain ethnic groups
(Latino, African-American)
Prevalence
Not available
Morbidity
• Maternal morbidity associated with
– Diabetic ketoacidosis (DKA) in ∼1–2% of diabetic pregnancies, related to Type I DM
– Severe hypoglycemia occurs in ∼50% of patients, higher incidence in Type 1 DM
– Pregnancy-induced hypertension (PIH) and preeclampsia occur with greater frequency in
parturients with GDM
– Progression of end-organ damage including retinopathy, nephropathy, and neuropathy
– Autonomic cardiovascular dysfunction
• Neonatal morbidity characterized by
– Hypoglycemia
– Hypocalcemia
– Respiratory distress syndrome from delayed release of surfactant in lungs
– Macrosomia with associated shoulder dystocia and birth injuries
– Birth defects (especially with pregestational DM)
Mortality
Pregestational DM perinatal mortality rate ∼5%
• Etiology of GDM: Presumed to be due to hormonal changes of pregnancy in order to spare
glucose for fetal utilization.
• Risk factors: Obesity, advanced maternal age, previous history of GDM, family history of
DM.
• Normal pregnancy results in
– Decreased insulin sensitivity by ∼50%.
– Increased insulin requirements due to increases in anti-insulin hormones of pregnancy.
Human placental lactogen (HPL) has a growth hormone (GH)-like effect that increases
glucose availability for the fetus.
• Fetus
– Maternal insulin does not cross the placenta
– Fatty acids cannot be utilized for energy until the 3rd trimester
• Gestational diabetes
– Impaired beta-cell function results in insufficient insulin release
– Insulin sensitivity is further decreased, compared to non-GDM pregnancies
• Impaired glucose control can result in placental degeneration and calcification
• Pain can elevate cortisol levels and further worsen insulin sensitivity
• Anticipate added risks with general anesthesia such as
– Difficult intubation due to stiff-joint syndrome (generally Class C)
– Aspiration from diabetic gastroparesis
– Autonomic cardiovascular dysfunction and hemodynamic instability
• Regional anesthesia with either spinal or epidural has been shown to be effective and
preferred to general anesthesia. Vasopressor therapy, however, may be needed following
bolus doses.
• Delivery complications include unexplained fetal demise with increasing gestational age.
Thus, it is suggested that patients with GDM should be delivered by 40 weeks;
pregestational diabetics should be delivered by 39 weeks.
SYMPTOMS
If undiagnosed, the patient may complain of increased thirst, frequent urination, blurry
vision, or orthostatic symptoms
History
• Assess glycemic control, episodes of hyperglycemia, and hypoglycemia
• Evidence of cardiovascular disease, autonomic dysfunction, or other coexisting morbidities
including neuropathies
Signs/Physical Exam
• Hypertension may be present secondary to preeclampsia/PIH.
• General assessment of cardiac and pulmonary status
• Brief neurologic exam to look for peripheral nerve palsies and neuropathies
• “Prayer sign” – inability to closely approximate the palms and fingers when hands placed
together may imply stiff-joint syndrome and potential difficult intubation due to poor neck
extension.
TREATMENT HISTORY
Fasting glucose >105 g often requires insulin therapy if diet and exercise fail to control the
condition.
MEDICATIONS
• Oral hyperglycemic agents (glyburide) may be used.
• Metformin is not generally used, but pregestational DM patients may have continued to take
it.
• Insulin regimen should be reviewed with consideration for insulin infusion.
• Pregestational DM patients have a 50% increase in insulin requirement by term.
• Anticipate sharply decreased insulin needs soon after delivery (as much as 15% on the first
postpartum day).
Labs/Studies
• Typically diagnosed on screening at 24–28 weeks gestation, either via fasting glucose (>126
mg) or oral glucose tolerance test (OGTT) (>200 mg at 2 hours).
• Frequent glucose measurements
• Hemoglobin (Hgb) A1C: 4–6% normal, >7% indicates impaired control.
• Platelets, coagulation factors, fibrinogen, and proteinuria in cases with suspected
PIH/preeclampsia.
• Fetal status followed by more frequent nonstress tests and biophysical profile
• Fetal lung maturity testing by amniocentesis for indications of maturity:
Lecthicin:sphingomyelin ratio >2, presence of phosphatidyl glycerol (component of
surfactant) and Lamellar bodies (surfactant vacuoles).
• Cardiovascular effects including hypertension, heart disease, and renal disease
• Neuropathy
• Proliferative retinopathy
• Delayed fetal production of surfactant
• Elective Cesarean section without documentation of fetal lung maturity at <39 weeks
gestation
• Moderate-to-severe hyperglycemia or hypoglycemia if fetal conditions allow time to treat
and optimize.
CLASSIFICATIONS
• White classification during pregnancy:
– Class A1: Gestational, diet controlled
– Class A2: Gestational, on insulin or oral antihyperglycemic
• White classification for pre-existing diabetes
– Class B: Diagnosis of DM for <10 years
– Class C: Diagnosis of DM for >10 years
– Class R: DM complicated by retinopathy
– Class F: DM complicated by nephropathy
– Class T: DM with renal transplant
TREATMENT
Premedications
• Antacids (sodium bicitrate) and promotility agents (metoclopramide)
• Adequate fluid resuscitation prior to induction of general or regional anesthesia
INTRAOPERATIVE CARE
Maternal safety is improved with regional anesthesia
• Assessment for, and anticipation of, stiff-joint syndrome with reduced neck movement
resulting in difficult intubation (Prayer sign)
• Cardiovascular instability should be monitored for and may require greater vasopressor use.
Maintenance
• During labor, an insulin infusion may be utilized (0.8–1.0 units/kg) to keep glucose 70–90
mg/dL (tight control) or 80–100 mg/dL. Glucose infusion 5–10 g/hour may be needed if
NPO
• Carefully pad extremities during Cesarean sections; diabetics are more prone to nerve
injuries/neuropathies
• Judicious fluid administration in patients with cardiovascular disease or preeclampsia
(increased risk of pulmonary edema)
In intubated patients, consider a leak test prior to extubation. Increased airway edema may be
present from excessive fluid administration.
FOLLOW-UP
BED ACUITY
• Higher nursing acuity for insulin infusions
• Coexisting moderate-to-severe maternal disease may warrant increased nursing care.
• Continued glucose monitoring through the peripartum period
• Can typically discontinue insulin infusion postdelivery
COMPLICATIONS
• Maternal
– Hyperosmolar hyperglycemic state
– Diabetic ketoacidosis
– Subsequent pregnancies have a 40–50% risk of GDM
– Development of type 2 DM (60%)
– Increased risk for infection (impaired WBC effectiveness)
• Neonatal
– Respiratory distress syndrome requiring supplemental oxygen or intubation
– Hypoglycemia requiring careful monitoring
– Increased risk of developing GDM (females)
REFERENCES
1. ridijian G,Benjamin TD. Update on gestational diabetes. Obstet Gynecol Clin N Am.
2010;37:255–267.
2. Pani N, Mishra SB, Rath SK. Diabetic parturient – Anaesthetic implications. Indian J
Anaesth. 2010;54:387–393.
ADDITIONAL READING
• American Diabetes Association
• American Congress of Obstetricians and Gynecologists Practice Bulletin 30 Gestational
Diabetes, Practice Bulletin 60 Pregestational Diabetes
• World Health Organization
• Pregnancy-induced hypertension
CODES
ICD9
648.83 Abnormal glucose tolerance of mother, antepartum condition or complication
ICD10
O24.419 Gestational diabetes mellitus in pregnancy, unsp control
CLINICAL PEARLS
• Avoidance of maternal hyperglycemia during pregnancy and labor allows for better
maternal and neonatal outcomes.
• Maintain tight glucose control; may need insulin and glucose infusion during labor.
• PIH and preeclampsia are twice as likely to occur in the setting of GDM
• Prayer sign can predict stiff-joint syndrome and the possibility of a difficult intubation.
• Insulin requirement in the postpartum period decreases and requires constant vigilance.
• Routinely check newborn glucose and evidence of hyperbilirubinemia.
GLOMERULAR FILTRATION RATE (GFR)
BASICS
DESCRIPTION
• Glomerular filtration rate (GFR) is widely considered to be the best overall index of renal
function.
• GFR is the rate (volume per unit time) that plasma fluid is filtered by functioning nephrons
and is used to detect, grade, and follow the course of kidney disease. Patients with a low
GFR have a greater likelihood of the following:
– Significant comorbidities.
– Intraoperative and postoperative complications such as worsening of renal failure,
cardiovascular complications, electrolyte disturbances, etc.
• Despite its utility, GFR is not easily measured and attained. To that extent, it is often
approximated by creatinine clearance (CCr) or other equations that estimate GFR based on
serum creatinine (SCr), each with its own pros and cons.
• The kidneys receive ∼20–30% of the cardiac output.
• Ultrafiltration:
– Blood flows from the afferent arteriole, through the highly permeable renal glomerular
capillaries, and out the efferent arteriole.
– Plasma is filtered through these capillaries into the surrounding Bowman’s capsule. The
ultrafiltrate then passes through the proximal tubule, loop of Henle, distal tubule, and
collecting ducts while being subjected to tubular reabsorption and secretion, prior to
being excreted as urine (the majority of glomerular filtrate is reabsorbed and returned to
the systemic circulation).
– The diameter of efferent arterioles is smaller than that of afferent arterioles, leading to a
pressure gradient that is countered by osmotic and hydrostatic pressures and drives
ultrafiltration.
• Regulation of GFR:
– Renal blood flow (RBF) and GFR are maintained via autoregulation across a wide range of
mean arterial pressures (∼70–170 mm Hg).
– Outside of this autoregulated range, GFR is dependent on systemic BP. Renal
autoregulation can be impaired by chronic hypertension (HTN), hyperlipidemia, obesity,
and insulin resistance.
– The ratio of GFR:renal plasma flow (RPF) is the filtration fraction (FF), and under normal
circumstances is ∼20%. Afferent arteriolar vasodilation or efferent arteriolar
vasoconstriction will increase the FF to maintain a constant GFR in the setting of a
decreased RPF.
– GFR decreases by increased renal tubular flow (tubuloglomerular feedback).
– GFR decreases by sympathetic stimulation, via renin-angiotensin system-mediated
constriction of renal afferent arterioles.
• GFR measurement:
– GFR can be calculated by measuring endogenous (e.g., creatinine) or exogenous (e.g.,
inulin) substances that have steady-state levels in blood, are freely filtered by glomeruli,
and are not (or only minimally) secreted or reabsorbed in the renal tubules. GFR = (urine
concentration × urine flow)/(plasma concentration)
– GFR can be approximated by CCr, although this will generally overestimate GFR by 5–
20% due to small amounts of tubular creatinine secretion. Tubular secretion of creatinine
can be competitively inhibited by cimetidine.
– CCr is best measured with a 24-hour urine collection and spot steady-state serum
measurements, but this is logistically challenging.
– Creatinine is produced by the breakdown of creatine in skeletal muscle. Increased muscle
mass (e.g., males, African-Americans) will lead to higher SCr at any level of CCr.
Conversely, decreased muscle mass (malnutrition, paraplegia) will result in lower
creatinine generation.
– Numerous equations (see below “Equations”) have been developed that estimate CCr or
GFR, based on factors including SCr, age, race, gender, height, weight, BUN, serum
albumin, etc.
– Most labs have recently changed SCr assays from an older alkaline picrate (Jaffe)
chromographic technique to a newer enzymatic technique that iscalibrated to isotope
dilution mass spectroscopy (IDMS). This results in ~5% lower SCr values, leading to
adjustments in previous GFR estimation formulas.
– A more recently investigated endogenous protein called cystatin C may offer improved
GFR estimation compared to creatinine, but most estimation formulae still rely on SCr.
• Normal values:
– Normal GFR for adults is 110–130 mL/min per 1.73 m2. (GFR is usually reported adjusted
for body surface area because renal function is proportional to kidney size, which in turn
is proportional to body surface area; 1.73 m2 is considered the normal mean for healthy
young adults.)
– Premature infants have correspondingly lower GFR.
• Slightly higher for men versus women
• GFR for full-term neonates is 15–40% that of adult values. GFR doubles over the first 2
weeks postnatally and then continues to increase slowly until reaching adult value at 1–2
years.
• Use Schwartz formula for GFR estimation in pediatric patients. (The Cockcroft–Gault,
Modification of Diet in Renal Disease [MDRD], and Chronic Kidney Disease Epidemiology
Collaboration [CKD-EPI] formulae were derived and validated using adult populations.)
• Elderly patients have lower muscle mass, which generates less steady-state creatinine, so
their SCr can be deceptively low (i.e., a SCr that is normal for younger adults may reflect a
significantly impaired GFR in the elderly).
• In the elderly, RBF and GFR are decreased due to vascular sclerosis and renal parenchyma
atrophy.
• GFR < 60 mL/min/1.73 m2 defines chronic kidney disease.
• GFR can decrease by half (e.g., 120 to 60 mL/min/1.73 m2) before becoming clinically
apparent (due to large functional kidney reserves).
• The prevalence of complications of chronic kidney disease increases significantly below 60
mL/min/1.73 m2.
• Chronic kidney disease staging:
– Stage 1: GFR > 90 mL/min/1.73 m2 (kidney damage with normal GFR)
– Stage 2: GFR 60–89 (mild)
– Stage 3: GFR 30–59 (moderate)
– Stage 4: GFR 15–29 (severe)
– Stage 5: GFR < 15 (kidney failure; on dialysis)
• Decreased preoperative renal function is a strong predictor for intraoperative and
postoperative acute renal failure.
• General anesthesia and, to a lesser extent, neuraxial anesthesia mildly and reversibly impair
GFR.
• Volatile anesthetic agents produce a dose-dependent decrease in RBF and GFR (and
consequently urine output), an effect likely secondary to their negative impact on cardiac
output and systemic BP. Volatiles do not directly affect autoregulation.
• Chronic renal failure (CRF) can contribute to the following:
– Anemia (decreased erythropoietin)
– Electrolyte disturbances (e.g., hyperkalemia)
– Heart disease (HTN, coronary artery disease, CAD)
– Coagulopathy (decreased platelet function)
– Hypoalbuminemia
– Increased gastric volumes
– Increased risk of infectious complications (e.g., sepsis)
• CRF patients are often diabetic.
• CRF patients may have arteriovenous (AV) fistulas that limit the placement of IV lines,
arterial lines, and BP cuffs.
• Perioperative management:
– Drug doses must be adjusted for those drugs that have significant renal elimination,
secretion, or metabolism such as antibiotics, some muscle relaxants (tubocurarine,
pancuronium), H2-receptor blockers, morphine and meperidine metabolites, contrast
agents, etc.
– Maintain a low threshold for the placement of an arterial line (due to cardiac
comorbidities and for arterial blood gases, ABGs) and central venous access (due to
volume disturbances).
– Carefully assess volume status intraoperatively and monitor fluid intake and urine output.
– Monitor electrolytes and consider replacement as needed.
EQUATIONS
Online calculators for each of these formulae are widely available (e.g., www.kidney.org/gfr).
• Cockcroft–Gault formula (1):
– Published in 1976
– Estimates CCr
– CCr = (140–Age) × Weight × (0.85 if Female)/(72 × SCr); where CCr is measured as
mL/min, Age in years, Weight in kg, and SCr in mg/dL.
– Does not account for race
– Does not adjust for body surface area
– Clearly demonstrates the dependence of CCr on age
– Most drug-dosing guidelines for impaired renal function are based on Cockcroft–Gault
estimates
• 4-variable MDRD formula (2):
– Estimates GFR
– Based on patients enrolled in MDRD study
– GFR = Const × (SCr)−1.154 × (Age)−0.203 × (0.742 if Female) × (1.210 if African-
American); where Const = 175 if the lab calibrates SCr to IDMS standard, or 186 if not;
GFR is measured in mL/min/1.73 m2; Age in years; SCr in mg/dL.
– Tends to underestimate GFR at higher (more normal) values above 60 mL/min/1.73 m2
– Does not adjust for body mass; will underestimate GFR for heavy patients
• 6-variable MDRD formula (3):
– Estimates GFR
– Expanded version of MDRD formula
– GFR = Const × (SCr)−0.999 × (Age)−0.176 × (0.762 if Female) × (1.18 if African-
American) × (BUN)−0.170 × (Albumin)+0.318; where Const = 160 if the lab calibrates
SCr to IDMS standard, or 170 if not; GFR is measured in mL/min/1.73 m2; Age in yrs; SCr
in mg/dL.
– Tends to underestimate GFR at higher (more normal) values
– Does not adjust for body mass; will underestimate GFR for heavy patients
• CKD-EPI formula (4):
– Estimates GFR
– Developed by CKD-EPI in effort to improve on existing MDRD models
– GFR = 141 × min(SCr/k,1)a × max(SCr/k,1)−1.209 × 0.993Age × (1.018 if Female) ×
(1.159 if African-American); where k is 0.7 for Females and 0.9 for Males; a is −0.329 for
Females and −0.411 for Males; GFR is measured in mL/min/1.73 m2; Age in yrs; SCr in
mg/dL.
– More accurate and less biased than MDRD formulae, especially improved at higher GFRs
• Schwartz pediatric formula (classic) (5):
– Estimates GFR in children
– GFR = k × Height/SCr
– k is 0.33 for premature infants, 0.45 for full-term infants, and 0.55 for children age 1–12
years
– GFR in mL/min/1.73 m2; Height in cm; SCr in mg/dL
• Schwartz pediatric formula (updated) (6):
– GFR = 0.413 × Height/SCr
– Reflects modern IDMS standardized SCr measurements
REFERENCES
1. Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine.
Nephron. 1976;16:31–41.
2. Levey AS, Greene T, Kusek JW, et al. A simplified equation to predict glomerular filtration
rate from serum creatinine (Abstract). J Am Soc Nephrol. 2000;11:155A (A0828).
3. evey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular
filtration rate from serum creatinine: A new prediction equation. Ann Intern Med.
1999;130:461–470.
4. Levey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration
rate. Ann Intern Med. 2009;150:604–612.
5. Schwartz GJ, Haycock GB, Edelmann CM Jr, et al. A simple estimate of glomerular
filtration rate in children derived from body length and plasma creatinine. Pediatrics.
1976;58:259–263.
6. Schwartz GJ, Munoz A, Schneider MF, et al. New equations to estimate GFR in children
with CKD. J Am Soc Nephrol. 2009;20:629–637. www.kidney.org (National Kidney
Foundation) Stevens LA, Coresh J, Greene T, Levey AS. Assessing kidney function –
Measured and estimated glomerular filtration rate. N Engl J Med. 2006;354:2473–2483.
7. K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease. Am J Kidney Dis.
2002;39:S1–S266. Also available at www.kidney.org/professionals/kdoqi.
• Chronic renal failure
• Renal blood flow
• Creatinine clearance
CLINICAL PEARLS
• GFR is considered to be the best overall index of renal function.
• Estimate GFR using well-established, validated models based on SCr values:
• Use CKD-EPI or modified MDRD formulae for clinical GFR estimates.
• Use Cockcroft–Gault formula to estimate GFR for drug-dosing purposes.
• Use modified Schwartz formula for children up to 12 years.
• Patients with low GFR (<60 mL/min/1.73 m2) have significant renal function impairment,
are more likely to have important comorbidities (anemia, volume disturbances, electrolyte
abnormalities, cardiac disease, etc.), and are at increased risk for intraoperative and
postoperative complications.
• Many drugs require reduced doses or dosing intervals (“renal dosing”) in patients with low
GFR.
HEART TRANSPLANT
Charles H. Brown IV, MD
Nanhi Mitter, MD
BASICS
DESCRIPTION
General
• Heart transplant is the gold standard for the treatment of end-stage heart failure. Mechanical
ventricular assist devices may be used as a “bridge to transplant.”
• Indications for cardiac transplant include (1)
– Severe, end stage disease that is refractory to surgical or medical therapy
– NYHA Class III–IV despite maximum therapy
– Compliant, motivated patient <70 years old
– Heterotopic transplant is indicated for severe pulmonary hypertension and extreme
donor/recipient size discrepancy.
• Contraindications for cardiac transplant (1)
– Fixed pulmonary vascular resistance (PVR) >5 Wood units
– Active tobacco, alcohol, or drug use
– Active neoplasm. Oncology consult regarding risk of recurrence for previous neoplasm
– Major debilitating disease
– Patient non-compilance
– Relative contraindications: BMI>30, diabetes with end organ
• Requires full cardiopulmonary bypass; cannula are inserted in the normal fashion (venous
drainage from the IVC and the SVC and return via the aortic canula). Surgeons may use
either a (2)
– Biatrial technique (traditional): The recipient’s ventricles are removed, while leaving the
right and left atrium and great vessels in place. The atrial cuffs of the transplanted heart
are sewn onto the recipient’s.
– Bicaval technique: The recipient’s ventricles and right atrium are excised while the left
atrium and great vessels are left in place. The transplanted IVC and SVC are sewn to the
free edges of the recipient’s SVC and IVC.
Position
Supine-careful attention to padding
Incision
• Sternotomy
• Prepare for possible groin cannulation, especially if previous sternotomy.
Approximate Time
• 6–8 hours. Repeat sternotomy patients require longer dissection time.
• Preparation of the recipient must be carefully timed with donor organ harvest; the
recommended ischemic time is <4 hours.
EBL Expected
• Frequent postbypass coagulopathy requiring antifibrinolytic agents and transfusion of
pRBCs, FFP, platelets, and cryoprecipitate. Coagulopathy generally occurs as a result of
cardiopulmonary bypass, as well as preoperative anticoagulation and liver dysfunction.
• Common surgical complications
– Cardiac dysfunction of left, right, or both ventricles
– Coagulopathy
– Organ failure (kidneys, lungs)
– Arrhythmias
– Rejection
Hospital Stay
Typical ICU discharge by POD #3 but may have protracted hospital course.
• Full cardiopulmonary bypass machine
• Pacing capability
• Availability of ventricular assist devices or intra-aortic balloon pumps
EPIDEMIOLOGY
Incidence
• In the US, ∼2,000 heart transplants are performed each year.
• The most frequent indications are idiopathic or ischemic cardiomyopathy.
Prevalence
Approximately 35% of patients listed for heart transplant will actually receive a transplant.
Morbidity
• Early: Graft failure
• Intermediate: Acute rejection or infection
• Late: Allograft vasculopathy, lymphoproliferative disease, chronic rejection.
Mortality
• 1 year survival: 80–90%
• Additional mortality: 4% per year.
• Approximately 20–30% of patients on the transplant list will die from cardiac causes before
a donor is found.
Maintain and be prepared to aggressively support an adequate rhythm, preload, contractility,
and afterload – Patients are exquisitely sensitive to changes in any of these parameters.
SYMPTOMS
• NYHA Class III–IV symptoms of heart failure
• Left-sided failure: Respiratory insufficiency, cyanosis, poor perfusion, orthopnea, paroxysmal
nocturnal dyspnea, easy fatigue.
• Right-sided failure: Peripheral edema, ascites, hepatomegaly.
History
• Assessment is often limited because of urgent surgery, but full transplant evaluation should
be available.
• Evaluate current symptoms, any changes in ischemic threshold or cardiac function, and NPO
status.
Signs/Physical Exam
Evaluate volume status and signs of pulmonary vascular congestion
• Lung auscultation
• JVD
• Peripheral edema
• Poor perfusion or cyanosis
MEDICATIONS
• Beta-blockers
• Diuretics
• ACE inhibitors or angiotensin receptor blockers.
• Digoxin
• Inotropes
• Anticoagulants
Labs/Studies
• Electrolytes are often altered due to diuretics or excessive fluid retention.
• Liver function tests may reflect hepatic venous congestion.
• EKG: Dysrhythmias are common.
• CXR to evaluate pulmonary venous congestion.
• Echocardiography to assess right and left heart function, valvular abnormalities, and the
presence of pericardial or pleural effusion.
• Left and right heart catheterization.
• Evaluation of pulmonary hypertension is critical.
• Rule out existing organ dysfunction that would lead to mortality soon after transplant.
• Reversible hepatic or renal dysfunction is often present.
• Endocrine and electrolyte abnormalities are common: Salt and water retention, glucose
abnormalities, and hypokalemia due to diuretics.
TREATMENT
Premedications
• Patients usually have elevated levels of catecholamines and are dependent on high preload
(2).
• Small doses of sedation may result in severe hemodynamic changes.
• Patients are generally anxious but are very well informed about their care.
• Postoperative intubation and mechanical ventilation
• Transfusion of blood products
• Patients will be immunosuppressed so meticulous attention to aseptic technique is vital.
• Use blood products free of cytomegalovirus for patients lacking antibodies to this organism.
INTRAOPERATIVE CARE
• General endotracheal anesthesia (2)
• Timing coordinated with donor heart availability
Monitors
• Arterial line (preinduction)
• Central venous catheter – Right IJ access may be utilized, although concern for access for
future biopsies.
• PA catheter – Insertion may be difficult in the dilated heart. Full insertion could possibly
wait until after the donor heart implantation.
• TEE
• Large bore access
• Repeat sternotomy: Consider placement of defibrillator pads and cross-matched and checked
pRBCs in the room prior to sternotomy.
• Concern for “full stomach,” preoxygenation, +/– rapid sequence induction with cricoid
pressure, unexpected difficult airway equipment readily available.
• Very sensitive to hemodynamic changes. Goal is to maintain heart rate, preload,
contractility, and afterload. Continue inotropic support if the patient was reliant on it.
• For induction, opioids and benzodiazepines are commonly used for hemodynamic stability.
Some patients may tolerate low volatile agent.
Maintenance
• Standard concerns for cardiopulmonary bypass.
• Insulin infusion will likely be necessary given the administration of steroids.
• Weaning from bypass
– The newly transplanted heart is preload dependent so special care should be given to
maintain adequate filling pressures.
– Particular attention should be paid to right ventricle function; it is the most common
etiology of failure to wean.
• Patients remain intubated with sedation
• Complications
– Primary allograft failure secondary to inadequate myocardial protection, prolonged
ischemic time, and reperfusion injury.
– Right ventricle dysfunction
Etiology may be secondary to residual pulmonary hypertension, air in the right coronary
artery, valve insufficiency, or prolonged ischemic time.
Increases in PVR can result from hypoxemia, hypercarbia, acidemia, and excessive tidal
volumes and should be avoided.
Treat with aggressive inotropic therapy and selective pulmonary vasodilators (inhaled
nitric oxide, prostaglandins).
– Coagulopathy, especially in patients with prior sternotomy.
POSTOPERATIVE CARE
BED ACUITY
• Patients require cardiac surgical ICU care.
• Cardiac issues
– Maintain adequate oxygenation and ventilation
– Meticulous optimization of hemodynamics.
– Treat coagulopathy and hypothermia.
• Transplant issues
– Immunosuppressive regimen is initiated.
ANALGESIA
Standard postcardiac surgical pain management
COMPLICATIONS
• Acute rejection during the first 6 months – Monitored by serial myocardial biopsies.
• Pulmonary and systemic hypertension
• Arrhythmias
• Respiratory and renal failure.
• Immunosuppression and subsequent risk of infection. Viral and fungal infections more
common in long term.
PROGNOSIS
• Recipient risk factors for increased mortality include age, race, prior transplant, poor HLA
matching, ventilator dependence, and size mismatching.
• Donor risk factors for increased mortality are age, race, gender, and long ischemic time.
REFERENCES
1. Mehra M, et al. Listing criteria for heart transplantation: International Society for Heart
and Lung Transplantation Guidelines for the Care of Cardiac Transplant Patients—2006. J
Heart Lung Transplant. 2006;25(9):1024–1042.
2. Fann JI, Reitz BA. Heart and lung transplantation. In Jaffe R, Samuels SI (Eds.),
Anesthesiologist’s Manual of Surgical Procedures. 3rd edn. Lippincott Williams & Wilkins.
Philadelphia, 2004:360–364.
3. Jacob S, Sellke F. Is bicaval orthotopic heart transplantation superior to the biatrial
technique? Interact CardioVasc Thorac Surg. 2009;9(2):333–342.
ADDITIONAL READING
• Ramakrishna, et al. Anesthesia for heart transplantation. Ann Cardiac Anesth. 2009;12(1):
71–78.
• Post-heart transplant
CODES
ICD9
V42.1 Heart replaced by transplant
ICD10
Z94.1 Heart transplant status
CLINICAL PEARLS
• Cardiac denervation occurs in heart transplant recipients
– Stimuli do not produce normal responses of increased chronotropy and inotropy.
– Instead, these patients respond to increased demand primarily by increases in stroke
volume and, thus, are very preload dependent.
– Vagolytic agents such as atropine will likely not affect heart rate. The heart continues to
respond to direct acting agents such as epinephrine.
• Anesthetic care of the donor follows general principles of brain-dead donor care
– Maintain normovolemia, normothermia, normal to high preload, MAP 80–90 mm Hg (may
need vasopressors).
– Avoid hypoxia and transfuse if oxygen supply is inadequate.
– ARDS or neurogenic pulmonary edema may necessitate high levels of PEEP.
– Central DI may lead to massive diuresis.
• Right ventricle function is paramount
– Preoperative assessment should demonstrate PVR <5 Woods units.
– Postoperative management should optimize RV function.
• Biatrial versus bicaval technique (3):
– The bicaval technique may be associated with the following short-term benefits: Decreased
atrial pressure, tricuspid valve regurgitation, and mortality, as well as quicker return to
sinus rhythm
– Long-term outcomes, however, do not appear to show a difference in survival at 1 and 3
years.
– The bicaval technique is considered more technically demanding and may be associated
with longer pump bypass and ischemic time.
HELLP SYNDROME
BASICS
DESCRIPTION
• HELLP is a syndrome of pregnancy characterized by Hemolysis, Elevated Liver enzymes, and
Low platelets.
• Diagnostic criteria for HELLP include thrombocytopenia (platelet count <100,000/L), AST
and/or ALT >70 IU/L, and hemolysis with LDH >600 IU/L.
• Twenty percent of patients with severe preeclampsia develop HELLP but the syndrome can
occur without hypertension (HTN) and/or proteinuria.
• Signs of HELLP usually manifest between 28 and 36 weeks gestation; however, ∼20% of
patients will show initial manifestations at >48 hours after delivery. Resolution of
symptoms usually occurs within 48 hours postpartum but can take up to 4 weeks.
EPIDEMIOLOGY
Incidence
• Overall deliveries: ∼0.6%
• Preeclampsia develops in ∼10% of all pregnancies in the US.
Morbidity
• Maternal morbidity: Hepatic rupture, disseminated intravascular coagulation (DIC), seizure,
pulmonary edema, renal failure
• Fetal morbidity: Intrauterine growth restriction (IUGR), placental abruption, preterm
delivery
Mortality
Maternal and fetal mortality are associated with hepatic rupture and/or seizure.
• Etiology unclear; HELLP is considered a severe form of preeclampsia.
• Maternal risk factors for preeclampsia
– Demographics: Age >40 years old, African-American ethnicity
– Pregnancy associated: Nulliparity, multiple gestations, molar pregnancy
– Comorbidities: HTN, renal disease, diabetes mellitus, factor V Leiden deficiency,
antiphospholipid antibody
• Paternal risk factors for preeclampsia: History of fathering a preeclamptic pregnancy with
another woman; history of having a mother with preeclampsia during his gestation
• HELLP recurrence is rare (∼3%).
PATHOPHYSIOLOGY
• Theories include abnormal implantation of trophoblastic tissue and imbalanced production
of mediators. An atypical maternal immune response to embryonic trophoblasts can result
in impaired invasion of trophoblastic cells into the uterine wall. This results in
maladaptation of myometrial spiral arteries (high-resistance, and hence reduced
uteroplacental flow). The hypoperfusion can cause placental hypoxia and the release of
inflammatory cytokines into the maternal circulation with consequent endothelial
dysfunction.
• An imbalance of placental production of prostacyclin and thromboxane can result in
systemic vasoconstriction and placental ischemia.
• Control HTN (target SBP <160 mm Hg; DBP <110 mm Hg).
• Seizure prophylaxis
• Accelerate fetal lung maturity for gestational age <36 weeks with betamethasone if preterm
delivery anticipated.
• Evaluate for hemorrhage risk factors including thrombocytopenia, coagulopathy, and
hepatic dysfunction.
• Identify increased risk of hepatic rupture including thrombocytopenia, elevated liver
enzymes, and right upper quadrant pain.
• Prepare for urgent/emergent delivery. Indications for emergent delivery include non-
reassuring fetal heart tones lasting >10 minutes, placental abruption, hepatic rupture,
seizure, and/or end-organ damage.
SYMPTOMS
• Pulmonary: Dyspnea.
• Hepatic: Abdominal pain, ascites, jaundice.
• Hematologic: History of petechiae, mucosal bleeding, bruising.
• Neurologic: Hyperexcitability, headaches, visual changes, seizure.
History
• Preeclampsia risk factors
• Evaluate for other causes of elevated liver enzymes and/or RUQ pain: Hepatitis,
cholecystitis, pancreatitis, appendicitis.
• Rule out other causes of thrombocytopenia: Idiopathic thrombocytopenic purpura (ITP),
thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), systemic
lupus erythematosus (SLE).
Signs/Physical Exam
• Airway: Pharyngolaryngeal edema
• Pulmonary: Pulmonary edema, hypoxemia.
• Cardiovascular: HTN, decreased central venous pressure (CVP).
• Hematologic: Evidence of DIC (bruising, petechial, bleeding around catheter sites).
• Renal: Oliguria.
• Hepatic: Hepatic edema.
• Neurologic: Signs of intracranial hypertension (headache, vomiting, altered mental status).
TREATMENT HISTORY
Preeclampsia therapy
MEDICATIONS
• Betamethasone
Labs/Studies
• Labs: Urinalysis for proteinuria, uric acid; complete blood count (platelets, hematocrit);
complete metabolic panel (including Mg2+), coagulation studies, serum transaminates; Type
and Cross.
• Imaging studies
– Abdominal ultrasound, CT, or MRI. Evaluate for hepatic infarction, hematoma, or rupture.
– Chest X-ray. Evaluate for pulmonary edema.
• Decreased glomerular filtration rate (GFR); increased proteinuria, uric acid, urine
protein:creatinine ratio.
• Cardiovascular: Decreased CVP; increased peripheral vascular resistance, sensitivity to
catecholamines; vasospasm, LV hypertrophy.
• Pulmonary: Airway edema, pulmonary edema, increased risk of gastric aspiration.
• Renal: Acute renal failure; decreased GFR, clearance of uric acid.
• Hematologic: Hemoconcentration (increased blood viscosity), thrombocytopenia,
coagulopathy.
• Hepatic: Liver hematoma, hepatocellular damage, periportal hepatic necrosis.
• CNS: Risk of cerebral edema, cerebral hemorrhage, alteration in cerebral autoregulation.
• Placental: Uteroplacental insufficiency may lead to fetal hypoxia, IUGR. Increased risk of
placental abruption, premature labor.
• Delivery of the fetus and placenta is the only curative therapy.
• Emergent delivery may be delayed in the absence of the following: Deterioration of clotting
function (progression of thrombocytopenia and/or DIC); evidence of hepatic dysfunction,
hematoma, and/or rupture; severe, refractory HTN >24 hours; renal failure; pulmonary
edema, eclampsia or onset of neurologic deficits; placental abruption; nonreassuring fetal
status.
CLASSIFICATIONS
• HELLP syndrome
• Preeclampsia
• Eclampsia
TREATMENT
Premedications
– Magnesium sulfate (first line): 4–6 g IV bolus over 15 minutes, followed by 1–2 g/hr.
Therapeutic level ∼ 6–8 mEq/mL.
– Phenytoin (second line): 10 mg/kg dose over 1 hour.
– Diazepam (second line): 5–10 mg IV over 15 minutes, may be repeated every 15 minutes
for a maximum dose of 30 mg.
• BP control
– Hydralazine (first line): 5–10 mg IV q15 minutes.
– Labetalol (first line): 20 mg IV every 10 minutes up to a maximum dose of 300 mg.
– Nifedipine (second line): 10 mg PO TID titrated to effect for a maximum dose of 120 mg
daily.
• Fetal lung maturity
– Betamethasone given in divided doses to accelerate fetal lung development in anticipation
of deliveries <36 weeks gestation.
• Regional anesthesia and coagulopathy.
• Blood products. Platelets rarely given for thrombocytopenia in the absence of hemorrhage.
• Possible need for invasive monitoring.
INTRAOPERATIVE CARE
• Neuraxial anesthesia (spinal or epidural) is preferred. A careful evaluation of the risks versus
benefits should be made in the setting of thrombocytopenia. Contraindications include
patient refusal, elevated ICP, inability to cooperate, evidence of coagulopathy, or signs of
local infection. Hypotension may accompany initiation of neuraxial anesthesia; patients
with preeclampsia are often hypovolemic.
• General anesthesia may be necessary in emergent deliveries (fetal distress, placental
abruption, hepatic rupture, severe pulmonary edema, seizure, and/or end-organ
dysfunction). Use is associated with increased risk of aspiration, transient neonatal
depression, severe HTN, and cerebral hemorrhage.
Monitors
• Pulse oximetry. Decrease in SpO2 in the setting of pulmonary edema, respiratory depression,
and/or pulmonary aspiration.
• BP monitoring. Consider invasive BP monitoring in the setting of refractory HTN (BP
>180/120) or for frequent blood sampling.
• CVP. May be useful in determining volume status and for infusion of vasodilators.
• Pulmonary arterial catheter rarely indicated.
• Urinary output. Useful in evaluation of volume resuscitation and renal function.
• Fetal heart tracing.
• Limit use of benzodiazepines and opioids prior to delivery; their use is associated with
neonatal (respiratory/CNS) depression.
• General anesthesia for emergent deliveries. A rapid sequence intubation with cricoid
pressure should be used to minimize the risk of aspiration. Airway edema may increase
difficulty of laryngoscopy. Avoid a hypertensive response to laryngoscopy by deepening of
the anesthetic or using remifentanil and/or esmolol.
Maintenance
• General anesthesia can be maintained with a combination of volatile anesthetic and nitrous
oxide. Volatile anesthetic at <0.5 MAC minimizes decreases in uterine tone. IV opioids and
benzodiazepines can be given following clamping of the cord.
• Magnesium sulfate prolongs the duration of nondepolarizing neuromuscular blockade.
• Extubation criteria include adequate oxygenation and ventilation as well as the ability to
protect the airway.
• Airway edema may necessitate reintubation.
• Severe HTN and cerebral hemorrhage may accompany emergence and extubation.
POSTOPERATIVE CARE
BED ACUITY
Consider ICU admission in patients with evidence of end-organ damage and/or need for
• Continue antihypertensive medication until BP normalizes.
• Continue seizure prophylaxis for 24 hours following last seizure.
• Labs. Follow platelets, INR/PT, hepatic enzymes, BUN/Cr until values normalize.
COMPLICATIONS
Hepatic rupture or dysfunction; pulmonary edema, renal failure, thrombocytopenia, DIC,
seizure, placental abruption, IUGR, preterm delivery, maternal or fetal death.
REFERENCES
1. Gasem T, Al Jama FE, Burshaid S, et al. Maternal and fetal outcome of pregnancy
complicated by HELLP syndrome. J Matern Fetal Neonatal Med. 2009;22(12):1140–1143.
2. Practice guidelines for obstetric anesthesia: An updated report by the American Society of
Anesthesiologists Task Force on Obstetric Anesthesia. Available at:
http://www.asahq.org/publicationsAndServices/OBguide.pdf. Accessed on January 08,
2011. Sibai BM, Stella CL. Diagnosis and management of atypical preeclampsia/eclampsia.
Am J Obstet Gynecol. 2009;200:481.e1–481.e7. Katz L, de Amorim MMR, Figueiroa JN, et
al. Postpartum dexamethasone for women with hemolysis, elevated liver enzymes, and low
platelets (HELLP) syndrome: A double-blind, placebo-controlled, randomized clinical trial.
Am J Obstet Gynecol. 2008;198:283.e1–283.e8.
3. Turner J. Diagnosis and management of preeclampsia: An update. Int J of Women’s Health.
2010;2:1–11.
ADDITIONAL READING
• American College of Obstetricians and Gynecologists (ACOG) Practice bulletin: Diagnosis
and management of preeclampsia and Eclampsia. Obstet Gynecol. 2002;99(1):159–167.
• Pregnancy induced hypertension
• Preeclampsia
• Eclampsia
CODES
ICD9
• 642.50 Severe pre-eclampsia, unspecified as to episode of care or not applicable
• 642.51 Severe pre-eclampsia, delivered, with or without mention of antepartum condition
• 642.52 Severe pre-eclampsia, delivered, with mention of postpartum complication
ICD10
• O14.20 HELLP syndrome (HELLP), unspecified trimester
• O14.22 HELLP syndrome (HELLP), second trimester
• O14.23 HELLP syndrome (HELLP), third trimester
CLINICAL PEARLS
• Hepatic rupture is associated with an increased risk of maternal and fetal mortality.
• Risk versus benefit of neuraxial analgesia/anesthesia must be carefully considered in the
setting of severe thrombocytopenia.
• Platelet transfusion is generally reserved only for cases of active or spontaneous bleeding.
HEMOGLOBIN
BASICS
DESCRIPTION
• Hemoglobin (Hb) is a molecular structure in red blood cells (RBCs) responsible for oxygen
transport and acid/base balance.
• Hb has an oxygen-binding capacity of 1.34 mL of oxygen per gram of Hb and provides a
very efficient mechanism for carrying and transporting the gas.
• The Hb molecule comprises four noncovalently bound polypeptide chains (α-1, α-2, β-1,
β-2). Each chain holds a heme group containing an iron atom responsible for binding
oxygen. The hydrophobic portion of the heme is buried within the protein, while the
hydrophilic “arms” are on the outer surface. This conformation results in a globular
structure with four heme groups, capable of binding 4 oxygen molecules.
• The primary function of Hb is to bind oxygen in pulmonary capillaries and then release it to
the tissues. Hemoglobin exists in 4 physiologic forms: oxyhemoblobin (bound to oxygen)
and deoxyhemoglobin (not bound to oxygen), as well as carbaminohemoglobin (bound to
carbon dioxide; thus functions to transport CO2) and methemoglobin (reduced hemoglobin,
cannot bind oxygen).
• The oxyhemoglobin dissociation curve describes the relationship between PaO2 and the
oxygen saturation of Hb. A normal oxyhemoglobin dissociation curve is characterized by
50% of Hb being saturated with oxygen at a PaO2 of 26 mm Hb (P50 value).
• Cooperative binding
– Oxygen binding to Fe2+ induces a conformational change in the Hb structure that
facilitates oxygen binding to the other heme groups.
– The shape of the oxyhemoglobin curve is sigmoid because as oxygen tensions increase it
becomes exponentially easier for Hb to bind oxygen molecules. Conversely, as oxygen
tension decreases, it becomes exponentially harder for Hb to bind oxygen. The splay of the
curve on both the left and right sides reflects these exponential relationships.
• A right-shifted oxyhemoglobin dissociation curve reflects a decreased affinity of Hb for
oxygen, which facilitates unloading of oxygen to the tissues. Conditions that shift the
oxyhemoglobin dissociation curve to the right:
– Acidemia (increased [H+]–Bohr effect)
– Increase in 2,3-diphosphoglycerate (chronic arterial hypoxemia or anemia), carbon
dioxide, or temperature
– Pregnancy (though it is reduced with preeclampsia)
– Sickle cell disease
• A left shift in the oxyhemoglobin curve reflects an increased affinity of Hb for oxygen. This
increased affinity is physiologically advantageous in situations where oxygen tension is low.
Conditions that shift the oxyhemoglobin dissociation curve to the left:
– Alkalemia
– Increased levels of fetal Hb (P50 = 19 mm Hg) and fetal circulation where HbF avidly
binds oxygen in the uterus to be unloaded in the very low oxygen tensions of the fetal
tissues.
– Methemoglobinemia or carboxyhemoglobinemia (see details below)
– High concentrations of transfused blood that has been stored.
• Emerging evidence suggests that Hb is involved in the transport of nitric oxide, a
vasodilator, to the tissues.
• Hb accomplishes its buffering action through exposed histidine residues on the polypeptide
chains.
• The viscosity of RBCs contributes to resistance. Resistance = [(viscosity ×
length)/diameter4]. Because pressure = Flow × resistance, viscosity is directly related to
pressure.
• Erythropoietin is a hormone produced in the kidneys and liver that promotes synthesis of
RBCs.
ANATOMY
• Adult Hb normally consists of HbA, HbA2, and HbF.
– 95–98% of adult hemoglobin is HbA.
– 2–3% of adult hemoglobin is HbA2.
– Less than 2% of adult hemoglobin is HbF.
• Anemia: “not enough” Hb
– Causes can be categorized as blood loss, decreased production of RBCs, and/or increased
destruction of RBCs.
– Iron deficiency anemia is common in menstruating females and can be treated with
dietary supplementation of iron.
– Pernicious anemia is caused by a lack of secretion of gastric intrinsic factor leading to low
absorption of vitamin B12.
– The decrease in blood viscosity can result in decreases in blood pressure.
• Polycythemia: An excess of Hb
– Polycythemia vera is a hereditary cause
– Acquired causes result from a compensatory response to chronic hypoxia. They include
COPD, sleep apnea, congenital heart disease. Athletes seeking a competitive advantage
have been reported to use erythropoietin to artificially increase RBC mass.
– Extreme levels of polycythemia can increase blood viscosity and cause thrombosis
resulting in cerebrovascular accidents or cardiac events; impairs ideal “rheology” through
blood vessels.
• Sickle cell disease
– HbS is the result of a mutation in the coding gene for HbA (substitution of a valine instead
of glutamic acid at the 6th position of the β-subunit); this creates a new hydrophobic spot
within the normally hydrophilic outer arm. In hypoxic environments, deoxygenated Hb
aggregates with hydrophobic spots on other deoxygenated Hb molecules, resulting in
polymerization. Homozygous patients are severely affected, while heterozygous patients
are carriers.
– Pathophysiology. HbS is less resilient than HbA with a RBC lifespan of 10–20 days instead
of the normal 120 days with resulting anemia. Sickled RBCs tend to clump together
leading to decreased organ blood flow and even infarction. Increased production of HbF is
a compensatory response.
– Management. Optimize volume status (avoid dehydration); exchange transfusions when
indicated; adequate pain control; avoid factors that favor sickling such as hypoxemia,
hypothermia, and stasis (tourniquets)
• Thalassemias
– α. Caused by a defect in the α-1 or α-2 gene. The severity of disease is dependent on the
number of affected genes.
– β. Caused by a defect in genes coding for β-globulin. The minor variant exhibits a
hypochromic, microcytic anemia. The intermediate variant has an increase in HbF and a
left shift on the oxyhemoglobin dissociation curve. The major variant (Cooley’s anemia)
can manifest with significant problems in infancy that include overgrowth of the maxilla,
CHF, pericarditis, SVT, cor pulmonale, and hepatomegaly. Treatment includes supportive
care and transfusion to keep Hb above 9 g/dL.
• HbC
– Glutamic acid is replaced by lysine at the 6th position on the β-globulin chain.
– Autosomal recessive disease with heterozygous asymptomatic carriers; in contrast,
homozygous patients have a mild hemolytic anemia.
• HbE
– Similar to HbC, glutamic acid is replaced by lysine, but at the 26th position of the β-
globulin chain.
– Similar to HbC, HbE is also autosomal recessive with heterozygotes as asymptomatic
carriers and homozygotes displaying a mild hemolytic anemia.
• HbA1c. Hb reacts with glucose molecules to form glycosylated Hb. The higher the glucose
concentration the Hb is exposed to, the higher the number of glycosylated molecules.
Therefore, HbA1c is a good measure of the glucose level over the previous several weeks
and is used to monitor glycemic control in diabetics.
– The iron in Hb can be oxidized to Fe3+ (from normal Fe2+). Oxidized Hb is unable to bind
oxygen and impairs oxygen delivery to the tissues.
– Methemoglobin absorbs light equally at the two wavelengths used in pulse oximetry,
giving a ratio of 1. This ratio is read by the conventional pulse oximeter to be a saturation
of 85%.
– Methemoglobinemia can be caused by administration of oxidizing substances, such as
prilocaine (EMLA cream), procaine (Hurricaine spray™), dapsone, nitrates, and aniline
dyes.
– Deficiencies in NADH methemoglobin reductase (G6PD deficiency, pyruvate kinase
deficiency) decrease the ability to convert methemoglobin to normal Hb.
– Treatment of methemoglobinemia is with methylene blue 1–2 mg/kg given as a slow IV
push over 5 minutes (contraindicated in G6PD deficiency due to resulting hemolysis).
• Carboxyhemoglobinemia
– Occurs most commonly as a result of smoke exposure (chronic smokers, structure fire
victims) or from improper ventilation in areas with car exhaust fumes.
– Carbon monoxide (CO) has a 300-fold greater affinity for Hb compared to oxygen.
– Hb saturated with CO cannot deliver oxygen to the tissues.
– A conventional pulse oximeter will not detect the abnormal oxygen saturation in CO
poisoning.
– Hyperbaric oxygen can overcome Hb’s preferential binding of CO in clinically significant
cases.
• Adequate oxygenation of tissues is dependent on appropriate levels of Hb saturated with
oxygen.
– Hb can be transfused in the form of packed RBCs (most common) and whole blood.
– The only indication for Hb transfusion is to increase the oxygen-carrying capacity of
blood. Unlike crystalloid and colloid solutions, transfusion of packed RBCs is not an
appropriate volume expander. However, because it can increase blood viscosity (and
hence resistance to flow), it can increase blood pressure.
• Transfusion “triggers”:
– Evidence of an existing or impending deficiency in oxygen delivery to the tissues
– Assessment of adequate oxygenation of tissues can be challenging and the entire clinical
picture needs to be taken into account. Review of vital signs, crystalloid and colloid
infusion, blood loss, acid/base status, presence of lactic acidosis, Hb/Hct, and possibly
mixed venous oxygen saturation can help guide the decision-making process.
– Based on viscosity and cardiac pump performance, the Hb level that maximizes oxygen
delivery to the tissues has been shown to be 10 g/dL. However, there are no absolute
“triggers” for Hb transfusion. Patients at risk for cardiac disease are generally maintained
at a Hb of 10 g/dL or greater. Otherwise healthy patients frequently tolerate a Hb as low
as 6 g/dL.
– Mostly supportive care involving optimization of volume status, oxygenation, and
temperature to avoid a vaso-occlusive crisis.
– Transfusion of RBCs is indicated when signs or symptoms of anemia are present (e.g.,
dyspnea, high output cardiac failure, and postural hypotension).
• Ischemic optic neuropathy
– Anemia is thought to be a risk factor in this rare perioperative event that involves
ischemia of the optic nerve and vision loss.
• Jehovah’s witnesses
– Patients will often refuse transfusion of blood products, even under life-threatening
circumstances.
– Jehovah’s witness patients have been reported to survive with Hb levels as low as 3 g/dL.
– Strategies to minimize blood loss. Some Jehovah’s witness patients will allow return of
autologous blood that has been salvaged intraoperatively. Individual patients will
sometimes insist that a complete circuit be connected between them and the salvaging
apparatus. Isovolemic hemodilution involves collecting whole blood from a patient in the
immediate perioperative period and replacing that volume with crystalloid or colloid. It
does not decrease the volume of blood loss (unlike controlled hypotension), but instead
decreases the mass of red blood cells that are lost (the blood that is lost has a lower
hematocrit). However, some Jehovah’s witnesses will not accept autologous blood
collected using this technique.
• Newer pulse oximeters can monitor Hb levels and variant forms of Hb continuously.
• Research into oxygen-carrying Hb substitutes, such as perfluorocarbons continues, but has
not yet produced a viable alternative to RBC transfusion.
Physiologic anemia of pregnancy. Plasma volume increases relative to red cell mass and
results in a dilutional anemia. A “normal” Hb in pregnancy is 11 g/dL. To compensate,
cardiac output increases and there is a right shift of the oxyhemoglobin dissociation curve.
The increase in oxygenation that occurs with normal breathing after birth, causes a sharp rise
in tissue O2 level; this causes a negative feedback on erythropoietin production with resultant
anemia. Normal Hb levels decrease for 6–8 weeks before production of erythropoietin
resumes. This anemia rarely requires intervention.
Elderly patients have a higher incidence of cardiac risk factors that favor maintaining an Hb
level above 10 g/dL.
EQUATIONS
Calculation of arterial content of blood: CaO2 = (SaO2 × Hb × 1.34) + 0.003(PaO2); where
CaO2 is the arterial content of oxygen in blood, SaO2 is the oxygen saturation, and PaO2 is the
partial pressure of oxygen in blood.
REFERENCES
1. Firth PG. Anesthesia and hemoglobinopathies. Anesthesia Clin. 2009;27(2):321–326.
2. Kamat V. Pulse oximetry. Indian J Anaesth. 2002;46(4):261–268.
ADDITIONAL READING
• www.umass.edu/molvis/tutorials/hemoglobin/sickle.htm
• Oxygen carrying capacity
• Hemolytic anemia
CLINICAL PEARLS
• Increasing oxygen-carrying capacity is the only indication for transfusion of RBCs.
• Hydroxyurea increases the amount of fetal Hb in sickle cell patients.
• Recombinant erythropoietin (EpogenTM, ProcritTM) can be administered to patients with
chronic anemia with the goal to avoid transfusion. The Food and Drug Administration
(FDA) has issued a “Black Box Warning” against erythropoietin administration to patients to
a target Hb >12 g/dL as it has been associated with an increased incidence of
thromboembolic events. The FDA recommends using the lowest dose possible to gradually
raise the Hb to the lowest level sufficient to avoid transfusion.
HEMOLYTIC ANEMIA
Malina M. Varner, MD
Kathleen S. Donahue, DO, FAAP
BASICS
DESCRIPTION
• Hemolytic anemia describes a low red blood cell (RBC) count that results from lysis of
erythrocytes.
• Over 200 causes exist and are either (1):
– Congenital: Hemoglobinopathies, enzyme defects, and cell membrane defects
– Acquired: Injury to the cells increases splenic sequestration and clearance by the immune
system; or abnormal immune complexes form and attach to the RBC (signals for
hemolysis).
• Perioperative management depends on the etiology. The preoperative evaluation,
optimization, intraoperative management, and postoperative care should be appropriately
tailored.
EPIDEMIOLOGY
Incidence
Accounts for 5% of all causes of anemia (1)
Morbidity
• Depends on the underlying etiology of anemia
• Patients can develop leg ulcers, folate deficiency, hemosiderosis, and gallstones
• Can precipitate angina and heart failure in patients with underlying cardiovascular disease
Mortality
Overall incidence of death is rare
• Congenital (commonly diagnosed in childhood) (1):
– Hemoglobinopathies: Sickle cell, thalassemia
– Enzyme defects: G6PD deficiency
– Cell membrane defects: Hereditary spherocytosis
• Acquired
– Mechanical injuries: Artificial valves, cardiopulmonary bypass (CPB), preeclampsia
– Hypersplenism
– Burns
– Drugs that impose oxidative stress on the erythrocyte (nitrates, methylene blue,
methyldopa, ribavirin)
– Infectious: Malaria, Escherichia coli 0157:H1, C. perfringens
– Autoimmune hemolytic anemia (AIHA)
– Transfusion-related
PATHOPHYSIOLOGY
• Inherited hemolytic anemias. Lysis is the final outcome to a variety of deficits within the
erythrocyte:
– Hemoglobinopathies. In sickle cell disease, the average red cell half-life is decreased. This
is due to the following: Mechanical cell membrane damage while traversing through
capillaries; injury from reactive oxygen species; and the formation of antibodies to
erythrocyte clusters seen during sickling (2).
– Enzymes. G6PD deficiency results in the inability to produce glutathione, which is
responsible for reducing hemoglobin during oxidative stress. The oxidized hemoglobin
precipitates in the RBC and forms Heinz bodies that are “flagged” and removed by the
spleen (3).
– Cell membrane structure. Hereditary spherocytosis and its abnormal sphere shape result in
splenic sequestration and hemolysis, thereby reducing its lifespan.
• Acquired hemolytic anemias.
– Mechanical injury: Prosthetic heart valves, CPB, eclampsia, hemolytic uremic syndrome
(HUS), disseminated intravascular coagulopathy (DIC)
– Exposure
– Disease (malaria invades the erythrocyte and causes destruction)
– Drugs may cause immune-mediated hemolysis
• Erythrocyte lysis causes release of hemoglobin molecules as well as lactate dehydrogenase
(LDH).
• Although hemolytic anemia comprises only 5% of all causes of anemia, it should be
considered and ruled out when anemia is present. When diagnosed, the underlying etiology
should be discerned and treatment and management should be tailored accordingly.
• A hematology consult prior to surgical intervention should be considered in patients with
rare etiologies.
SYMPTOMS
• Anemia: Angina, dyspnea, and weakness due to decreased oxygen carrying capacity (2).
• Right upper quadrant (RUQ) pain due to gallstone formation from excessive bilirubin.
History
• Often suspected after an incidental laboratory finding
• Known family history if hereditary
Signs/Physical Exam
• Generalized pallor (1)
• Pale conjunctiva
• Tachycardia, tachypnea, and hypotension
• Splenomegaly, RUQ tenderness
• Leg ulcer
• Acute chest syndrome (sickle cell disease)
TREATMENT HISTORY
• Depends on the cause
• Sickle cell disease: Blood transfusions, splenectomy
• Autoimmune: Corticosteroids, plasmapheresis
• Drug induced: Discontinue possible medications as precipitating factors
MEDICATIONS
Depends on the etiology but can include folic acid, iron replacement, and corticosteroids (1).
Labs/Studies
• CBC: Low hemoglobin levels; normal MCV. Increased erythrocyte levels may be associated
with MCV elevation (1).
• Haptoglobin levels are decreased due to binding with free hemoglobin.
• Reticulocyte counts are increased and reflect the bone marrow’s attempt to restore
erythrocyte levels.
• LDH levels are elevated due to release into the circulation when erythrocytes are destroyed.
• Bilirubin: Indirect levels are often elevated due to an increased load that “backs up” before
being conjugated by the liver.
• Peripheral smears may demonstrate the etiology of hereditary causes.
• WBC and platelet counts may provide information about underlying malignancy or
hematologic disease.
• Type and screen for operative procedures where blood loss may occur.
• Type and cross for patients with transfusion dependent anemia or patients with difficult to
cross blood due to rare antibodies (always consider in patients with a history of mulitple
transfusions).
• CXR if there is concern for hemodynamic compromise or acute chest syndrome (2).
• Splenic infarct in sickle cell
• Myocardial stress due to poor oxygen supply
• Renal failure
• Acute cardiovascular decompensation
• Acute chest syndrome
• Sepsis if underlying infectious cause
• Need for exchange transfusion or plasmapheresis
CLASSIFICATIONS
• Congenital
• Acquired
TREATMENT
Premedications
• Avoid oxidative stress (hemolytic crisis) from anxiety and pain by appropriately titrating
benzodiazepines and fentanyl in patients with known G6PD deficiency (3).
• Exchange transfusions and appropriate hydration may be performed in sickle cell patients.
There is no general consensus regarding preoperative hemoglobin levels, but some clinicians
transfuse to maintain a hemoglobin level of 10 g/dL (2).
• For AIHA, controversy exists whether pretreatment with high-dose corticosteroids is
beneficial; however, these patients may be on chronic immunosuppression. Consider
administering a stress dose of steroids, if appropriate (1).
Patients should be informed about the possible need for blood transfusion.
INTRAOPERATIVE CARE
• Based primarily on the surgical procedure and patient comorbidities.
• Avoid medication that may cause hemolysis under oxidative stress (3).
– Acetaminophen
– Antibiotics including penicillin, nitrofurans, isoniazid, and chloramphenicol
– Sulfa derivatives such as furosemide
– Antimalarial drugs
– Miscellaneous including methylene blue, quinidine, vitamin K analogs, probenecid, and
possibly nitroprusside.
• Regional and/or neuraxial anesthesia may be considered to optimize postoperative pain
control and decrease stress. Significant sedation for these procedures may cause hypoxia
and hypercarbia that can precipitate sickling in susceptible patients (2).
Monitors
• Additional invasive monitoring is primarily dictated by the type and length of the surgery as
well as comorbid conditions. The necessity for frequent labwork should be considered.
• Foley catheters may be helpful as hemoglobinuria may be visually diagnosed.
• Depends on the surgical procedure
• Avoid hypoxia and hypotension that could provoke sickling or a hemolytic crisis in G6PD
deficiency.
Maintenance
• G6PD deficiency. Avoid oxidative stressors such as hypoxia, hypovolemia, and hypothermia
as well as select drugs. The use of benzodiazepines, fentanyl, propofol, and ketamine has
not been shown to cause a hemolytic crisis (3).
• Sickle cell crises may be avoided with aggressive hydration, avoidance of hypoxia,
hypothermia, and acidosis.
• Acute hemolytic transfusion reactions are manifest by hypotension, tachycardia, rash,
hyperthermia, and hematuria (1).
– Immediately stop the transfusion
– Begin resuscitative measures in the form of hemodynamic support and aggressive
hydration and diuresis (to combat acute renal failure, ARF)
– Send additional donor and recipient blood to be retested in the laboratory.
Careful attention should be paid to adequate pain control and oxygenation to avoid stress that
could trigger an acute hemolytic crisis.
POSTOPERATIVE CARE
BED ACUITY
Determination based primarily on the type of surgery
• Hematology consult
• Postoperative CBC should be followed
COMPLICATIONS
• Hemodynamic compromise due to acute hemolysis and decreased oxygen carrying capacity
• ARF precipitated by elevated free hemoglobin
REFERENCES
1. Lucio L.Hemolytic Anemias and Anemia Due to Acute Blood Loss (Chapter 101). In: Fauci
AS, Braunwald E, Kasper DL, et al. (eds.). Harrison’s Principles of Internal Medicine, 17th
ed. McGraw-Hill Professional. New York, New York; 2008.
2. irth PG, McMillan KN, Haberkern CM, et al. A survey of perioperative management of
sickle cell disease in North America. Paediatr Anaesth. 2011;21(1):43–49.
3. Elyassi AR, Rowshan HH. Perioperative management of the glucose-6-phosphate
dehydrogenase deficient patient: A review of literature. Anesth Prog. 2009;56(3):86–91.
• Anemia
• Preeclampsia
CODES
ICD9
• 282.0 Hereditary spherocytosis
• 283.9 Acquired hemolytic anemia, unspecified
ICD10
• D58.0 Hereditary spherocytosis
• D59.9 Acquired hemolytic anemia, unspecified
CLINICAL PEARLS
• Acute causes of hemolytic anemia in the operating room are likely related to blood
transfusion or medication administration. The inciting agent should be discontinued
immediately and supportive measures provided.
HEMOPHILIA
Neesa Patel, MD
BASICS
DESCRIPTION
• Hemophilia is an inherited disorder of hemostasis characterized by a deficiency in clotting
factors.
– Hemophilia A: Deficiency of factor VIII (FVIII) coagulant protein; X-linked recessive
inheritance.
– Hemophilia B: (Christmas disease) Deficiency in factor IX (FIX) coagulant protein; X-
linked recessive inheritance
– Hemophilia C: Deficiency of factor XI (FXI); autosomal-recessive inheritance (rare)
• Hemophiliacs pose the risk of increased surgical and postoperative bleeding; their care
should be tailored and coordinated between the anesthesia provider, surgeon, and
hematologist.
EPIDEMIOLOGY
Incidence
• Hemophilia A: 1 in 10,000 male births. Severe form is found in 7 out of 10 with the disease
• Hemophilia B: 1 in 50,000 male births
• The ratio of hemophilia A to B is 9:1
• Hemophilia C: Very rare; seen more commonly in Ashkenazi Jews
Prevalence
In the US: ∼20,000 people
Morbidity
Intracranial hemorrhage and complications associated with blood transfusions
Mortality
Overall mortality is twice that of a healthy male
• Results from large inversions, insertions, deletions, or point mutations of FVIII or FIX genes;
located on the long arm of chromosome X.
• The disease is typically inherited, but acquired disease is also a possibility.
PATHOPHYSIOLOGY
• FVIII and FIX circulate in the plasma in an inactive form. When activated, these two factors
cooperate to cleave and activate FX (controls the conversion of fibrinogen to fibrin).
• Lack of either of these factors significantly alters clot formation resulting in clinical
bleeding. Factor activity is described as a percentage; for example, normal patients have
100% activity, whereas severe disease is defined as <1% activity.
• The hallmark of hemophilia is hemorrhage into joints that causes long-term inflammation
and deterioration of the joint. Human synovial cells in joints synthesize high levels of tissue
factor pathway inhibitor, resulting in a higher degree of FXa inhibition, mainly for
moderate-to-severe forms. There is no excessive bleeding after minor cuts or abrasions for
mild-to-moderate disease.
• Acquired hemophilia is the development of FVIII inhibitors (autoantibodies) in persons
without a history of FVIII deficiency (1). Associated conditions include idiopathic, collagen
vascular disease, drug reaction (e.g., to penicillin), and lymphoproliferative malignancies.
• Patients pose an increased risk of bleeding and hemorrhage perioperatively. Hematology
consultation should be considered to aid with perioperative management.
• In elective cases, specific coagulant factor replacement (mild, moderate, severe) or 1-
deamino-8-d-arginine vasopressin (DDAVP) (mild disease) are typically administered. Levels
of the deficient coagulation factor should be assayed 48 hours before surgery and restored
to 40% of normal before surgery (higher for major surgeries and orthopedics).
• For emergent surgery, consider fresh frozen plasma (FFP) (mild-to-moderate disease),
DDAVP, concentrate replacement, and FVIIa (refractory bleeding).
SYMPTOMS
Hematuria, GI bleeds, easy bruising
History
• Bleeding (seldomly from small cuts or venipuncture). Patients with severe disease commonly
report a history of intraarticular and intramuscular bleed.
• The majority of patients are known to have hemophilia because of family history.
Signs/Physical Exam
Joint deformities, large subcutaneous, and soft-tissue hematomas.
TREATMENT HISTORY
• Multiple transfusions
• Hospital admissions for bleeding post-trauma
MEDICATIONS
Factor concentrate. Severe hemophiliacs are commonly placed on prophylactic IV infusions
for reduction in arthropathy and to prevent bleeding (2).
Labs/Studies
• PTT values are prolonged, whereas `PT’ is typically normal.
• Factor levels VIII or IX
• Preoperative screening for factor inhibitors (IgG antibodies) should be measured in severe
disease states (FVIII antibodies seen in ∼25% and FIX in ∼3–5%) (3). Inhibitors can result
in a diminished, inhibitory, or anaphylactic response to concentrates.
• Synovitis and joint destruction in patients with hemarthroses. This results in permanent
deformities, misalignment, loss of mobility, and extremities of unequal lengths.
• Transfusion-related infections have markedly reduced with improvements in donor
screening, virucidal techniques, and the development of recombinant products.
• Commonly associated with von Willebrand’s disease. Women may be “symptomatic carriers”
of hemophilia. FVIII and von Willebrand factor (VWF) levels tend to rise during pregnancy
and then often fall abruptly following delivery. Coagulation parameters should be obtained
in the 3rd trimester to evaluate for the safety of epidural placement (4).
Elective surgery should be delayed for proper evaluation of activity levels and treatment with
concentrates, as appropriate.
CLASSIFICATIONS
• Severe disease: <1% normal factor activity (<0.01 IU/mL). Spontaneous bleeding may
occur, classically hemoarthrosis.
• Moderate disease: 1–5% normal factor activity (0.01–0.05 IU/mL).
• Mild disease: 5–40% normal factor activity (>0.05 to <0.40 IU/mL).
TREATMENT
Premedications
• Desmopressin (DDAVP)—may administer to control or prevent bleeding in mild-to-moderate
hemophilia A. DDAVP is a synthetic analogue of vasopressin (antidiuretic hormone) that
lacks pressor activity; It increases circulating FVIII levels 2–4 times above baseline via
release from endothelial storage sites; in those with FVIII levels 9% of normal, it can
increase circulating FVIII levels 4–6 times above baseline (5). Dosage: 0.3 μg/kg IV over 15–
30 minutes; should be administered 30 minutes prior to scheduled procedure while
monitoring BP and pulse.
• Recombinant FVIII and FIX (moderate and severe disease) should be administered in
consultation with a hematologist. For every 1 U/kg of concentrate that is administered,
activity levels rise by ∼1–2%.
– In elective surgery, the goal is to attain 40% activity. In severe disease, an initial dose of
20 U/kg can be given within 1 hour of surgery, followed by 1.5 U/kg/hour of FVIII or 2
U/kg/hour of FIX.
– For major surgical procedures, factor levels should be between 60% and 100% prior to
surgery and maintained at 30–50% until the wound has healed (typically for 10–14 days)
(3).
– For orthopedic procedures, activity levels of 80–100% are suggested and should be
maintained at 30% for several days after the procedure.
• Presence of inhibitors to FVIII and FIX may make therapy with concentrates not an option.
Instead, recombinant FVIIa may be given as an initial IV bolus of 90–120 μg/kg over 2–5
minutes and redosed every 2 hours until hemostasis is attained (6).
Jehovah’s witness: Consent must be detailed for any plasma-derived clotting factor
replacement.
INTRAOPERATIVE CARE
• General or sedation depending on the surgical procedure
• Neuroaxial blocks are contraindicated given the risk of epidural hematoma.
• Peripheral nerve blocks (PNBs) may be safely performed in a hemophiliac patient, provided
that FVIII and IX activity levels are appropriate (7). Consider ultrasound assisted to decrease
the risk of tissue trauma or vessel puncture.
Monitors
• Dependent on surgery. High-risk or prolonged procedure should consider invasive monitors.
• Arterial line may be beneficial in patients for serial PTT and factor level evaluation in severe
hemophiliacs.
• A second large bore IV line should be placed for infusion of factors.
Concerns for bleeding from airway trauma are decreased if factor replacement has been
initiated.
Maintenance
Intraoperative bleeding poses the greatest risk despite optimizing preoperatively. Be prepared
to administer FFP, FVIIa, or increase the infusion rate of factor concentrate.
Standard criteria apply depending on the patient’s medical history, airway concerns, and type
of surgery.
POSTOPERATIVE CARE
BED ACUITY
• Depends on the risk of postoperative bleeding, type of surgery, and severity of disease
• Depending on the institution, factor concentrate infusion may not be administered on the
floor.
• Ongoing consultation with hematologist
• Labs: Factor levels, inhibitors, and PTT levels should be checked postoperatively and as
needed.
• Additional factor replacement should be guided by the activity of clotting factors for about
6–10 days postoperatively (depending on the surgical procedure) (8), and in conjunction
with a hematologist.
COMPLICATIONS
Ongoing surgical bleeding beyond the initial postoperative period is a concern.
REFERENCES
1. Bitting RL, Bent S, Li Y, Kohlwes J. The prognosis and treatment of acquired hemophilia: A
systematic review and meta-analysis. Blood Coagul Fibrinolysis. 2009;20(7):517–523.
2. erntorp E. Consensus perspectives on prophylactic therapy for haemophilia: Summary
statement. Haemophilia. 2003;9(Suppl 1):1–4.
3. Martlew VJ. Peri-operative management of patients with coagulation disorders. Br J
Anaesth. 2000;85(3):446–455.
4. Varughese J, Cohen AJ. Experience with epidural anaesthesia in pregnant women with von
Willebrand disease. Haemophilia. 2007;13(6):730–733.
5. Mannucci PM, Ruggeri ZM, Pareti FI, et al. 1-Deamino-8-d-arginine vasopressin: A new
pharmacological approach to the management of haemophilia and von Willebrands’
diseases. Lancet. 1977;1(8017):869–872.
6. Shapiro AD, Gilchrist GS, Hoots WK, et al. Prospective, randomised trial of two doses of
rFVIIa (NovoSeven) in haemophilia patients with inhibitors undergoing surgery. Thromb
Haemost. 1998;80(5):773–778.
7. Sripada R, Reyes JJ, Sun R. Peripheral nerve blocks for intraoperative management in
patients with hemophilia A. J Clin Anesth. 2009;21(2):120–123.
8. Brettler DB, Levine PH. Factor concentrates for treatment of hemophilia: Which one to
choose? Blood. 1989;73:2067.
9. Ramsahoye BH, Dasani H, Pearson JF. Obstetric management in von Willebrand disease: A
report of 24 pregnancies and a review of the literature. Haemophilia. 1995;1:140–144.
10. Logan AC, Goodnough LT. Recombinant factor VIIa: An assessment of evidence regarding
its efficacy and safety in the off-label setting. Hematology Am Soc Hematol Educ Program.
2010;2010:153–159.
• von Willebrand’s disease
CODES
ICD9
• 286.0 Congenital factor VIII disorder
• 286.1 Congenital factor IX disorder
ICD10
• D66 Hereditary factor VIII deficiency
• D67 Hereditary factor IX deficiency
CLINICAL PEARLS
• Early consultation with a hematologist is critical to evaluate the extent of disease and
treatment options.
• If a patient has had a history of multiple factor replacements in the past, there is an
increased likelihood that inhibitors may have formed.
• Obstetrical literature suggests maintaining FVIII levels to more than 30% to minimize the
risk of bleeding after delivery (9).
• Recombinant factor VIIa is FDA approved to treat bleeding secondary to hemophilia (10).
When administered in pharmacological doses (~1000 times greater than normal circulating
levels), rFVIIa improves the coagulation process at the site of injury by:
– Directly (without forming a complex with tissue factor [TF]) activating factor X on the
activated platelets at the site of injury, and thus bypassing the need for factors VIII and IX.
– Boosting the TF-dependent pathways
• Cardiopulmonary bypass. Preoperative preparation includes attaining a factor activity level
of 100%. During bypass, it is not necessary to administer an infusion to counteract the
dilutional effect of the pump circuit. A repeat bolus of factor concentrate is given post
bypass and prior to wound closure followed by factor infusion. It is safe to administer
standard heparinization doses during cardiac bypass as well as protamine reversal.
HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)
James D. Boone, MD
BASICS
DESCRIPTION
• Describes a drug-induced thrombocytopenia after exposure to any dose or type of heparin
• Two types of heparin-induced thrombocytopenia (HIT) exist:
– Type I most likely has a nonimmune mechanism. Heparin causes mild platelet
aggregation, especially in patients with activated platelets. This results in increased
platelet sequestration in the spleen, leading to thrombocytopenia.
– Type II is an autoimmune complication after heparin exposure. Unlike other drug-induced
thrombocytopenias, HIT does not cause bleeding. Instead, it causes thrombosis and carries
an increased risk for thromboembolic complications. For the purpose of this chapter, HIT
will refer to type II.
EPIDEMIOLOGY
Incidence
• Type I: 1–4% following exposure to unfractionated heparin and in <1% of patients treated
with low molecular weight heparin (LMWH).
• Type II: 0.5–5% after exposure to unfractionated heparin for more than 4 days.
Morbidity
In association with thrombosis 9–11%
Mortality
• Overall 1%
• If thrombosis develops: 8–20% (despite treatment)
• Longer duration of heparin therapy (>4 days)
• Use of unfractionated heparin rather than LMWH
• Bovine in origin rather than porcine
• Surgical rather than medical patients; highest risk after cardiac, orthopedic, and
neurosurgical procedures
• Female gender
• Rare in pediatric, obstetric, and patients receiving hemodialysis
• Malignancy
• Severe thrombocytopenia
• High heparin-PF4 antibody titer
• Heparin is a highly sulfated and negatively charged glycosaminoglycan that has a high
affinity for platelet factor 4 (PF4).
– PF4 is highly positively charged. It is found in the alpha-granules of platelets and exists in
the plasma in low levels (following platelet activation, the PF4 plasma concentration
rises).
– PF4 binds to heparin, forming a heparin-PF4-complex. A conformational change in PF4
occurs, that leads to the exposure of new epitopes. These epitopes act as immunogens, and
stimulate the production of IgG antibodies.
– The heparin-PF4 complex binds to platelets via heparin binding sites.
– When IgG binds to this complex, platelets become activated and further release PF4. This
leads to
Platelet consumption
Thrombocytopenia
Thrombin release
Tissue factor activation; sets off the cascade and leads to a prothrombotic state.
• Since LMWH has a shorter molecular length than unfractionated heparin, it binds weakly to
PF4 and is less likely to cause HIT.
• Heparin avoidance
• Early recognition and treatment to avoid complications
DIAGNOSIS
• Type I:
– Mild thrombocytopenia with an early-onset (usually within 2 days)
– The platelet count is rarely <80 × 109/L
– Spontaneous resolution within a few days even if heparin is continued.
– Patients are usually asymptomatic and have no thrombosis.
• Type II. Diagnosis should initially be made on a clinical basis: Development of
thrombocytopenia while on heparin, exclusion of other causes of thrombocytopenia, and
resolution of thrombocytopenia after cessation of heparin administration.
– The moderate-to-severe reduction in platelet count usually occurs gradually after 5–10
days. Delayed-onset HIT can present with a fall in platelet count days or weeks after
heparin exposure.
– Platelet count is usually around 50 × 109/L (alternatively, there is a 50% reduction from
baseline). However, the platelet count can also be normal if a 50% reduction occurred
after an elevated baseline count.
– Unless heparin is stopped, the platelet count will not return to baseline.
– Thrombotic complications are common, whereas bleeding is rare. Thromboses can occur
in veins, arteries or both, depending on the clinical setting.
– In postoperative patients, deep vein thrombosis (DVT) and pulmonary embolism are more
common. Venous thrombosis can be severe and can even cause venous gangrene.
– In patients with a history of peripheral vascular disease and advanced artherosclerosis,
arterial thrombosis is more common and can lead to limb gangrene and leg amputation.
• Laboratory testing. Can be helpful in the confirmation of HIT, but is less important if the
clinical picture is clear. Additionally, the assays with the highest sensitivity and specificity
may not be readily available and have a slow turnaround time. If laboratory tests are
needed to make a diagnosis decision, treatment should not be withheld. They are divided
into either functional tests or immunoassays:
– Functional tests assess platelet activation and altered platelet function caused by HIT
antibodies.
C-serotonin release assay (SRA) is considered the gold standard with a 90–98%
sensitivity. It has a 95% specificity for early-onset HIT and a 80–97% specificity for late-
onset HIT.
Heparin-induced platelet aggregation (HIPA) has a 90–98% sensitivity. It has a 95%
specificity for early HIT and 80–97% specificity for late-onset HIT.
– Immunoassays. Enzyme-linked immunosorbent essay (ELISA) is the most common. The
solid-phase anti-PF4/heparin ELISA complex detects HIT antibody binding. ELISA can
show false positives since it detects all antibodies (even those not causing HIT). ELISA has
a >91–97% sensitivity. It has a >95% specificity with early platelet fall and a 50–93%
specificity with a late platelet fall.
• Doppler of extremities should be considered to rule out thrombosis.
Thrombocytopenia caused by
• Drugs such as glycoprotein IIb/IIIa inhibitors and antibiotics
• Sepsis
• Disseminated intravascular coagulopathy
• Bone marrow disease
• Intra-aortic balloon pumps
• Hemofiltration therapies
TREATMENT
• Type I: Since type 1 is usually transient and clinically insignificant most patients remain
asymptomatic and no specific treatment is required. If it is difficult to differentiate between
type I and type II, the patient should be treated as having type II.
• Type II:
– Discontinuation of all sources of heparin, including LMWH and heparin-coated catheters.
– Avoid prophylactic platelet transfusions.
– Give alternative anticoagulant to avoid clot formation while the platelet count recovers
and antibody formation decreases. Alternative anticoagulation includes either direct
thrombin inhibitors (lepirudin, bivalirudin, argatroban) that reduce activity of thrombin
or heparinoids (danaparoid, fondaparinux) that reduce thrombin formation. These drugs
act immediately and should be continued for at least 5 days or until thrombosis is under
control.
– Warfarin is not an option for immediate alternative anticoagulation. Since warfarin
initially decreases protein C levels faster than the coagulation factors, it can worsen
thrombosis and cause leg gangrene and cutaneous necrosis. Treatment with danaparoid,
lepirudin, bivalirudin, or argatroban should overlap warfarin therapy for a few days.
– Thrombolytic therapy may be needed in patients with severe DVT and limb gangrene or
pulmonary embolism.
– In patients who cannot be anticoagulated, an inferior vena cava filter can be placed.
– Embolectomy might be necessary in some cases.
FOLLOW-UP
• Serial platelet counts should be performed.
• HIT antibodies usually disappear in a 100 days after the onset of HIT.
• To prevent the recurrence of thrombosis, long-term treatment (e.g., for 6 months) is usually
required.
• Re-exposure. Heparin is unlikely to result in a recurrence of HIT; however,
recommendations lean toward heparin avoidance in the future if possible.
– If no heparin alternative is available, negative HIT antibodies need to be confirmed and
heparin should only be used for a short period of time.
– Patients with positive HIT antibodies needing noncardiac surgery with anticoagulation
(e.g., vascular surgery) can be given argatroban as an alternative to heparin.
– Elective cardiac surgery with cardiopulmonary bypass (CPB) should be postponed in
patients with positive HIT antibodies until the platelet count is restored and HIT
antibodies are eliminated from the circulation. Heparin should only be used during the
surgery, and an alternative anticoagulant should be used pre- and postoperatively.
– If cardiac surgery cannot be postponed and HIT antibodies are still present, consider the
following alternatives:
Bivalirudin for anticoagulation on CPB
Lepirudin during off-pump cardiac surgery
Heparin plus the antiplatelet agent tirofiban or danaparoid.
REFERENCES
1. Chong BH. Heparin-induced thrombocytopenia. J Thromb Haemost. 2003 Jul;1(7):1471–
1478.
2. Shantsila E, et al. Heparin-induced thrombocytopenia: A contemporary clinical approach to
diagnosis and management chest. 2009;135(6):1651–1664.
ADDITIONAL READING
• www.heparininducedthrombocytopenia.com
CODES
ICD9
289.84
ICD10
D75.82 Heparin induced thrombocytopenia (HIT)
CLINICAL PEARLS
• Recognize thrombocytopenia in the setting of heparin administration. Thrombocytopenia is
defined as a >50% reduction from baseline platelet count or absolute values <100 ×
109/L after 5–10 days of heparin administration
• HIT carries a high risk for thrombosis and thromboembolic events.
• If Type 2 HIT is suspected, heparin, LMWH, and all heparin sources need to be discontinued
and alternative anticoagulation should be started.
HEPATIC ENCEPHALOPATHY
Allyson J.A. Morman, MD
BASICS
DESCRIPTION
• Hepatic encephalopathy (HE) is a serious, progressive, and reversible metabolic
encephalopathy characterized by neuropsychiatric abnormalities and neuromuscular
dysfunction that range from mild cognitive and motor impairment to coma and death.
• HE results from the abnormal accumulation of toxic substances that are normally cleared
(detoxified) by the liver.
EPIDEMIOLOGY
Incidence
New or worsening HE occurs in 30–35% of patients following a transjugular intrahepatic
portosystemic shunt (TIPS) procedure (1).
Prevalence
• Minimal HE occurs in 60–80% of patients with cirrhosis.
• Overt hepatic encephalopathy (OHE) can be seen in 30–45% of patients with advanced liver
disease.
Morbidity
Severely impairs driving skills and/or work performance.
Mortality
After the 1st occurrence of OHE, mortality at 1 year was 42% and 23% at 3 years (2).
• GI bleeding (excess protein load)
• Sepsis
• Dehydration (excessive diuretics, vomiting, diarrhea)
• Hyponatremia, hypokalemia
• Postsurgical states
• Medication noncompliance
• Sedative use (opiates, benzodiazepines, antidepressants)
• TIPS placement
• Constipation
• Excessive dietary protein
PATHOPHYSIOLOGY
• Elevated levels of ammonia in the presence of an inflammatory response cause astrocyte
swelling and fluid accumulation in the brain (cerebral edema).
– Ammonia is normally converted to urea by the liver; however, with liver failure, ammonia
concentrations rise.
– An alternative pathway in muscle (via glutamine synthetase enzyme) serves to metabolize
ammonia to glutamine. Saturation of this secondary pathway leads to accumulation of
ammonia in plasma that easily passes through the blood-brain-barrier and comes into
contact with astrocytes.
– Astrocytes convert excess ammonia to glutamine intracellularly. This process will lead to
cellular swelling, cerebral edema, and ultimately increased intracranial pressure (ICP).
• Historically, the role of ammonia accumulation has dominated explanations of pathogenesis,
but it is now recognized that the pathogenesis is multifactorial. Oxidative stress,
endogenous benzodiazepine-like ligands, astrocyte swelling, GABA-like molecules, abnormal
histamine and serotonin neurotransmission, endogenous opioids, neurosteroids,
inflammatory cytokines, and manganese toxicity are other potential mediators of
pathogenicity.
• Assess the severity of HE and treat underlying as well as precipitating causes prior to
surgery. Emergent cases may require proceeding with concurrent perioperative
management.
• Pharmacokinetic alterations can include: Decreased hepatic metabolism; decreased albumin
leading to less protein binding (more free drug available); and increased volume of
distribution due to ascites and increased total body water compartments.
SYMPTOMS
Difficulty concentrating, increasing pruritus
History
• Course of HE
• Assess for the presence of comorbidities: History of esophageal varices, easy bruising,
ascites, orthodeoxia/platypnea, renal dysfunction
• Recent paracentesis
Signs/Physical Exam
• Altered mental status, ascites, peripheral edema, jaundice, asterixis.
• In severe cases (e.g., type A), may see muscular rigidity or clonus, extensor plantar
responses, slurred speech, tremor, or decerebrate posturing.
TREATMENT HISTORY
Liver transplantation
MEDICATIONS
• Lactulose; first-line therapy with a direct effect on the GI system. It is a nonabsorbable
disaccharide that is fermented in the colon and reduces the intestinal production and
absorption of ammonia.
• Rifaximin; direct effect on the GI system. A nonabsorbable antibiotic that is very expensive
and reserved for patients who are either intolerant or refractory to lactulose. Its cost,
however, may be justified by the reduced need for hospitalization.
• Flumazenil; direct neurological therapy. A GABA antagonist that can produce short-term
reversal of HE symptoms. Has fallen out of favor secondary to its potential to decrease the
seizure threshold and its transient efficacy.
• Metronidazole and neomycin; antibiotics that reduce intestinal ammonia production.
However, it lacks data that support its efficacy.
– Long-term neomycin administration is associated with nephrotoxicity and ototoxicity.
– Long-term metronidazole administration is associated with peripheral neuropathy.
Labs/Studies
• Arterial ammonia levels. In acute liver failure, ammonia levels >200 μg/L were found to be
almost invariably associated with cerebral uncal herniation in patients with grade 3 and 4
HE (3). Otherwise, ammonia levels (especially ones that are drawn venously) are not
reliable indicators of severity of HE.
• Sodium levels. Hyponatremia is present in ~25% of patients with acute liver failure; it
becomes more prominent with severe encephalopathy.
• CBC, PT/PTT/INR
End stage liver disease
• Overt hepatic encephalopathy (OHE) should be optimized medically and the underlying
etiology addressed prior to an elective and possibly an urgent procedure. This may not
always be possible, as with GI bleeding (etiology) or other emergent cases.
• Coagulopathy
• Poor nutrition status
• Hypovolemia
CLASSIFICATIONS
• Overt hepatic encephalopathy (OHE). Combination of neurological and neuropsychiatric
abnormalities that can be detected by bedside clinical tests.
• Minimal hepatic encephalopathy (MHE). Normal mental and neurological function but
abnormal results on formal neuropsychometric testing.
• World Congresses of Gastroenterology Classification System
– Type A: Associated with acute liver failure. Increased incidence of elevated ICP that can
lead to brain stem herniation and death. Thirty percent mortality rate if the ICP is
elevated (4).
– Type B: Associated with portosystemic bypass without intrinsic liver disease
– Type C: Associated with cirrhosis
• West Haven Criteria. Grades the severity of HE and is based on intellect/behavior as well as
level of consciousness and neurological findings.
– Grade 1 – Trivial lack of awareness; euphoria or anxiety; shortened attention span;
impaired performance of addition or subtraction.
– Grade 2 – Lethargy or apathy; minimal disorientation for time or place; subtle personality
change; inappropriate behavior.
– Grade 3 – Somnolence to semistupor, but responsive to verbal stimuli; confusion; gross
disorientation.
– Grade 4 – Coma (unresponsive to verbal or noxious stimuli).
• Childs–Pugh class score measures lab values (total bilirubin, serum albumin, PT/INR) and
clinical symptoms (ascites, hepatic encephalopathy) to assess perioperative mortality risk.
Class A is 10%, Class B is 30%, Class C is 82%.
• Model for end-stage liver disease (MELD) score. Originally developed to predict short-term
mortality in patients undergoing a TIPS procedure, but currently being used as a predictor
for 30-day postoperative mortality and organ allocation in the US (5). It provides an
objective measure and is based on laboratory values (INR, bilirubin, creatinine). A score of
5 has a 5% risk; a score of 10 has a 7% risk; a score of 15 has a 11% risk; a score of 20 has a
17% risk; and a score of 25 has a 26% risk.
TREATMENT
Premedications
• If benzodiazepines are needed, they should be short-acting and given in reduced doses (drug
clearance is reduced, half-life increased).
• Fentanyl can be used safely despite being almost completely metabolized by the liver.
• Patient may not be able to provide consent.
• Increased risk of morbidity and mortality that need to be weighed against the urgency of the
procedure.
• Potential for postoperative intubation.
INTRAOPERATIVE CARE
• General endotracheal anesthesia is commonly chosen to provide airway protection in grade
III or IV HE (bleeding varices, ascites, obtundation), or manage ICPs, esophageal varices,
severe ascites, or obtundation.
• Any patient presenting with moderate encephalopathy has impaired liver failure and
drugs/dosages should be modified appropriately.
Monitors
• Consider neurosurgical consultation for the placement of an ICP monitoring device.
• Consider an arterial line in high-risk patients in order to closely monitor acid/base status.
• Consider a rapid sequence induction or awake intubation in patients with concurrent GI
bleeding/history of esophageal varices.
• Pharmacokinetic profile of propofol is not significantly altered in the presence of liver
disease and is thus a safe induction agent; however, may cause hypotension.
• Nondepolarizing muscle relaxants selection. Most have prolonged half-lives because of
impaired biliary excretion. Atracurium and cisatracurium do not rely on hepatic or renal
excretion (Hoffmann elimination).
• Anticipate hypotension as endogenous stores of catecholamines are often depleted and wider
swings in BP can be expected.
Maintenance
• Volatile anesthetics. Isoflurane and desflurane are preferred (low hepatic metabolism, less
effects on hepatic blood flow); however, sevoflurane is probably also appropriate. Avoid
halothane and enflurane: Decreases total hepatic blood flow and their higher hepatic
metabolism leads to formation of adducts. Adducts are formed with liver proteins that can
be recognized as neoantigens. They are associated with the production of humoral and
cellular immune responses that are involved in hepatotoxicity.
• Opioid selection. Fentanyl has advantages already noted. When utilized, other opioids
should be given at reduced doses secondary to their toxic metabolites (meperidine) and/or
prolonged duration of action (morphine, hydromorphone).
• Maintain ICP <20–25 mm Hg with a CPP >50–60 mm Hg. Prolonged ICP >40 mm Hg and
CPP <50 mm Hg have been shown to be associated with poor outcome (3). Mannitol,
hyperventilation, head-up position, and hypertonic saline may be considered.
• Consider empiric antibiotics if the precipitating cause of the HE episode remains undefined.
• Meperidine has prolonged duration of action as does its major metabolite, normeperidine
(more susceptible to seizures), and should be avoided.
If the ICP is increased, or there is a risk for aspiration (AMS, grade III or IV HE), consider
leaving the patient intubated to manage PaCO2 most effectively.
POSTOPERATIVE CARE
BED ACUITY
Admit to ICU if surgery is prolonged, cardiac and/or pulmonary surgery were performed,
intraoperative hypotension, excessive blood loss, or Grade III/IV HE.
• Continue preoperative lactulose and antibiotics.
• Carefully titrate sedatives and pain medications to prevent exacerbation.
• Consider hepatology or GI consult.
COMPLICATIONS
• Worsening jaundice, encephalopathy, and ascites
• Hepatorenal syndrome
• Development of sepsis and secondary disseminated intravascular coagulation.
REFERENCES
1. Somberg KA, Riegler JL, LaBerge JM, et al. Hepatic encephalopathy after transjugular
intrahepatic portosystemic shunts: Incidence and risk factors. Am J Gastroenterolgy.
1995;90:549–555.
2. ustamante J, et al. Prognostic significance of hepatic encephalopathy in patients with
cirrhosis. J Hepatol. 1999;30(5):890–895.
3. roglu Y, Byrne WJ. Hepatic encephalopathy. Emerg Med Clin N Am. 2009;27:401–414.
4. Shawcross D, Jalan R. The pathophysiological basis of hepatic encephalopathy: Central role
for ammonia and inflammation. Cell Mol Life Sci. 2005;64:2295–2304.
5. Northup PG, et al. Model for end-stage liver disease (MELD) predicts nontransplant surgical
mortality in patients with cirrhosis. Ann Surg. 2005;242(2):244–251.
6. Bajaj JS. The modern management of hepatic encephalopathy. Aliment Pharmacol Ther.
2010;31:537–547.
7. Furst SM, Chen M, Gandolfi AJ. Use of halothane as a model for investigating chemical-
induced autoimmune hepatotoxicity. Drug Inf J. 1996;30(1):301–307.
ADDITIONAL READING
• The American College of Gastroenterology Clinical Practice Guidelines:
http://www.acg.gi.org/physicians/clinicalupdates.asp
• Hoffman elimination
CODES
ICD9
572.2
ICD10
K72.90 Hepatic failure, unspecified without coma
CLINICAL PEARLS
• Infection/inflammation and oxidative stress act synergistically with ammonia to create the
pathogenesis of the clinical syndrome. Most commonly, the precipitating incident is either
medication noncompliance or infection. Empiric antibiotics should be started.
• Serum ammonia levels are elevated in 90% of patients, but encephalopathy can be present
with normal serum ammonia levels as well.
• Catecholamine and other neurohormonal responses are impaired in patients with liver
disease. Thus, intraoperative hypovolemia or hemorrhage may not be able to trigger
adequate compensatory mechanisms. Subsequent decreases in oxygen delivery to the liver
can further worsen hepatic dysfunction.
HEPATITIS C
Neesa Patel, MD
BASICS
DESCRIPTION
• Hepatitis C is a virus that can cause acute and chronic inflammation of the liver. Clinical
presentation can range from inactive, dormant carrier states to severe fibrosis, cirrhosis,
end-stage liver disease, or hepatocellular carcinoma.
• Patients with hepatitis C can present perioperatively for procedures that are related (e.g.,
liver transplantation, transjugular intrahepatic portosystemic shunt (TIPS), and liver
resection) and unrelated to liver disease.
• Healthcare workers are at an increased risk for exposure due to needlestick injuries. The
average incidence of seroconversion to hepatitis C virus (HCV) after unintentional needle
sticks or sharps exposures from an HCV-positive source is 1.8% (range of 0–7%) (1).
• Unfortunately, at this time there is no proven effective postexposure prophylaxis for persons
exposed to HCV blood or contaminated body fluids.
EPIDEMIOLOGY
Prevalence
• In the US: 28,000 new infections/year
• Chronic hepatitis develops in about 85% of those infected.
Prevalence
In the US, there are an estimated 3.2 million persons (1.3% of the population) (2).
Morbidity
It is the leading cause of liver transplantation, accounting for 30% of all liver transplants.
Mortality
Chronic HCV accounts for 8–10,000 deaths/year
The US Centers for Disease Control and Prevention (CDC) recommend assessment of HCV risk
factors; those with risk factors should be screened for HCV antibodies (anti-HCV). The
American Association for the Study of Liver Diseases rates the level of evidence for screening
in all of the following risk groups as class 1B (3):
• High risk: IV drug abusers, hemophilia patients treated with clotting factor concentrates
produced before 1987, HIV-positive patients
• Intermediate risk: Recipients of blood transfusions or solid organ transplants before 1992,
patients with unexplained elevated aminotransferase levels, patients born from infected
mothers.
• Low risk: People who have had sexual relations with multiple or infected partners;
healthcare workers exposed to HCV (e.g., needlestick) (4).
• HCV replicates within hepatocytes but can be found in multiple sites throughout the body. It
is not directly hepatotoxic.
• Liver parenchyma damage is mediated by inflammatory cytokines that lead to varying
degrees of hepatic fibrosis. Only some patients develop progressive fibrosis and eventually
cirrhosis. Predictors of progression include
– Advanced age at the time of infection
– Male gender
– Excessive alcohol use
– Co-infection with hepatitis B virus (HBV)
– Hemophiliacs with multiple transfusions
– Injection drug users and HIV
– Persistently elevated aminotransferase activity
– Concomitant liver disease (5–7)
• Because the immune system’s antibody response cannot clear the infection, there is slow
progress in the development of a vaccine.
• Hepatitis C infection alone without end-organ damage usually does not require specific
perioperative considerations. However, even asymptomatic patients should be screened
before elective surgery; the INR is the most sensitive indicator of disease severity.
• Patients who have developed liver disease or cirrhosis should be carefully evaluated and
optimized prior to surgery. Perioperative goals should include maintaining hepatic
perfusion and avoiding factors that might precipitate liver failure or hepatic
encephalopathy.
• Elective surgery should be delayed in patients with acute hepatitis of any etiology until
resolution (8).
SYMPTOMS
• Chronic hepatitis C infection is usually asymptomatic.
• In the acute phase, look for signs of acute hepatitis: Malaise, nausea, and right upper
quadrant pain, followed by dark urine and jaundice.
• Patients with uncompensated end-stage liver dysfunction can present with signs of
encephalopathy.
History
• Assess for risk factors and consider screening as appropriate
• Clinically important hepatic dysfunction is more likely to occur in patients with preexisting
liver disease.
Signs/Physical Exam
Acute hepatitis: Myalgia, right upper quadrant pain, anorexia. However, it is also frequently
asymptomatic (many patients may hence be unaware of infection or carrier status).
TREATMENT HISTORY
• Liver transplantation
• TIPS
• Large volume paracentesis
• Endoscopic variceal ligation
MEDICATIONS
• Interferon-alpha and oral ribavirin during the first 6 months of infection.
• Diuretics (spironolactone) for ascites
• Antibiotics (cephalosporins) for spontaneous bacterial peritonitis
• Lactulose and poorly absorbable antibiotics (rifaximin, neomycin, metronidazole) for
hepatic encephalopathy.
Labs/Studies
• Enzyme immunoassays (EIAs) for diagnosing HCV infection are recommended as the initial
serologic test for screening populations at risk.
• A positive anti-HCV EIA requires HCV RNA measurement to discriminate between current
infection on the one hand, and either resolved HCV infection or a false-positive result on the
other (4)
• CBC
• Coagulation studies: INR is the most sensitive indicator of severity of disease
• Complete metabolic panel
Cirrhosis and end-stage liver disease manifest as impaired hepatic synthesis and metabolism
as well as increased hepatic vascular pressures:
• CNS: Encephalopathy, asterixis, peripheral neuropathy
• Cardiovascular: Decreased systemic vascular resistance, high output cardiac failure
• Pulmonary: Pulmonary shunting may cause hypoxemia and pulmonary hypertension; pleural
effusions
• Hepatic: Cirrhosis, portal hypertension, varices, ascites, splenomegaly
• Renal: Insufficiency or failure; hepatorenal syndrome describes renal disease in the absence
of primary disease and may be related to hypoperfusion.
• Coagulation: Decreased production of hepatic synthesized factors, thrombocytopenia
• Infectious: Spontaneous bacterial peritonitis
• Cutaneous: Jaundice, palmar erythema, spider nevi, male gynecomastia
• Elective surgery should be delayed in patients with acute hepatitis of any etiology until
resolution of hepatocellular dysfunction (1).
• When surgery cannot be avoided, meticulous care should be taken perioperatively to
maintain hepatic perfusion and avoid factors that might precipitate liver failure, hepatic
encephalopathy, or both.
CLASSIFICATIONS
• Acute infection
– Symptoms consistent with acute viral hepatitis along with jaundice/dark urine or serum
alanine aminotransferase levels >400 IU/L
– Positive hepatitis C antibody (anti-HCV), recombinant immunoblot assay (HCV RIBA), or
nucleic acid test (NAT).
– Combined with a negative IgM antibody to hepatitis A virus and hepatitis B core antigen
• Chronic infection
– Symptoms may range from none to severe
– Positive anti-HCV by EIA combined with either a more specific assay or HCV RIBA, or
NAT.
TREATMENT
Premedications
• Anxiolysis may be administered safely in asymptomatic patients with normal liver function
tests.
• Correct coagulopathies with vitamin K and fresh frozen plasma.
• Correct electrolyte abnormalities
• Intravascular volume repletion
Depending on the severity of liver dysfunction, anesthetic morbidity, and mortality rise
INTRAOPERATIVE CARE
• Asymptomatic without ESLD can be performed with general, regional, or deep sedation
depending on the surgical procedure and patient preference.
• In coagulopathic patients, neuroaxial blocks should be avoided. Regional techniques may be
acceptable but risks of bleeding should be weighed against the benefits of avoiding general
anesthesia.
Monitors
• Standard ASA monitoring
• Invasive monitoring such as an arterial or central line may be appropriate depending on the
extent of the procedure and liver disease severity.
• A standard induction may be appropriate in patients without (or only minimal) liver
dysfunction
• If significant liver dysfunction, use caution with benzodiazepines, morphine, demerol,
neuromuscular agents.
Maintenance
Volatile agents. Halothane and enflurane appear to reduce hepatic artery blood flow via
systemic vasodilation and a mild negative inotropic effect. Halothane is also associated with
hepatotoxicity.
Standard precautions
FOLLOW-UP
BED ACUITY
• Depends on extent of liver disease, surgical procedure, and intraoperative course.
• Monitor for signs of acute liver failure, including worsening jaundice, encephalopathy, and
ascites.
• Patients with preoperative acute hepatitis or cirrhosis from hepatitis C are at increased risk
of postoperative jaundice.
• Patients with more advanced liver disease (CTP class B or C cirrhosis) are at increased risk
of encephalopathy, cerebral edema, coagulopathy, hemorrhage, and portal hypertension.
COMPLICATIONS
• Infectious exposure to the hepatitis C patient
– Cuts or needle-stick injuries may occur in up to 15% of all surgeries.
– The risk of HCV transmission depends on the volume of blood transmitted, but <0.5% of
such injuries are considered high risk (e.g., hollow-bore needle) (9).
– There is no vaccine or immunoglobulin to protect against transmission. Additionally,
prophylactic post-exposure treatment with interferon and/or ribavirin is not
recommended.
– At this time, the following recommendations are:
Baseline testing of the injured for anti-HCV and ALT activity
Follow-up testing 4–6 months for anti-HCV and ALT activity or HCV RNA at 4–6 weeks
Careful monitoring for laboratory abnormalities and signs/symptoms of acute infection
Avoidance of blood, plasma, organ, tissue, or semen donation
REFERENCES
1. holson CF, Provenza JM, Bacon BR. Hepatologic considerations in patients with
parenchymal liver disease undergoing surgery. Am J Gastroenterol. 1990;85:487–496.
2. Armstrong GL, Wasley A, Simard EP, et al. The prevalence of hepatitis C virus infection in
the United States, 1999 through 2002. Ann Intern Med. 2006;144:705–714.
3. Ghany MG, Strader DB, Thomas DL, et al., American Association for the Study of Liver
Diseases. Diagnosis, management, and treatment of hepatitis C: An update. Hepatology.
2009;49:1335–1374.
4. Albeldawi M, Ruiz- Rodriguez E, Carey WD. Hepatitis C virus: Prevention, screening, and
interpretation of assays. Cleve Clin J Med. 2010;77(9):616–626.
5. Thomas DL, Astemborski J, Rai RM, et al. The natural history of hepatitis C virus infection:
Host, viral, and environmental factors. JAMA. 2000;284:450–456.
6. Seeff LB. Natural history of chronic hepatitis C. Hepatology. 2002;36:S35–S46. Shakil AO,
Conry-Cantilena C, Alter HJ, et al. Volunteer blood donors with antibody to hepatitis C
virus: Clinical, biochemical, virologic, and histologic features. Ann Intern Med.
1995;123:330–337.
7. Gholson CF, Provenza JM, Bacon BR. Hepatologic considerations in patients with
parenchymal liver disease undergoing surgery. Am J Gastroenterol. 1990;85:487–496.
8. U.S. Public Health Service. Updated U.S. Public Health Service Guidelines for the
Management of Occupational Exposures to HBV, HCV, and HIV and Recommendations for
Postexposure Prophylaxis. MMWR Recomm Rep. 2001;50(RR-11):1.
• Liver resection
• Transjugular intrahepatic portosystemic shunt (TIPS)
• Cirrhosis
• Hepatic encephalopathy
• Infectious disease exposure in the healthcare worker
CODES
ICD9
• 070.51 Acute hepatitis C without mention of hepatic coma
• 070.54 Chronic hepatitis C without mention of hepatic coma
• 070.70 Unspecified viral hepatitis C without hepatic coma
ICD10
• B17.10 Acute hepatitis C without hepatic coma
• B18.2 Chronic viral hepatitis C
• B19.20 Unspecified viral hepatitis C without hepatic coma
CLINICAL PEARLS
• Patients with asymptomatic Hepatitis C infection alone usually tolerate anesthesia without
sequela.
• Elective surgery should be delayed in patients with acute hepatitis.
• Care should be taken when clinical signs of cirrhosis are apparent.
HERNIORRHAPHY
BASICS
DESCRIPTION
General
• A hernia is defined as a protrusion of any viscous structure from its proper cavity.
• Hernias can occur at any point in the abdominal wall, but some of the more common are
– Inguinal and femoral (groin hernias) occur from defects in the transverse abdominis layer.
Direct hernias protrude through the posterior wall of the inguinal canal, whereas indirect
hernias protrude through the internal inguinal ring.
– Umbilical hernias may be congenital or acquired. Congenital hernias arise from a
weakness in the area where the fetal vessels exited the muscular layer of the abdominal
wall. Umbilical hernias may also develop later in life, as continued tension in the same
area leads to progressive weakening of the muscular layer and eventual protrusion of
abdominal contents.
– Incisional hernias occur from prior surgical incisions. They are more common following
midline incisions, wound infection, or trauma.
• Hernia descriptions
– Reducible hernias refer to the ability to replace the contents of the hernia sac within their
proper cavity with pressure.
– Nonreducible hernias cannot be replaced with pressure.
– Incarcerated hernias occur when a portion of bowel becomes trapped in the defect and the
blood supply to that portion is compromised.
• The size of the hernia is not as important as the size of the defect in the abdominal wall, as a
small defect is more prone to entrap and strangulate bowel.
• Elective versus emergent repair
– Elective repair is performed to avoid the complication of incarceration and bowel
obstruction.
– Emergent repair is performed when symptoms and physical exam indicate the hernia is
incarcerated and to avoid bowel necrosis and intra-abdominal sepsis.
• Mesh may be used as an adjunct to the primary repair in order to reinforce the repair or
“plug” the defect. The use of mesh is possible with umbilical or groin hernias, depending on
the approach taken for the repair.
• Laparoscopic versus open depends on surgeon preference and characteristics of the hernia
such as location, size, and adherence of intra abdominal contents to the site of defect.
– Groin hernia: Laparoscopic or open; the laparoscopic approach may be preperitoneal or
intraperitoneal.
– Ventral hernia: Laparoscopic or open
– Umbilical hernia: Laparoscopic or open
Position
• Inguinal: Supine
• Ventral: Supine
Incision
• Ventral, umbilical, incisional: Incision at the site of defect
• Inguinal
– Open: Three- to four-inch groin incision
– Laparoscopic: Three or four one-inch incisions for trochar insertion
Approximate Time
• Length of case depends on the extent of the hernia.
• Open inguinal hernia repairs last approximately 1 hour.
EBL Expected
• Minimal
• Large abdominal hernia repairs with extensive lysis of bowel adhesions may result in
significant blood loss that is difficult to quantitate because it is not captured with the
suction.
Hospital Stay
• Straightforward hernia repairs may be performed on an outpatient basis.
• More extensive repairs, incarcerated hernias, or defects causing bowel obstruction require
more extensive hospitalizations for pain control and return of bowel function.
• Laparoscopic repairs: Laparoscopy monitors, cameras, trochars, etc.
• Mesh
EPIDEMIOLOGY
Incidence
• In the US: >1 million hernia repairs are performed annually; it is the most commonly
performed general surgery procedure.
• Inguinal hernias are the most common type.
• Men are affected more than women, by as much as a 19:1 ratio.
• Inguinal hernia incidence in children is as high as 4.4%.
Prevalence
Inguinal hernia estimated at 4.6%
Morbidity
• Related to complications of repair
– Adhesions
– Infection
– Chronic pain
– Hernia recurrence
• Related to complications of missed diagnosis
– Incarcerated bowel
– Bowel obstruction
– Peritonitis
Mortality
• Insignificant for elective hernia repairs
• Emergent hernia repairs carry up to a seven-fold increased mortality risk; this is related to
advanced age, ischemic bowel/need for bowel resections.
• Neuraxial techniques may be utilized as a sole technique (inguinal, femoral) or an adjunct to
a general anesthetic (incisional, umbilical).
• Minimize postoperative morbidity that can delay discharge home (nausea, pain).
SYMPTOMS
• It is very common to have an asymptomatic hernia.
• Fullness at site
• Ache or pain radiating into site
• Incarcerated hernia can present with pain at the site, nausea, and vomiting.
History
• Swelling or fullness at site that is associated with increases in intra-abdominal pressure
• History or prior abdominal surgery
• Family history of hernia
• Medical condition, such as BPH or chronic cough, that lead to increases in intra-abdominal
pressure.
• New onset nausea, vomiting, and abdominal pain may indicate a hernia involving bowel
obstruction.
Signs/Physical Exam
• Mass at site, visible with standing or increased intra-abdominal pressure
• If mass or fullness is present, assessing the mobility is important.
MEDICATIONS
None
Labs/Studies
• Preoperative labs as indicated for patient’s comorbidities
• KUB or CT scan to evaluate for obstruction and extent of hernia.
• If incarceration is suspected, WBC and/or BMP are indicated to evaluate for sepsis and
electrolyte abnormalities.
Incarcerated hernias may have other organs involved; the most common is small bowel or
colon, presenting as obstruction or strangulation.
TREATMENT
Premedications
• Standard, unless evidence of obstruction
• Incarcerated hernia carries a high-risk for aspiration; consider an H2 blocker. Avoid
metoclopramide in the setting of obstruction
If the planned procedure is laparoscopic, consent for open as well.
• First-generation cephalosporin
• Skin flora, including staphylococcus and streptococcus, are most common
INTRAOPERATIVE CARE
• Groin hernias
– Local with a genitofemoral, iliohypogastric, or ilioinguinal nerve block
– Paravertebral block
– Neuraxial block
– General anesthesia
• Ventral and umbilical hernias
– General
– Neuraxial
• Laparoscopic procedures must be performed with general endotracheal anesthesia.
Monitors
Standard ASA
• For open procedures, an LMA may be appropriate if muscle relaxation is not necessary
(groin hernias).
• Consider rapid sequence induction with cuffed endotracheal tube intubation in patients at
risk for aspiration or emergent repairs.
Maintenance
• Balanced inhaled or IV agent with or without muscle relaxant as needed for surgical
exposure and closure.
• For groin hernia under local anesthesia, consider small boluses of benzodiazepines, opioids,
or propofol (consider infusion).
• Avoidance of coughing and bucking is desired to avoid increases in abdominal pressure with
resultant tearing of sutures or displacement of mesh. A deep or comfortable extubation may
be considered, if appropriate.
• If bowel obstruction is present preoperatively, then the patient should be extubated when
fully awake, fully reversed, and capable of protecting their airway.
• Groin hernias are the most common in children.
• Pediatric patients have lower recurrence rates once the hernia defect is fixed.
• Caudal blocks provide excellent postoperative analgesia.
• Infants with significant pulmonary comorbidities are good candidates for hernia repair
under spinal anesthetic.
• There is no clear benefit to laparoscopic hernia repair in children, and it may increase
operative time, cost, and postoperative discomfort.
POSTOPERATIVE CARE
BED ACUITY
• Elective hernia repair appears to carry minimal increased risk of morbidity or mortality
(particularly when groin hernia repair is performed under local anesthesia).
• Emergent hernia repairs may be complicated by postoperative sepsis related to bowel
involvement.
ANALGESIA
• Local infiltration of the wound appears to provide the best postoperative pain relief
• Regional anesthesia (caudal, continuous epidural catheter, long acting epidural morphine,
tranversus abdominus plane (TAP) block)
• Opioid of choice
• NSAIDs such as IV ketorolac or PO ibuprofen; PO acetaminophen
COMPLICATIONS
• Recurrence of hernia
– 10% with open repair
– 1% if mesh utilized
• Damage to surrounding structures, that is, bowel, bladder, spermatic cord, nerves, blood
vessels
• Bleeding
• Infection
• Chronic postoperative pain
• Postoperative urinary retention
PROGNOSIS
• Excellent overall prognosis, excluding recurrence risk
• Emergent repair carries a significant increase in 30-day postoperative mortality.
REFERENCES
1. Kendell J,Wildsmith JAW, GrayIG. Costing anaesthetic practice. An economic comparison
of regional and generalanaesthesia for varicose vein and inguinal hernia surgery.
Anaesthesia.2000;55:1106–1126.
2. Song D, Greilich NB, White PF, et al. Recovery profiles and costs of anesthesia for
outpatient unilateral inguinal herniorrhaphy. Anesth Analg. 2000;91:876–881.
3. Koivusalo AI, Korpela R, Wirtavuori K, et al. A single-blinded, randomized comparison of
laparoscopic versus open hernia repair in children. Pediatrics. 2009;123(1):332–337.
• Laparoscopy
• Deep extubation
CODES
ICD9
• 553.8 Hernia of other specified sites without mention of obstruction or gangrene
• 553.9 Hernia of unspecified site without mention of obstruction or gangrene
ICD10
• K46.0 Unsp abdominal hernia with obstruction, without gangrene
• K46.1 Unspecified abdominal hernia with gangrene
• K46.9 Unspecified abdominal hernia without obstruction or gangrene
CLINICAL PEARLS
• For non-emergent groin hernias, open hernia repair under local anesthesia with sedation has
the best risk and cost profile as well as patient satisfaction.
• Emergent surgery for hernia repair carries a significant mortality risk; thus elective repair,
when feasible, is preferable, especially if the defect is small.
HIATAL HERNIA
BASICS
DESCRIPTION
• Hiatal hernia is a protrusion of a portion of the stomach through the diaphragmatic
esophageal hiatus into the thoracic cavity.
• The impaired ability of the lower esophageal sphincter (LES) to protect against reflux of
gastric contents, places the patient at an increased risk for aspiration. Thus, there is a
potential for patients in the perioperative period to have an
– Aspiration pneumonitis
– Aspiration pneumonia (a more delayed manifestation)
• The majority of patients with hiatal hernia are treated medically for the symptoms of
gastroesophageal reflux disease (GERD). Patients whose symptoms are not well controlled
prior to surgery should be treated as having an increased aspiration risk.
EPIDEMIOLOGY
Incidence
• Increases with age: ~10% in patients <40 years of age compared to ~70% in patients >70
years of age.
• Increased incidence with morbid obesity
Prevalence
Hiatal hernia is common; 30% of patients undergoing upper GI examination by radiography
were found to have a sliding type hiatal hernia.
Morbidity
Surgical repair exposes patients to an approximately 24% postoperative morbidity.
Mortality
Surgical repair carries an increased risk of mortality (as high as 2.4%) in elderly patients
secondary to comorbidities and surgical complications.
• Hiatal hernia may be congenital or acquired
• Predisposing factors for acquired hiatal hernia:
– Weakening of muscle and loss of elasticity when people age
– Women, which may result from the increased intra-abdominal pressure during pregnancy
– Obesity from increased abdominal pressure
– Chronic constipation due to low fiber diet
– Abdominal ascites
PATHOPHYSIOLOGY
• The upper part of the lower esophageal sphincter (LES) normally lies within the
diaphragmatic hiatus, while the lower portion is normally intra-abdominal. The LES is
maintained within the abdominal cavity by the phrenoesophageal ligament. The angle of
His between the cardia of the stomach and the distal esophagus prevents reflux of gastric
contents into the esophagus.
• There are two types of hiatal hernia
– Sliding hiatal hernia: A portion of the stomach and lower esophagus slide up into the
thoracic cavity. This is the most common type.
– Paraesophageal hernia: A portion of the stomach herniates through the hiatus, while the
esophagogastric junction remains in its normal anatomical location. It is less common, but
can lead to ischemia of the herniated part of the stomach if it becomes incarcerated.
• Symptoms of hiatal hernia present as GERD. It may also present as chest pain mimicking
angina. GERD in patients with a hiatal hernia can result from
– The backward flow of gastric acid into the esophagus and trapping into the hernia sac
during swallowing.
– Contraction of the crural diaphragm during inspiration leads to a compartmentalization of
the stomach between the LES and the diaphragm
• Any sudden increase in intra-abdominal pressure will increase the LES pressure by acting on
the portion of the LES below the diaphragm.
• Diabetic gastroparesis and gastric ulcers may delay gastric emptying leading to worsening of
symptoms in hiatal hernia patients.
• Certain drugs that may slow gastric emptying, including opioids, beta-blockers, tricyclic
antidepressants, and aluminum hydroxide antacid may increase the risk of aspiration in
hiatal hernia patients.
• The goal of anesthesia management is to prevent aspiration; appropriate techniques prior to
induction and emergence should be considered.
• An open or laparoscopic Nissen fundoplication may be performed to surgically repair a
hiatal hernia. While the results are comparable to an open procedure, laparoscopic
fundoplication may decrease postoperative pain and hospital stay while providing a more
rapid return to work and better cosmetic results. Downsides of the surgery include a
recurrence of symptoms, swallowing difficulties, failure, and increased bloating and
discomfort.
SYMPTOMS
• Indigestion, epigastric pain, nausea and vomiting, regurgitation, and chest pain. In patients
with concomitant cardiovascular diseases, chest pain of cardiac origin needs to be ruled out
before the treatment of the GERD.
• Chronic aspiration may present as an acid taste or sensation of refluxing liquid into the
mouth or paroxysms of coughing and/or wheezing.
History
Quality of heart burn and inciting factors
Signs/Physical Exam
Epigastric tenderness may be present in patients with severe acid reflux symptoms.
TREATMENT HISTORY
Failed Nissen fundoplication
MEDICATIONS
• H2-receptor antagonists: Decrease gastric acid secretion for both gastric pH and volume.
• Proton pump inhibitors are the most powerful medications for GERD. They block the final
steps in the hydrogen ion secretion by the parietal cells and raise stomach pH
• Antacids: Usually raise the pH of the gastric fluid, but at the same time increase gastric
volume.
• Metoclopramide: Shortens gastric emptying time, increases LES tone, and is an antiemetic. It
does not affect gastric pH.
Labs/Studies
• Complete blood count, electrolytes, urea, and creatinine
• CXR; if aspiration is suspected.
• Barium radiography
• Gastric endoscopy examination
• GERD
• Chronic aspiration
If the patient is believed to have a “full stomach” due to recent food intake, and the surgical
procedure is elective, the operation should be postponed.
CLASSIFICATIONS
• Sliding hiatal hernia (Type I)
• Paraesophageal hernia (Types II, III, and IV)
TREATMENT
Premedications
• GERD medications should be continued until surgery.
• Antacids are immediately effective in decreasing gastric acidity, but may increase gastric
volume slightly.
• Metoclopramide can be administered to decrease the gastric volume.
Risk for aspiration
INTRAOPERATIVE CARE
• For general anesthesia, quick control of the airway with an endotracheal tube (rapid
sequence induction) is indicated to prevent refluxing of gastric content into the oropharynx
and lungs. If a difficult intubation is anticipated, intubation should precede induction
(awake fiberoptic intubation).
• General anesthesia delivered via a mask or laryngeal mask airway is contraindicated.
• For monitored anesthesia care (MAC), avoid oversedation which can lead to a loss of the gag
reflex and aspiration.
• Regional anesthesia with minimal sedation may be considered, if it is practical for the
procedure.
Monitors
• Suction should be checked and immediately available.
• Rapid sequence induction is indicated in patients with symptomatic hiatal hernia, without a
difficult airway. Despite the need for rapidly securing the airway, adequate time needs to be
given to allow for the onset of induction agents and neuromuscular blockade to avoid
coughing, straining, and bucking (can cause strong forceful movement of stomach contents
upwards).
• Succinylcholine 1.5 mg/kg or rocuronium 1–1.2 mg/kg is usually used in addition to the
induction agents, including propofol, thiopental, or etomidate.
• Sellick’s maneuver (firm pressure over cricoid cartilage prior to induction) is used to
collapse the esophagus and prevent gastric content reaching the oropharynx and lungs.
• Consider placing the patient in reverse Trendelenburg to reduce passive reflux (gravity).
• A wide assortment of cuffed endotracheal tubes and laryngoscopy blades should be prepared
in advance to facilitate quick intubation.
Maintenance
• An orogastric tube may be gently inserted to suction any stomach contents after
endotracheal intubation, and left in place until the end of the procedure.
• Short-acting anesthetics should be considered to enhance rapid wakening of patients
• Nondepolarizing muscle relaxants should be used cautiously to avoid persistent
postoperative paralysis.
• Removal of the orogastric tube while on suction.
• Ensure full recovery or reversal if muscle relaxants are used.
• Patients should be extubated only after they are fully awake and regain the ability to protect
their airway.
• Consider placing the patient in a reverse Trendelenburg position to reduce the incidence of
passive reflux.
• Prophylaxis for postoperative nausea and vomiting.
POSTOPERATIVE CARE
BED ACUITY
Depends on the surgical procedure, patient comorbidities, and intraoperative events. If
pulmonary aspiration is suspected, a higher level of care is warranted to monitor for
respiratory dysfunction and hypoxia
Administration of narcotics for postoperative pain should be done carefully, as they may
delay gastric emptying as well as inhibit the gag reflex (from oversedation).
COMPLICATIONS
• Perioperative aspiration: Treat with supportive measures including suctioning of the
oropharynx, protection of the airway with endotracheal intubation, supplemental oxygen,
and ventilatory support in severe cases as well as bronchoscopy and pulmonary lavage.
• Additional surgical complications of Nissen fundoplication include pneumothorax, injury to
the stomach, esophagus, and liver in addition to bleeding and infection.
REFERENCES
1. Schieman C, Grondin SC. Paraesophageal hernia: Clinical presentation, evaluation, and
management controversies. Thorac Surg Clin. 2009;19(4):473–484.
2. Koerber JP, Roberts GE, Whitaker R, et al. Variation in rapid sequence induction
techniques: Current practice in Wales. Anesthesia. 2009;64(1):54–59.
3. Neumann L, Poulton B, Ridley S. Life-threatening complications of hiatus hernia.
Anaesthesia. 1999;54(1):93–94.
• Gastric esophageal reflux disease
• Aspiration
CODES
ICD9
• 553.3 Diaphragmatic hernia without mention of obstruction or gangrene
• 553.3 Hiatal hernia
ICD10
K44.9 Diaphragmatic hernia without obstruction or gangrene
CLINICAL PEARLS
• In patients with a diagnosed hiatal hernia, perioperative care should be tailored to reduce
the incidence of aspiration.
• Aspiration may lead to pneumonitis or pneumonia, both potentially fatal illnesses.
• Special care must be taken when using transesophageal echocardiography in patients who
may have hiatal hernia, because there is an increased risk of esophageal perforation.
HICCUPS
Dierk A. Vagts, MSc, DEAA, EDIC
BASICS
DESCRIPTION
• Hiccups are caused by intermittent, involuntary contractions of the diaphragm and
inspiratory muscles. The characteristic sound arises from very fast shutting of the glottis (1).
• Perioperatively, brief bouts of hiccups are most often precipitated by medications, irritation
of the diaphragm, or gastric distention from swallowing blood, gas, or debris.
• Chronic or intractable hiccups can adversely affect the quality of a patient’s life by causing
fatigue, sleep disorders, dehydration, depression, anorexia and weight loss, and death (from
the underlying disorder) (2).
EPIDEMIOLOGY
Incidence
1–4% of patients develop hiccups with the placement of a laryngeal mask airway (LMA).
Prevalence
No data available
Morbidity
Risk of
• Hyperventilation during anesthesia
• Aspiration during induction, extubation, or emergence
• Wound dehiscence
• Reflux esophagitis
• Interference with the surgical field (2)
Mortality
Not known
• Etiology might be organic, idiopathic or psychogenic.
• Anesthetic: Induction medications; LMA insertion (expansion of the oropharyngeal and/or
upper esophageal space may stimulate the vagus nerve); carbon dioxide (laparoscopic
procedures); gastric distention (2)
• Gastrointestinal: Hepatic failure, cholelithiasis, pancreatitis, hiatal hernia, gastroesophageal
reflux disease (atypical manifestation) (3)
• Psychiatric: Anorexia, hysteric neurosis, personality disorder traits
• Central nervous system: Ventriculoperitoneal shunt, multiple sclerosis, arteriovenous
malformation, epidural or subdural hematoma, traumatic brain injury, hyperdopaminergic
states
• Cardiac: Deviant cardiac pacemaker electrodes, myocardial infarction, pericarditis
• Pulmonary: Lung contusion, bronchial carcinoma, bronchitis, pleural empyema, asthma
• Head and Neck: Neck tumors
• Renal: Insufficiency, uremia
• Metabolic: Hypocalcemia, hyponatremia (4)
• Not completely understood; there are several hypotheses to explain the phenomenon of
hiccups.
– Protective mechanism to reduce the intake of large amounts of nutrition
– Support the development of the respiratory system in utero
– Phylogenetic residual phenomenon of gill breathing (2)
• There are three general components
– Afferent limb: Vagal, phrenic, and sympathetic (T6–T12) branches
– Central processor: Spinal cord (C3–C5), brain stem, midbrain. Processing is believed to be
mediated by several poorly defined neurotransmitters, including GABA and dopamine
– Efferent limb: Phrenic nerve, recurrent laryngeal nerve, accessory nerves to the
diaphragm, glottis, anterior scalenes, external intercostals, lower esophageal sphincter
muscles (2)
Not known
DIAGNOSIS
• Self-limited hiccups are often from peripheral sources such as the epigastrium, and occur
secondary to gastric distention, irritation, or reflux.
• Intractable hiccups are often from central mechanisms such as CNS disorders.
In the case of intractable hiccups (longer than 1 month), the infiltration of a tumor into the
phrenic nerve must be excluded.
TREATMENT
• Perioperative hiccups are usually self-limited and resolve without treatment. If they interfere
with the procedure or exceed 2 hours, treatment may be considered. There is currently no
evidence-based treatment. Options can be divided into pharmacological,
nonpharmacological, and invasive measures.
• Pharmacological
– Intraoperatively
Ephedrine 5–10 mg IV; may act on central receptors
Neuromuscular blocking drugs, if appropriate
Gastric acid reducers such as proton pump inhibitors and H2 blockers may be effective
when hiccups are the result of GERD.
Metoclopramide; aids with gastric emptying
Atropine 0.5 mg IV; may act directly on the esophagus by decreasing intraesophageal
pressure and hence peripheral mechanoreceptor-mediated reflexes, or indirectly on the
CNS via enhancement of sympathetic nerve activity (5).
Antidopaminergics such as chlorpromazine 25–50 mg IV or IM, droperidol, or
haloperidol; have inhibitory effects at the hypothalamus.
Propofol 0.25–0.5 mg/kg IV; titrate to effect
Ketamine (6)
Lidocaine 1 mg/kg IV; may follow with a continuous infusion.
Serotonin-5HT-1-A-receptor antagonists; receptors are located in the medulla in regions
involved with respiratory control. Inhibition shortens inspiratory discharges (8).
– Postoperatively
Ephedrine, gastric acid reducers, metoclopramine, atropine, antidopaminergics, propofol,
ketamine, lidocaine, serotonin-5HT-1-A-receptor antagonists may be appropriate
Baclofen 5 mg PO TID; a GABA agonist, typically used to treat spastic movement by
decreasing excitability and synaptic transmission at the level of the spinal cord. It is
believed that a similar mechanism is responsible for decreasing the hiccup reflex.
Gabapentin 300 mg PO TID; slow onset and more appropriate for chronic or intractable
hiccups (4,7).
Carvedilol 6.25 mg QID; unclear mechanism; may be an alternative to antidopaminergic
medications (9).
Antiepileptic drugs; phenytoin inhibits the transmission of motor activity; valproic acid
increases the function of GABA; carbamazepine blocks post-tetanic potentiation.
For psychogenic hiccups: Try distraction by assigning a new task
• Nonpharmacological intraoperative and postoperative (2)
– Increase PaCO2 by
Holding or decreasing ventilation
Rebreathing CO2
– Reduction of Hering–Breuer reflex by inflating and keeping the lungs extended with
Continuous positive airway pressure (CPAP) (10)
Valsalva maneuver
– Induction of contrairritation to inhibit the reflex for hiccups with a different reflex
Traction on the tongue
Bilateral orbital compression
Carotid massage
Rectal massage
Stimulation of nasopharynx with a catheter or nasopharyngeal airway (11)
Gastric lavage
The Heimlich maneuver is not recommended.
• Invasive measures for intractable or chronic hiccups
– Paravertebral block C3–C5, right or left side
– Cervical peridural anesthesia at C7 with 8 mL lidocaine 1.5% (12)
– Phrenic nerve block
Electrical nerve stimulation between the sternocleidomastoid and anterior scalene
muscle (may perform unilaterally or bilaterally)
Surgical blockade (13,14)
– Recurrence of hiccups is common after a single-injection technique for phrenic nerve
blockade; thus a catheter technique should be considered. All techniques try to interrupt
the neural pathway (15).
FOLLOW-UP
There is no evidence for any of the possible treatment options. However, as it is necessary to
stop hiccups to reduce the risk of aspiration during general anesthesia, patients may benefit
from sharing of the events.
CLOSED CLAIMS DATA
Not available
REFERENCES
1. Fass R. Stimulusand site specific induction of hiccups in the oesophagus of normal subjects.
Gut.1997;41:590–593.
2. zibor-Krisen U, Devide A, Hoetzel A, et al. Persistent intractable hiccup in the perioperative
period. AINS. 2008;43:674–676.
3. Becker DE Nausea, vomiting, and hiccups: A review of mechanisms and treatment. Anesth
Prog. 2010;57(4):150–156.
4. Tegeler ML, Baumrucker SJ. Gabapentin for intractable hiccups in palliative care. Am J
Hosp Palliat Care. 2008;25(1):52–54.
5. Kanaya N, Nakayam M, Kanaya J, et al. Atropine for the treatment of hiccup after
laryngeal mask insertion. Anesth Analg. 2001;93(3):791–792.
6. Shants RT. Ketamine for the treatment of hiccups during and following anesthetic. A
preliminary report. Anesth Analg. 1973;52:822–824.
7. Alonso-Navarro H, Rubio L, Jimenez-Jimenez F. Refractory hiccup: Successful treatment
with gabapentin. Clin Neuropharmacol. 2007;30:186–187.
8. Takahashi T, Murata T, Omori M, et al. Successful treatment of intractable hiccups with
serotonin (5-HT)1A receptor agonist. J Neurol. 2004;251:486–487.
9. Stueber D, Swartz CM. Carvedilol suppresses intractable hiccups. J Am Board Fam Med.
2006;19:418–421.
10. Saitto C, et al. Treatment of hiccups by continuous positive airway pressure (CPAP) in
anesthetized subjects. Anesthesiology. 1982;57:345.
11. angar D. Elimination of hiccups with a nasopharyngeal airway. J Clin Anesth. 1992;4:86.
12. Sato S. Cervical epidural block can relieve postoperative intractable hiccups.
13. Okuda Y. Use of a nerve stimulator for phrenic nerve block in treatment of hiccups.
14. Renes SH, van Geffen GJ, Rettig HC, et al. Ultrasound-guided continuous phrenic nerve
block for persistent hiccups. Reg Anesth Pain Med. 2010;35:455–457.
15. Lierz P, Felleiter P. Anesthesia as therapy for persistent hiccups. Anesth Analg.
2002;95:494–495.
ADDITIONAL READING
• Kranke P, Eberhart LH, Morin AM, et al. Treatment of hiccup during general anaesthesia or
sedation: A qualitative systematic reviews. EJA. 2003;20:239–244.
• Straus C, Vasilakos K, Wilson RJA, et al. A phylogenetic hypothesis for the origin of
hiccough. Bioesssays. 2003;25:182–188.
• Tardive dyskinesia
• Laryngeal mask airway
CODES
ICD9
786.8 Hiccough
ICD10
R06.6 Hiccough
CLINICAL PEARLS
• Hiccups are a sudden contraction of the diaphragm and intercostal muscles followed
immediately by laryngeal closure.
• Mostly occurs during inspiration and is inhibited by elevations in PaCO2.
HOFMANN ELIMINATION
Corey C. Downs, MD
BASICS
DESCRIPTION
• The chemist August Wilhelm von Hofmann (1818–1892) was the first to synthesize
quaternary amines, a cationic salt in which the nitrogen atom is bound to four groups and
carries a positive charge (NR4+). When subjected to the harsh conditions of basic solutions
and high temperatures, quaternary amines will undergo a chemical reaction, Hofmann
degradation, breaking into two fragments–a tertiary amine and an alkene.
• If a drug could undergo a similar spontaneous degradation reaction under the milder,
physiological conditions that exist within the body, it would allow for organ-independent
and enzyme-independent termination of its effect.
• Hofmann elimination describes the mechanism by which some drugs based on a quaternary
amine structure can undergo spontaneous degradation in vivo to inactive metabolites; it is a
temperature and pH-dependent process. At this time, only the neuromuscular blocker
atracurium and one of its isomers, cisatracurium, appear to harness this effect.
• Quaternary amines. Prepared by alkylation of tertiary amines in a process called
quaternization. The newly added alkyl group is typically a large, weak base, thus making it
a good “leaving” group under the appropriate conditions (high temperatures and a strong
basic solution).
• Hofmann elimination
– Breakdown of quaternary amines. Can occur under physiologic conditions: pH = 7.4,
temperature = 37°C
– Temperature-dependent metabolism
– pH-dependent metabolism
– Organ-independent metabolism
– Enzyme-independent metabolism
• Currently available drugs. Despite the benefits of spontaneous degradation under
physiologic conditions, the arsenal of anesthetic medications undergoing Hofmann
elimination to a clinically significant degree is limited to two neuromuscular blockers.
– Neuromuscular blocking drugs share a common structure, a quaternary ammonium group
that is essential for their function (binding to nicotinic acetylcholine receptors).
– Atracurium besylate was specifically chosen to take advantage of Hofmann elimination.
The beta-positional relationship between its nitrogen and carbonyl group results in a
molecular structure that allows Hofmann elimination to occur under physiological
conditions (1).
A small portion of atracurium also undergoes metabolism via ester hydrolysis.
Its side effects of histamine release (hypotension, tachycardia, bronchospasm), as well as
the potentially toxic effects of the tertiary amino alkaloid, laudanosine, have limited its
clinical use.
– Cisatracurium besylate is the R, cis-R’-isomer of atracurium.

More potent
Lacks or has significantly less histamine release and related side effects
Although elimination results in the production of laudanosine, the amount is

significantly less than with atracurium.
• Liver and renal disease. Because of its organ independence, the rate of Hofmann elimination
is essentially unaffected in these disease states.
– The dose requirements and recovery profiles of atracurium and cisatracurium in liver
failure patients are not significantly different from those in patients with normal liver
function (2).
– No significant difference was found in recovery parameters of patients with renal failure
receiving atracurium when compared to normal controls (3).
• Temperature derangements. Hofmann elimination will accelerate with increasing
temperature, while slowing for decreasing temperature. However, the clinical significance
of this change within ranges compatible with life is minimal or only requires minor dose
adjustments.
– Cisatracurium’s duration of action can be prolonged while on hypothermic
cardiopulmonary bypass (4).
– Hyperthermic states, as seen in malignant hyperthermia, hyperthyroidism, or
hyperthermic intraperitoneal chemotherapy, may cause a higher clearance of atracurium
(5).
– Slow infusions of either of these drugs through hot-lines containing basic carrier solutions
theoretically could lead to accelerated breakdown.
• pH derangements. Hofmann elimination will accelerate as the body becomes more alkaline,
while slowing in acidic conditions. Over the narrow pH range compatible with life this
effect is likely of little significance.
• Genetic variations. As a nonenzymatic process, Hofmann elimination is unaffected by
genetic variations and mutations in enzymes. For example, unlike succinylcholine,
cisatracurium is not affected by atypical plasma cholinesterase.
• Age does not appear to affect Hofmann elimination. Obesity does not change the rate of
Hofmann elimination.
In patients with renal or liver impairment, there is often concern over prolongation of a drugs
effect. For neuromuscular blockers this unpredictable duration can lead to an inability to
extubate, case delays, and airway compromise. Because they are processed primarily by
Hofmann elimination, atracurium and cisatracurium can be part of an anesthetic plan with
minimal or no change in dose requirements regardless of the patient’s pathology.
REFERENCES
1. Stenlake JB, Waigh RD, Urwin J, et al. Atracurium: Conception and inception. Br J
Anaesth. 1983;(Suppl 1):3S–10S.
2. De Wolf AM, Freeman JA, Scott VL, et al. Pharmacokinetics and pharmacodynamics of
cisatracurium in patients with end-stage liver disease undergoing liver transplantation. Br J
Anaesth. 1996;76:624–628.
3. Fahey MR, Rupp SM, Fisher DM, et al. The pharmacokinetics and pharmacodynamics of
atracurium in patients with and without renal failure. Anesthesiology. 1984;61:699–702.
4. Withington D, Menard G, Varin F. Cisatracurium pharmacokinetics and pharmacodynamics
during hypothermic cardiopulmonary bypass in infants and children. Pediatr Anesth.
2011;21:341–346.
5. Jonker G, Hoogenboom LJ, van Ramshorst B, et al. Atracurium during induced
hyperthermia. J Anesth. 2009;23(3):442-444.
ADDITIONAL READING
• Kisor D, Schmith V, Wargin W, et al. Importance of the organ-independent elimination of
cisatracurium. Anesth Analg. 1996;83:1065–1071.
• Prielipp R, Coursin D, Scuderi P, et al. Comparison of the infusion requirements and
recovery profiles of vecuronium and cisatracurium 51W89 in intensive care unit patients.
Anesth Analg. 1995;81:3–12.
• Neuromuscular blockade
• Chronic renal failure
CLINICAL PEARLS
• Hofmann elimination is a nonenzymatic, organ-independent degradation of quaternary
amines that for some drugs can occur at physiological temperatures and pH thus
terminating their clinical effect.
• Atracurium and cisatracurium primarily are inactivated via Hofmann elimination leading to
a more predictable duration of action with minimal or no dose adjustment in patients with
liver failure, renal impairment, or genetic variations in enzymes.
• Perhaps future research will develop additional drugs to take advantage of Hofmann
elimination, thus extending the options and safety margins for these patient populations.
HYPERBARIC OXYGEN THERAPY
Shawn T. Simmons, MD
BASICS
DESCRIPTION
• Hyperbaric oxygen (HBO) therapy is defined as the breathing of 100% oxygen inside a
pressure vessel at greater than one atmosphere absolute (ATA).
– Application of 100% oxygen to isolated body parts or breathing oxygen at surface (sea
level) pressure is not HBO.
• Terminology is often marine related due to the close relationship between hyperbarics and
diving:
– Dive = treatment
– Depth = treatment pressure
– Descent = compression of the chamber
– Ascent = decompression of the chamber
• There are two general types of chambers:
– Monoplace
Capacity limited to one patient at a time
Generally compressed with oxygen
Limited patient access. Monitors and IVs must enter chamber through a specially
designed “pass-through.”
Less expensive to purchase and run than multiplace units
– Multiplace
Capacity for more than one patient at a time
Generally compressed with air; oxygen is delivered to the patient via hood, mask, or
other airway (endotracheal tube, tracheostomy tube)
Most often have an inside attendant that is compressed with the patient(s). This allows
for easier patient care and manipulation of ventilators, IVs, etc., but requires the use of
dive tables to avoid decompression illness (“the bends”) in the attendant.
More expensive to purchase (each is custom built for the specific location), maintain, and
staff
• In general, a hyperbaric oxygen treatment consists of breathing 100% oxygen for 60–120
minutes at pressures of 2.0–2.4 ATA. The pressure, duration, and number of treatments are
varied depending on the disease being treated and the chamber type used (multiplace
chamber are often able to achieve higher pressures than monoplace chambers).
• Boyle’s gas law: The volume of a gas is inversely proportional to its pressure when the
temperature is held constant.
– Increased pressure directly shrinks gas bubbles in the blood and tissues.
– Patients must equalize the pressure in the middle ear to the external environment via the
Eustachian tube or risk eardrum rupture.
– An untreated pneumothorax may transform into a tension pneumothorax on
decompression as the extrapleural gas in the chest cavity expands.
– Implanted devices, such as pacemakers, must be certified for hyperbaric environments as
the change in pressure can result in malfunction and/or damage.
– Air must be eliminated from IV tubing and bags to avoid air embolism on decompression.
– Drains must be open to air during compression and decompression to allow equalization
of pressure.
– Endotracheal tube cuffs must be filled with saline or constantly adjusted during descent
and ascent.
• Henry’s gas law: The partial pressure of a gas dissolved in a liquid is directly proportional to
the pressure of the gas on the surface of the liquid.
– Increased ambient pressure and 100% oxygen increase the amount of oxygen dissolved in
the plasma.
Oxygenation of ischemic tissues
Promotes angiogenesis
Increased diffusion gradient to enhance elimination of inert gases
Bacterial control via direct killing of anaerobic species and enhanced leukocyte function
Hyperoxia causes arterial vasoconstriction; there can be a ∼10% increase in systemic
vascular resistance under hyperbaric conditions.
CNS oxygen toxicity can provoke seizures in susceptible patients.
Pulmonary oxygen toxicity can result in pulmonary fibrosis during prolonged exposures.
ANATOMY
• Oxygen is delivered to tissues via the bloodstream, so a minimum capillary density is needed
to observe a benefit.
• Tissue oxygenation decreases geometrically as distance from the capillary increases.
• Only certain diseases and conditions have been approved as appropriate for HBO therapy by
the Undersea and Hyperbaric Medicine Society (1)[A]
• Air or gas embolism
– Air is introduced into the vascular system, usually via medical devices or trauma.
– Hyperbaric effects
Increased pressure directly shrinks gas bubbles in the bloodstream and tissues.
Elevated oxygen tension provides an enhanced diffusion gradient for the elimination of
inert gas.
Therapy: Depending on severity, prolonged treatments at high pressures (3.0–6.0 ATA)
may be needed to resolve symptoms.
• Carbon monoxide (CO) poisoning
– CO is produced from incomplete combustion
– CO has ∼200 times the affinity for hemoglobin (Hgb) than O2 and is also a direct cellular
toxin (can cause acute cardiac and acute/delayed neurological dysfunction).
HBO greatly accelerates the elimination of CO from the blood.
Can help prevent delayed neurologic sequela (2)[A].
Therapy: A short series (1–3) of higher pressure (2.8–3.0 ATA) treatments.
• Clostridial myositis and myonecrosis (gas gangrene) is caused by organisms in the clostridia
family.
– Clostridia organisms secrete exotoxins that impair host defenses and produce the toxic
host reaction.
Inhibits bacterial growth (clostridia is a facultative anaerobe and is not directly killed by
oxygen).
Stops alpha-toxin production (the exotoxin produced by clostridia that is most associated
with morbidity and mortality).
Therapy: A short series of treatments, the first being at higher pressure (3.0 ATA), until
the patient stabilizes. The initial three treatments are delivered in 24 hours, then twice
daily after that.
• Crush injury, compartment syndrome, and other types of acute ischemia
– Trauma reduces blood flow to tissues, which then become ischemic, resulting in vasogenic
edema, further compromising blood flow and tissue oxygenation.
Oxygenates ischemic tissues
Reduces compartment edema due to decreased inflow due to arteriolar constriction from
hyperoxia and unchanged venous outflow.
Therapy: A short series of twice daily treatments at 2.0–2.4 ATA until the acute ischemia
is resolved.
• Decompression sickness
– Breathing air at increased ambient pressures (such as when scuba diving) causes increased
levels of nitrogen to be dissolved in the tissues and blood.
– During decompression/ascent, this nitrogen comes out of solution and forms bubbles in
the tissues and bloodstream if adequate decompression time is not allowed (i.e., nitrogen
comes out of solution faster than it can be eliminated through the lungs).
– These bubbles lodge in capillaries, resulting in decreased blood flow (joint pain,
myocardial and neurologic ischemia, V/Q mismatch, etc.), platelet aggregation, and
activation of the complement cascade.
Shrinks bubbles in plasma and tissues.
Enhanced diffusion gradient for inert gases.
Therapy: Depending on severity, prolonged treatments at high pressures (3.0 ATA) may
be needed to resolve symptoms.
• Enhancement of healing in selected problem wounds
– Problem wounds often fail to heal due to inadequate oxygen delivery secondary to
impaired microvascular injury, such as in diabetes.
– Transcutaneous oxygen monitoring can be used to assess potential benefit of hyperbaric
therapy (3)[B].
Bacterial control
Oxygenate ischemic tissues
Enhanced fibroblast activity
Therapy: 20–30 daily treatments at 2.0–2.4 ATA.
• Exceptional anemia
– Massive bleeding without the possibility of transfusion (religious beliefs, difficult cross-
match).
At 3.0 ATA on FiO2 1.0, enough oxygen can be dissolved in plasma to support basic
metabolic function without hemoglobin.
Therapy: Short series of high pressure (2.8–3.0 ATA) treatments until blood products are
available or until Hgb has increased to acceptable levels. Interval between treatments
should be guided by evidence of recurring ischemia (ECG change, acidosis, etc.).
• Intracranial abscess
– Adjunctive HBO therapy indicated for patients with: Multiple abscess or those in deep
tissues or dominant locations, immunocompromised, contraindications to surgery, or no
response to standard treatment.
Bacterial control
Oxygenate ischemic tissues
Therapy: Once to twice daily treatments at 2.0–2.4 ATA. Optimal duration of treatments
unknown.
• Necrotizing soft tissue infections
– Multiorganism, rapidly spreading infections that often tract along fascial layers.
Bacterial control
Therapy: Short series twice daily treatments at 2.0–2.4 ATA
• Osteomyelitis (refractory)
– Infection of bone that is difficult to clear due to impaired blood flow and ischemic
environment.
Bacterial control
Oxygenation of ischemic bone
Enhanced osteoclast function
Therapy: 20–30 (or more) daily treatments at 2.0–2.4 ATA.
• Delayed radiation injury (soft tissue and bony necrosis) (4)[B]
– Radiation therapy causes endovascular injury that results in decreased capillary density.
– Capillary density continues to decrease over time, even after radiation therapy ends,
resulting in ischemic tissues in the irradiated field.
– This ischemia can result in tissue breakdown either spontaneously or after trauma,
including surgery.
Bacterial control
Oxygenates ischemic tissues
Therapy: 20–30 daily treatments at 2.0–2.4 ATA
Marx protocol: Used in the case of osteoradionecrosis of the jaw when a tooth extraction
is planned in a previously irradiated area. The patient is given 20 treatments prior to the
extraction and 10 treatments postextraction.
• Skin grafts and flaps
– Compromised blood flow to grafts and flaps can result in ischemia and loss of the graft.
Therapy: A short series of twice daily treatments at 2.0–2.4 ATA until the acute ischemia
is resolved.
• Thermal burns
– Thermal injury impairs oxygenation via vascular coagulation and edema.
Therapy: A series of treatments at 2.0–2.4 ATA.
• Hyperbaric treatment performed immediately prior to debridement can help differentiate
viable from dead tissue.
• Myringotomies will need to be performed on intubated patients and others who are unable
to clear their ears (equalize the pressure in the inner ear with the external environment).
EQUATIONS
• Boyle’s law: P1V1 = P2V2; where P is pressure and V is volume
• Alveolar oxygen equation
– PAO2 = FiO2(PB – PH2O) – (PaCO2/RQ)
PaO2 = alveolar oxygen pressure.
PB = barometric pressure (mm Hg).
PH2O = water vapor pressure (usually 48 mm Hg).
RQ = respiratory quotient (usually 0.8)
21% O2 at 1 ATA: PaO2 = 100 mm Hg
100% O2 at 3 ATA: PaO2 = 1,500 mm Hg
• Arterial oxygen content
– CaO2 = 1.34(Hgb)(%sat) + (0.003)(PaO2)
1.34(Hgb)(%sat) = oxygen attached to Hgb
(0.003)(PaO2) = oxygen dissolved in plasma.
At 3 ATA on 100% oxygen, 5 mL/dL of oxygen can be dissolved in the plasma, which
can support resting metabolism.
• 1 ATA = 33 feet of seawater = 14.2 psi
REFERENCES
1. Gesell LB, Chairman and Editor. Hyperbaric Oxygen Therapy Indications: The Hyperbaric
Oxygen Committee Report, 12th edn. Durham, NC: Undersea and Hyperbaric Medicine
Society, 2008.
2. Weaver LK, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med.
2002;347(14):1057–1067.
3. Fife CE, et al. The predictive value of transcutaneous oxygen tension measurement in
diabetic lower extremity ulcers treated with hyperbaric oxygen therapy: A retrospective
analysis of 1,144 patients. Wound Repair Regen. 2002;10(4):198–207.
4. Feldmeier JJ. Hyperbaric oxygen for delayed radiation injuries. Undersea and Hyperb Med.
2004;31(1):133–145.
ADDITIONAL READING
• Clark RE. Hyperbaric oxygen treatment of chronic refractory radiation proctitis: A
randomized and controlled double-blind crossover trial with long-term follow-up. Int J
Radiat Oncol Phys. 2008;72(1):134–143.
• Kindwall EP, Whelen HT. Hyperbaric Medicine Practice, 3rd edn. Best Publishing Company,
Flagstaff, Arizona, 2008.
• www.UHMS.org
• PaO2
• Partial pressure
CLINICAL PEARLS
• For acute indications (CO, crush injury, failing graft, etc.), benefits are decreased with
increased delay in the start of treatments.
• In the case of delayed radiation injury (osteoradionecrosis or soft-tissue radionecrosis), it
takes ∼8 treatments to start to see clinical evidence of angiogenesis, which becomes
maximized at roughly 80% of preradiation levels at ∼20 treatments.
• Wounds must have an element of hypoxia (diabetes, radiation injury, trauma, etc.) to be
helped by hyperbaric oxygen.
– Hyperbaric treatments will not help normally oxygenated wounds heal faster.
– Wounds that are not healing for other reasons (pressure, venous insufficiency, etc.) will
not benefit from HBO therapy.
• Contraindications to HBO therapy:
– Untreated pneumothorax
– Concurrent chemotherapy with adriamycin (heart failure in hyperoxic environment) or
cisplatinum (wound breakdown in hyperoxic environments).
– Concurrent or prior exposure to bleomycin (reports of acute pulmonary fibrosis when
exposed to high oxygen concentrations. No known safe interval between treatment with
bleomycin and exposure to hyperoxia).
• There is little-to-no evidence in the peer-reviewed literature to support the use of HBO to
treat chronic CNS injuries/dysfunction (stroke, cerebral palsy, autism, etc.).
HYPERGLYCEMIA
BASICS
DESCRIPTION
• Hyperglycemia (>180–200 mg/dL) is common in diabetics as well as critically ill patients
without diabetes. It can result from
– Insulin deficiency
– Insulin receptor resistance
– Excess of glucagon
– Glucose over-administration
• Stress-induced hyperglycemia compared to diabetic hyperglycemia has been reported to
increase the length of hospital stay and in-hospital mortality.
EPIDEMIOLOGY
Prevalence
• Approximately 23 million patients have diabetes.
• Type 2 diabetes is seen in ~12.9% of people older than 20 years of age.
Morbidity
Diabetes is associated with a higher risk of acute myocardial infarction, stroke, and heart
failure
Mortality
• Three-fold increase in mortality in patients with hyperglycemia following acute myocardial
infarction.
• Poor outcome has been observed in non-diabetic patients with acute stroke and stress-
induced hyperglycemia.
• Underlying diabetes mellitus (DM)
• Inadequate insulin dosing in diabetics
• Concurrent medical illness: Stroke, acute myocardial infarction, trauma, sepsis, hypoxia
• Medication side effect
• Obesity
• In healthy individuals, the blood glucose level is closely regulated by insulin production,
hepatic glucose uptake, and production.
• Insulin actions include
• Increased transport of glucose, potassium, and amino acids into cells
• Protein synthesis
• Glycogen synthesis
• Inhibition of gluconeogenesis
• Counterregulatory hormones (cortisol, catecholamine, growth hormone) decrease peripheral
glucose uptake, inhibit hepatic glucose uptake, and increase hepatic gluconeogenesis and
glycogenolysis.
• Hyperglycemia
• Insulin deficiency (or insulin resistant states) can result in fat catabolism and increased
formation of acetyl CoA. Acetyl CoA will then form ketone bodies.
• Immune function. Impairs phagocytic function (adherence and chemotaxis) of neutrophils
and monocytes. Believed to be secondary to elevated cytosolic calcium in
polymorphonuclear (PMN) leukocytes that result in reduced ATP synthesis as well as
reduced superoxide formation in leukocytes.
• Fluid balance. Glycosuria promotes dehydration and various electrolyte imbalances. It can
cause serum hypertonicity and acidosis.
• Cardiovascular system. Hyperglycemia can increase systolic and diastolic BP, prolong the
QTc, and elevate catecholamine levels. Hyperglycemia can increase platelet activation and
adhesion, leading to thrombosis; as well as inflammatory markers such as TNFα, IL-6, and
IL-18. Studies have also demonstrated that it affects ischemic preconditioning of the heart
and reduced coronary collateral blood flow.
• Central nervous system (CNS). The penumbra area that surrounds the ischemic zone in the
brain is at increased risk for further infarction in hyperglycemic states because of the
ensuing acidosis and high lactate levels. High levels of lactate can damage astrocytes,
endothelial cells, and neurons.
• Glycemic control. Studies have yielded varying results.
• In critically ill surgical patients, tight glycemic control using intensive insulin therapy
(between 80 and 110 mg/dL) has shown improved outcomes.
• However, subsequent studies in the medical intensive care unit (ICU) have failed to show
similar benefits in all patients and more hypoglycemic episodes observed in patients with
more than 3 days of hospital stay.
• Furthermore, glucose variability has been shown to be more important than maintaining the
glucose level in a certain range. Fluctuation of blood glucose can cause increased apoptosis,
cytokine expression, and oxidative stress markers.
Surgical and anesthetic techniques that can minimize hyperglycemia responses:
• Minimally invasive surgery. The stress of surgery can reduce insulin sensitivity and the
release of counterregulatory hormones that can cause hyperglycemia.
• Avoid hypovolemia which can trigger a hyperosmolar hyperglycemic nonketotic (HHNK)
state (severe hyperglycemia often >600 mg/dL, hyperosmolarity often >320 mOsm/kg,
glycosuria with worsening hypovolemia, and central nervous system depression).
Dehydration combined with baseline impaired insulin production can further decrease
insulin levels and worsen hyperglycemia (compared to diabetic ketoacidosis, HHNK has
sufficient levels of insulin to prevent lipolysis and ketone production).
• Prevent nausea and vomiting (can lead to hypovolemia and electrolyte imbalances). Identify
patients at risk and avoid drugs with emetic properties (if possible) and administer
prophylactic treatment.
• Appropriate pain relief management to reduce the stress of surgery
• Neuraxial blockade. General anesthesia can result in a greater release of stress hormones
compared to local or epidural anesthesia. Volatile anesthetic agents can inhibit insulin
release and increase hepatic glucose output.
DIAGNOSIS
• Preoperative blood sugar testing in all diabetics.
• Intraoperative blood sugar testing should be considered in brittle diabetics and critically ill
patients.
• Postoperative blood sugar testing is typically performed in all diabetics in the recovery
room. Cases that are short in duration, ambulatory, minimal stress, and/or performed with
sedation may not require repeat testing in the recovery room (e.g., cataract, skin biopsies,
etc).
Inaccurate monitor results
TREATMENT
• A multidisciplinary approach involving the anesthesia provider, surgeon, endocrinologist,

intensivist, cardiologist, and dietitian may be necessary to minimize the perioperative
morbidity and mortality in diabetic patients.
• Preoperatively, blood glucose should be adequately controlled as per American Diabetes
Association (ADA) recommendations.
• HbA1C should ideally be <7%
• Preprandial glucose between 90 and 130 mg/dL
• Postprandial glucose <180 mg/dL
• Schedule elective cases for diabetic patients early in the day.
• On the day before surgery
• Oral hypoglycemic drugs should be dosed normally
• Long or intermediate acting insulin can be given in usual doses while taking a normal diet.
Evening or night doses are normally decreased to avoid hypoglycemia on the day of
surgery.
• While NPO, order blood sugar checks frequently. If hypoglycemic, treat with 15–20 gm of
glucose. Options include clear liquids, in the form of sugary drinks and fruit juices, sodas, or
electrolyte solutions.
• On the morning of the surgery
• Hold oral hypoglycemic agents to prevent reactive hypoglycemia
• Withhold short-acting insulin, but insulin pumps can be maintained at basal rate
• Intermediate insulin may be given according to the following formula: Fraction = [(Dosing
interval in hours) – (Hours of fast during interval)]/Dosing interval in hours. For example, a
patient is scheduled for hernioplasty. He will be eating normally at 10 am after minimally
invasive anesthesia.
– If he takes 24 U NPH daily at 7 am, then the fraction of intermediate insulin to give is (24
– 3)/24 = 7/8. Thus, at 7 am, he will receive 7/8th of his morning dose or 21 U of NPH.
– If he takes 24 U of NPH twice a day at 7 am and 7 pm, then the fraction of insulin to give
is (12 – 3)/12 = 3/4. Thus, at 7 am, he will receive 3/4th of his morning dose or 18 U of
NPH.
• For cases later in the day
• Maintain a basal rate for patients on insulin pump
• Consider advising that the patient takes a fraction of the intermediate acting insulin
according to the formula above.
• Consider allowing a small/light early snack such as toast (center-dependent).
• Intraoperatively
• Insulin-dependent diabetics: Consider administering an insulin infusion starting at 0.02
U/kg/h (100 U of insulin is mixed with 100 mL of IV fluid to yield a concentration of 1
U/mL) with a separate D5% or D5NS drip at 100–125 mL/h, for adult patients. Subsequent
titration should be based upon the desired glucose target.
• Alternatively, for insulin-dependent diabetics undergoing short procedures or minor
surgeries, or noninsulin-dependent diabetics, scheduled glucose testing may be performed
and treated as needed.
• Correction of hyperglycemia may be performed with correction doses of ultra short-acting
insulin; 1–4 U IV typically decreases blood sugar by 50 mg/dL.
• Recovery room or on the inpatient ward. While the patient is NPO, sliding scale insulin
dosing is commonly performed. When oral intake has resumed, oral medications may be
restarted alongside a sliding scale regimen. In insulin dependent diabetics, regular insulin
dosing may be restarted alongside a sliding scale regimen.
• In the ICU
• Some studies have documented decreased morbidity and mortality with normalization of
blood glucose within a range of 140–150 mg/dL.
• Type 1 diabetic patients require basal amounts of insulin.
• Type 2 diabetic patients: Withhold all oral hypoglycemia agents to prevent reactive
hypoglycemia. Patients with renal disease are at increased risk of lactic acidosis if treated
with biguanides.
• Initiate a sliding scale insulin infusion with a basal longer acting preparation to provide
more consistent glucose control.
• Subcutaneous insulin administration during critical illness may be unpredictable.
• Transition from the intensive care to general care with basal-bolus insulin has been shown
to demonstrate superior glycemic control. Ideally, the transition should take place either
before leaving the ICU or shortly thereafter. Several techniques have been described and are
often institution or practitioner specific.
• The starting dose for subcutaneous insulin should be 50–80% of the total IV insulin dose
over the last 24 hours; it may be given daily or divided into twice daily dosing as a long-
acting insulin analog (insulin detemir or insulin glargine). For example, if 72 U of IV insulin
have been administered over 24 hours, then the subcutaneous insulin dosing would range
from 36 to 58 U (QD or BID).
– Alternatively, the Miami 4/12 formula can be utilized. Dosage of basal insulin = body
weight (kg)/4. For example, a patient who weighs 72 kg needs 72/4 = 18 U of basal
insulin. Dosage of bolus insulin = body weight (kg)/12. For example, a patient who
weighs 72 kg needs 72/4 = 6 U of rapid-acting insulin before a meal.
– The first dose of long-acting insulin should be given 2–3 hours and the short-acting insulin
1–2 hours before stopping an insulin infusion.
FOLLOW-UP
• Patients, who were diagnosed as stress-induced hyperglycemia, requiring intensive insulin

therapy or not known to be diabetic before, need outpatient follow-up to confirm the
diagnosis of DM in an unstressed state.
• Long-standing and uncontrolled diabetes can cause a myriad of intraoperative events:
• Difficult intubation due to joint rigidity seen in Type 1 DM.
• Risk of aspiration due to gastroparesis
• Wide hemodynamic disturbances during induction
REFERENCES
1. Cowie CC,Rust KF, FordES, et al. Full accounting of diabetes and pre-diabetes in the U.S.
population in1988–1994 and 2005–2006.
2. Diabetes Care.2009;32(2):287–294.
3. Fahy BG, Sheehy AM, Coursin DB. Glucose control in the intensive care unit. Crit Care
Med. 2009;37(5):1769–1776.
4. Lipshutz AK, Gropper MA. Perioperative glycemic control: An evidence-based review.
Anesthesiology. 2009;110(2):408–421.
5. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes
Care. 2005;28(Suppl 1):S37–42.
6. Marik PE. Glycemic control in critically ill patients: What to do post NICE-SUGAR? World J
Gastrointest Surg. 2009;1(1):3–5.
7. Raju TA, Torjman MC, Goldberg ME. Perioperative blood glucose monitoring in the general
surgical population. J Diabetes Sci Technol. 2009;3(6):1282–1287.
8. Vann MA. Perioperative management of ambulatory surgical patients with diabetes
mellitus. Curr Opin Anaesthesiol. 2009;22(6):718–724.
ADDITIONAL READING
• Joshi GP, Chung F, Vann MA, et al.; Society for Ambulatory Anesthesia. Society for
Ambulatory Anesthesia consensus statement on perioperative blood glucose management in
diabetic patients undergoing ambulatory surgery. Anesth Analg. 2010;111(6):1378–1387.
• Meneghini LF. Perioperative management of diabetes: Translating evidence into practice.
Cleve Clin J Med. 2009;76(Suppl 4):S53–59.
• NICE-SUGAR Study Investigators; Finfer S, Chittock DR, Su SY, et al. Intensive versus
conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283–
1297.
• Hypoglycemia
CODES
ICD9
790.29 Other abnormal glucose
ICD10
R73.9 Hyperglycemia, unspecified
CLINICAL PEARLS
• Postoperative hyperglycemia is associated with increased risk of infection, longer hospital
stay, and myocardial infarction.
• Hyperglycemia is a common complication in patients receiving enteral and parenteral
nutrition.
• Hypoglycemia is a barrier for the achievement of euglycemia in patients with diabetes.
HYPERKALEMIA
BASICS
DESCRIPTION
• Hyperkalemia is defined as a serum potassium >5.5 mEq/L. If it goes unrecognized or there
is a delay in treatment, it can lead to cardiac and respiratory arrest.
• Potassium is predominantly an intracellular cation and is important in electrophysiological
functions. The body has several regulatory mechanisms to maintain the potassium
concentration within narrow levels; to avoid hyperkalemia, the cation is shifted
intracellularly and/or excretion is enhanced.
• Hyperkalemia may present preoperatively or develop intraoperatively. The anesthesia
provider must be vigilant in the identification and treatment of this potentially life-
threatening electrolyte abnormality.
EPIDEMIOLOGY
Incidence
Hospitalized patients: 1.1–10%
Prevalence
• End-stage renal disease: 5–10%
• Male:female ratio of 1:1
Morbidity
Increased in elderly patients with diabetes, chronic renal disease, and hypertension.
Mortality
Untreated cases: 67%
• Altered internal balance: Acidosis, insulin deficiency, renal failure, decreased aldosterone
levels, increased tissue breakdown.
• Altered external balance: Blood transfusions, drugs that affect renal excretion or internal
balance.
• Pseudohyperkalemia: Thrombocytosis, leucocytosis, hemolyzed sample, increased release
from abnormal cells.
• Nearly 98% of total body potassium is intracellular; the remaining 2% is extracellular. The
total potassium load in the body is ~50 mEq/kg (average 70 kg human has ~3500 mEq).
Serum potassium is usually maintained from 3.5 to 5.0 mEq/L.
• Na+/K+ ATPase is located in the cell membrane. It is a counter-exchange mechanism that
pumps Na+ extracellularly and K+ intracellularly in a 3:2 ratio. The pump functions to
maintain the resting cell membrane potential, cell volume, and intracellular calcium
concentration. It is further regulated by insulin, acidosis, drugs, and catecholamines.
• Hyperkalemia from intracellular to extracellular shifting:
– Insulin directly stimulates the Na+/K+ ATPase pump in the liver, skeletal muscle, and fat
cells. It promotes intracellular uptake of potassium. Insulin deficiency can hence impair
the transcellular uptake of glucose as well as the Na+/K+ ATPase pump.
– Excessive tissue breakdown or increased cellular catabolism can result in a release of
excessive amounts of potassium to the extracellular environment. Examples include
malignant hyperthermia, rhabdomyolysis, massive hemolysis, and tumor lysis syndrome.
– Beta-2 adrenergic agonists promote intracellular uptake of potassium by stimulating the
Na+/K+ ATPase pump. Conversely, non-selective beta-blockers may decrease uptake.
– Metabolic acidosis promotes potassium efflux via hydrogen ion exchange. For every 0.1
mmol/L decrease in pH, there is a 0.6 mmol/L increase in serum potassium. The Na+ -
H+ ion exchanger allows for the cells to function as a buffer against alkalemia or
acidemia. In acidemia, H+ ions move intracellularly, in exchange for Na+ moving
extracellularly. This reduces intracellular shifting of K+ via the Na+ - K+–ATPase. The
opposite occurs in alkalemic states.
– Hypertonicity leads to a loss of intracellular water and concentrates the intracellular
potassium concentration. This creates a driving force that favors potassium movement out
of the cell.
– Medications, including NSAIDS and digoxin, impair the movement of potassium into the
cell by inhibiting the Na+/K+ ATPase pump in the cell membrane.
– Succinylcholine causes rapid transient hyperkalemia from “cellular leak.”
• Hyperkalemia from impaired excretion occurs primarily from renal and gastrointestinal
derangements. In the kidneys, excretion occurs mainly at the cortical collecting duct and
aldosterone is a hormonal regulator of serum K+. Approximately 60–75% of filtered
potassium in the glomerulus is reabsorbed in the proximal tubule and 15–20% in the thick
ascending limb of the loop of Henle. Hyperkalemia stimulates aldosterone production with
resultant renal tubular elimination of K+ and reabsorption of Na+ and water.
– In patients with a glomerular filtration rate (GFR) of 5–10 mL/min, potassium excretion is
impaired at the distal collecting duct as a result of a decrease in sodium and water
delivery. Conditions like severe heart failure, dehydration, or hypovolemia also limit the
sodium and water delivery to the distal collecting ducts.
– Mineralocorticoid deficiency (aldosterone) can decrease excretion at the cortical collecting
duct.
– Medications such as potassium sparing diuretics (amiloride, triamterene) and antibiotics
(trimethoprim-sulfamethoxazole, pentamidine) can decrease urinary potassium excretion
by inhibiting the sodium channels in the kidney.
– Aging results in decreased renal mass, renal blood flow, GFR, and loss of tubular transport
function. This predisposes elderly patients to hyperkalemia. Additionally, elderly patients
are more likely to take NSAIDS, ACE inhibitors, beta-blockers, digitalis, and potassium
sparring diuretics.
• Hyperkalemia from increased intake
– In patients with intact renal function, a supranormal intake is needed to cause
hyperkalemia. In patients with impaired renal function (GFR <15 mL/min/1.73 m2), only
a slight increase in potassium intake can cause severe hyperkalemia.
• Electrophysiologic effects of hyperkalemia in heart muscles:
– Hyperkalemia leads to an increased resting membrane potential (less negative; e.g., –90
mV to –80 mV) secondary to a decrease in the transmembrane potassium gradient. This
result manifests as a shortening in the duration of the action potential in all cardiac cells.
– Phase 0. When the membrane is partially depolarized, there are fewer sodium channels in
the resting state that are ready for opening and ion conductance. This results in a decrease
in the Vmax (phase 0), slowing of the impulse conduction, and prolongation of membrane
depolarization. On the EKG, this is manifested by a prolonged P wave, PR interval, and
QRS complex.
– Phase 2 and 3. The potassium current in the myocyte membrane is responsible for the
potassium efflux during these phases. Potassium currents increase during hyperkalemic
states, via unknown mechanisms, leading to acceleration of repolarization. On the EKG,
this is manifested by a peaked T wave.
– Atrial tissue is more sensitive to hyperkalemia than the ventricles and nodal cells. At a
potassium level of 8–9 mEq/L, the SA node may stimulate the ventricle without evidence
of atrial activity, producing a sinoventricular rhythm. On the EKG, this is manifested as an
absent P wave with a wide QRS complex.
– As hyperkalemia worsens, SA node conduction ceases, and the passive junctional
pacemaker becomes the primary electrical stimulation for myocardium. On the EKG, this
is manifested as a QRS complex that continues to widen, blends with the T wave, and
produces the classic sine wave pattern. At this point, ventricular fibrillation and asystole is
imminent.
• Pseudohyperkalemia is defined as a [K+] increase of at least 0.5 mEq/L and results from
difficult phlebotomy, excessive alcohol swabbing of the skin, or clenching of the fist. When
the value is excessive or does not fit the clinical picture, the lab draw should be repeated to
confirm true hyperkalemia.
• Additional care and strict monitoring of serum potassium is needed for patients with
impaired renal function or heart failure who are on spironolactone and ACE inhibitor.
• Serial measurement of serum potassium coupled with EKG monitoring and management of
the patient’s overall clinical condition can prevent fatal cardiac arrhythmia.
• In patients with normal renal function, temporarily shifting potassium intracellularly can be
therapeutic. In patients with poor renal function, shifting potassium intracellularly may
need to be combined with hemodialysis.
DIAGNOSIS
• Plasma concentration >5.5 mEq/L
– Mild hyperkalemia: 5.5–6.5 mEq/L
– Moderate hyperkalemia: 6.5–7.5 mEq/L
– Severe hyperkalemia: >7.5 mEq/L
• Symptoms: Often asymptomatic thus, a clinical history of kidney disease or certain
medications, coupled with laboratory and EKG results, aid in the diagnosis of hyperkalemia.
• EKG changes are progressive and depend on the speed at which hyperkalemia manifests or
changes. Progressive EKG manifestation are
– Peaked T waves (5.5–6.5 mEq/L)
– ST segment depression
– Widening of the PR interval (>6.5 mEq/L)
– Widening of the QRS interval
– Loss of P wave (>8.0 mEq/L)
– Sine wave pattern
– Ventricular fibrillation
– Asystole
Pseudohyperkalemia
TREATMENT
• Membrane stabilization with calcium in severe hyperkalemia or EKG manifestations

(immediate)
– IV calcium gluconate 10%: Infuse 10 mL over 10 minutes while monitoring the EKG. If no
improvement, or EKG deterioration after initial improvement, repeat the dosage. Onset of
action: <3 minutes. Duration of action: 30–60 minutes.
– IV calcium chloride 10%: Provides three times more calcium. Infuse 3–10 mL over 10
minutes. Can cause tissue necrosis if extravasation occurs.
• Redistribution of potassium into cells (quick)
– Regular insulin 10 units IV with 50 mL of dextrose 50% is concomitantly given to prevent
hypoglycemia. Onset of action is within 10–20 minutes and the peak effect is seen at 30–
60 minutes and persists for 4–6 hours.
– IV or nebulized albuterol may be used as adjunctive therapy in severe hyperkalemia.
Stimulates the Na+/K+ ATPase through beta-2 receptor agonism. The recommended dose
is 0.5 mg IV or 20 mg nebulized.
– Epinephrine 0.05 μg/kg/minute IV infusion, similarly, stimulates the Na+/K+ ATPase
through beta-2 receptor agonism.
– Sodium bicarbonate functions by increasing plasma pH and producing metabolic alkalosis.
It is usually reserved for cases with severe acidosis, or if other indications for bicarbonate
therapy are present. NaHCO3 is less effective for patients with renal failure.
– Hyperventilation will transiently move K+ into cells by causing a temporary alkalosis.
• Elimination of potassium from the body
– Diuretics may be used for patients who are not volume depleted or do not have severe
renal impairment. Loop diuretics alone, or in combination with thiazide diuretics, may
promote potassium excretion by enhancing distal sodium and water delivery to the
principal cells in the cortical collecting ducts.
– Hemodialysis is the most effective mechanism to eliminate potassium from the body.
REFERENCES
1. Lehnhardt A,Kemper MJ. Pathogenesis, diagnosis and management ofhyperkalemia.
Pediatr Nephrol. 2010;25(3):403–413.
2. Palmer BF. A physiologic-based approach to the evaluation of a patient with hypokalemia.
Am J Kidney Dis. 2010;56(6):1184–1190.
3. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246–
3251.
4. Einhorn LM, Zhan M, Hsu VD, et al. The frequency of hyperkalemia and its significance in
chronic kidney disease. Arch Intern Med. 2009;169(12):1156–1162.
5. Naderi AS, Palmer BF. An unusual case of acute hyperkalemia during pregnancy. Am J
Obstet Gynecol. 2007;197(3):e7–8.
6. Parham WA, Mehdirad AA, Biermann KM, et al. Hyperkalemia revisited. Tex Heart Inst J.
2006;33(1):40–47.
ADDITIONAL READING
• Prough DS, Funston JS, Svensen CH, et al. Fluids, electrolytes, and acid-base physiology. In
Barash PG et al. (Eds.), Clinical Anesthesia, 6th edn. Philadelphia: Lippincott Williams &
Wilkins, 2009, p. 311.
• Hypokalemia
• Acid-base physiology
CODES
ICD9
276.7 Hyperpotassemia
ICD10
E87.5 Hyperkalemia
CLINICAL PEARLS
• Exclude pseudohyperkalemia by repeating serum potassium in patients with normal EKG
and no obvious risk factor for hyperkalemia.
• Hyperkalemia is seen in diabetic ketoacidosis; it is caused by insulin deficiency that impairs
normal intracellular potassium movement.
• Calcium gluconate protects the myocardium from fatal arrhythmia by reducing (more
negative) the threshold potential of myocytes thus restoring the resting membrane potential.
• Succinylcholine can cause elevation of serum potassium by 0.5–1 mEq/L with standard
dosing.
HYPERNATREMIA
BASICS
DESCRIPTION
• Hypernatremia is defined as a serum [Na+] >145 mEq/L; it indicates an absolute or
relative water deficit.
• Major causes include
– Excessive loss of water
– Inadequate water intake
– Lack of antidiuretic hormone (ADH)
– Excessive sodium intake from iatrogenic causes or accidental administration
• Hypernatremia results in a hypertonic, hyperosmolar state within the extravascular
compartment that draws water from the intracellular compartment causing cell shrinkage.
This concept is harnessed therapeutically in patients with intracranial hypertension to
decrease intracranial volume.
EPIDEMIOLOGY
Incidence
Found in ∼1% of hospitalized patients.
Prevalence
• Increased in patients who are intubated, have altered mental status, and where access to
water is compromised (e.g., infants and elderly). In infants, it is usually associated with
diarrhea or severe febrile illness.
• Diagnosed equally among males and females.
Morbidity
• Severe hypernatremia, defined by a [Na+] >160 mEq/L, or rapid onset of less than 12
hours, can result in intracranial bleeding, convulsions, neurologic deficits, and coma.
• Chronic hyperosmolality and hypotonic fluid treatments can also cause cerebral edema,
convulsions, coma, and death.
Mortality
Varies widely and is dependent on the severity of the condition and the rapidity of onset.
• Acute changes: 42–75%
• Chronic changes: 10–60%
• Inadequate water intake (no gain in sodium)
– Restricted access to water; seen in nursing home or hospitalized persons who are
dependent on others to meet fluid requirements.
– Impaired thirst mechanisms can result from a defect in the osmoreceptor or cortical thirst
center as well as structural lesions involving the hypothalamus.
• Hypotonic fluid loss
– Diabetic insipidus: Both central and nephrogenic causes
– Gastrointestinal (GI) losses: Diarrhea, vomiting, fistula
– Burns
– Peritoneal dialysis
– Insensible losses: Skin (excessive sweating), respiratory tract
– Renal losses: Osmotic diuresis as a result of hyperglycemia or diuretic therapy (mannitol),
postobstructive diuresis
• Sodium overload (in excess of body water)
– Excessive sodium intake: Iatrogenic causes include IV sodium bicarbonate or hypertonic
saline (3% normal saline contains 30 g/L of sodium chloride which is equivalent to a
[Na+] of 513 mEq/L); excessive PO salt intake.
– Mineralocorticoid excess: Cushing’s syndrome, hyperaldosteronism
• Medications that affect the function of the renal collection system: Lithium, glyburide,
foscarnet, demeclocycline, amphotericin B, methoxyflurane.
• Under normal conditions, the sodium concentration is tightly regulated and maintained
within a narrow range. Increases in sodium stimulate a strong thirst sensation and ADH
release from the pituitary gland to re-establish normal levels. Physiological values are
crucial to a myriad of functions within the human body:
– Maintains normal electrophysiological balance of the cell membrane. The normal
transmembrane potential is maintained by the Na+/K+-ATPase pump, which pumps 3
sodium ions out of the cell for every 2 potassium ions transported into the cell.
– Maintains water homeostasis (water follows sodium)
– Maintains normal extracellular and intracellular osmolality
– Conducts electrical impulses in nerves, muscle, and cardiac tissue via specialized sodium
channels.
– Regulates blood pressure BP via aldosterone’s effects
• General effects of hypernatremia: Hypertonic hyperosmolality that causes movement of
water from the intracellular to extracellular space and results in intracellular compartment
shrinkage.
• Hypernatremia and the central nervous system: To offset cellular shrinkage, the brain
increases intracellular solute uptake. Adverse effects include
– Intracranial bleeding. The brain is pulled away from the calvarium and can cause tearing
of the bridging veins. Intraparenchymal bleeding results from capillary enlargement and
rupture from cell shrinkage.
– Encephalopathy. Cellular shrinkage disrupts synaptic transmission and brain cell function.
• Hypernatremia and the cardiovascular system. Rapid increases in serum sodium result in
volume overload (fluid shifting out of the intracellular space) and can overwhelm the left
ventricle with resultant dysfunction. Fluid may “backup” into the pulmonary vasculature
and result in cardiogenic pulmonary edema. Conversely, the administration of hypertonic
saline has been used to treat severe hypovolemia (e.g., trauma) by drawing water into the
vasculature/circulation.
• Hypernatremia and the renal system. Studies in rats have shown that an acute increase in
serum sodium leads to renal vasodilatation. Hypertonic saline infusions stimulate
vasopressin and oxytocin, alter sympathetic activity, cause transient hypertension, and
result in a sustained increase in renal blood flow.
• Central diabetes insipidus (DI) describes impaired ADH synthesis that manifests as polyuria
and defects in the ability to concentrate urine. The kidneys cannot produce/maintain the
hypertonic medullary interstitium that is required to concentrate urine; this results in a
solute (osmotic) diuresis and excessive free water loss. Central DI may be seen after
pituitary surgery, severe head trauma (damage to the neurohypophyseal stalk), or basilar
skull fracture.
• Nephrogenic diabetic insipidus describes renal resistance to ADH; it manifests similarly to
central DI (polyuria and an inability to concentrate urine). Hereditary nephrogenic DI can
result from a gene mutation of the ADH receptor or the AQP-2 water channel. Acquired
nephrogenic DI is commonly due to lithium toxicity or metabolic abnormalities, particularly
hypokalemia and hypercalcemia.
• Mineralocorticoid excesses will increase aldosterone levels, leading to potassium depletion
and sodium retention (increase in total body sodium). Aldosterone acts on the distal
collecting ducts to increase tubular reabsorption of sodium and potassium excretion.
Free water loss via the GI, respiratory, and urinary tract should be replaced in critically ill
patients.
DIAGNOSIS
Symptoms include hyperpnea, muscle weakness, restlessness, a characteristic high pitched
cry, insomnia, lethargy, and coma.
Signs and symptoms
• Lethargy, mental status changes, irritability
• Thirst, shock, peripheral edema, ascites, and myoclonus
• Muscular tremor, rigidity, hyperactive reflexes, and spasticity
• Serum [Na+] >145 mEq/L
• If the urine output is >100 mL/hour with hypernatremia, the patient should be evaluated
for DI. A urine osmolality <300 mOsm/L and serum sodium >150 mEq/L makes the
diagnosis of DI likely.
Must make a distinction between the three types:
• Low total body sodium (loss of water >sodium); also referred to as hypovolemic
hypernatremia
– Renal: Osmotic diuresis from hyperglycemia or mannitol. Urine [Na+] >20 mOsm/L
– Extrarenal: Diarrhea, insensible fluid losses, vomiting. Urine [Na+] <10–20 mOsm/L
• Normal total body sodium (water loss); also referred to as euvolemic hypernatremia
– Renal: Central and renal DI. Urine osmolality: Low. Urine [Na+]: Variable.
– Extrarenal: Impaired water intake. Urine osmolality: High Urine [Na+] >20 mOsm/L.
• High total body sodium (gain of sodium >water) and includes hypertonic saline; also
referred to as hypervolemic hypernatremia. Urine [Na+] >20 mOsm/L
TREATMENT
• Depends on the underlying cause and course of development

– In chronic hypernatremia, brain cells accumulate organic osmoles when intracellular
water is lost, thus minimizing cell shrinkage. If corrected too fast, cerebral edema will
occur as a result of rapid uptake of water into brain cells that outpaces the extrusion of
organic osmoles and electrolytes from the brain cells. To that extent, a reduction in serum
[Na+] by <10 mEq/day, or 0.5 mEq/hour in chronic hypernatremia, is recommended.
– In acute hypernatremia, rapid correction (e.g., 1 mEq/hour) may not increase the risk of
cerebral edema.
• High total body sodium/hypervolemic hypernatremia. Excessive salt and water can be
corrected with a potent diuretic (e.g., furosemide) combined with a hypotonic solution such
as D5%W. Alternatively, hemodialysis may be utilized.
• Normal total body sodium/euvolemic hypernatremia.
– Central DI. Intranasal DDAVP 5–10 μg once or twice daily or aqueous vasopressin SC 5–10
U twice daily. In an emergency, IV DDAVP 1–2 μm BID or TID.
– Nephrogenic DI. Thiazide diuretics with or without prostaglandin synthetase inhibitors
(e.g., indomethacin or amiloride) and modest sodium restriction.
• Low total body sodium/hypovolemic hyponatremia. Correct hypovolemia using 0.9%
normal saline followed by correction of the water deficit with a hypotonic solution. The free
water deficit can be estimated as follows: Total body water (TBW) × [(serum Na+/140) –
1]. The TBW for males and females are 0.6 and 0.5 multiplied by the lean body weight,
respectively. In elderly patients and those with significant dehydration, a more conservative
estimate is needed (0.5 for males and 0.4 for females).
– For example, a male patient with a body weight of 70 kg presenting with a serum sodium
of 160 mEq/L would have a free water deficit = 70 × 0.6 × [(160/140) – 1]; this is
equal to 42 × 0.143 or 6 L.
– Correction of the water deficit can occur with oral intake, a G tube, or IV replacement
using D5%W or 0.45% NaCl.
REFERENCES
1. Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493–1499.
2. Wakil A, Atkin SL. Serum sodium disorders: Safe management. Clin Med. 2010;10(1):79–
82.
3. Prough DS. Physiologic acid-base and electrolyte changes in acute and chronic renal failure
patients. Anesthesiol Clin North America. 2000;18(4):809–833.
4. Robertson G, Carrihill M, Hatherill M, et al. Relationship between fluid management,
changes in serum sodium and outcome in hypernatraemia associated with gastroenteritis. J
Paediatr Child Health. 2007;43(4):291–296.
5. Leung C, Chang WC, Yeh SJ. Hypernatremic dehydration due to concentrated infant
formula: Report of two cases. Pediatr Neonatol. 2009;50(2):70–73.
ADDITIONAL READING
• Prough DS, Funston JS, Svensen CH, et al. Fluids, electrolytes, and acid-base physiology. In
Barash PG et al. (Eds.), Clinical Anesthesia, 6th edn. Philadelphia: Lippincott Williams &
Wilkins, 2009, p. 309.
• Cushing’s syndrome
• Crystalloids
CODES
ICD9
276.0 Hyperosmolality and/or hypernatremia
ICD10
E87.0 Hyperosmolality and hypernatremia
CLINICAL PEARLS
• Hypernatremia increases the minimum alveolar concentration of inhaled anesthetic agents,
possibly because of enhanced sodium conductance during depolarization of excitatory
membranes.
• Common errors in the correction include underestimation of fluid deficit, ongoing fluid
losses, and maintenance fluid requirement.
HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC (HHNK)
COMA
Jeffrey Katz, MD
Ori Gottlieb, MD
BASICS
DESCRIPTION
• Hyperosmolar hyperglycemic nonketotic (HHNK) coma is defined as a
– Severe hyperglycemic state (often >600 mg/dL)
– Hyperosmolarity (often >320 mOsm/kg)
– Hypovolemia from glycosuria
– Central nervous system (CNS) depression
• It is more commonly seen in older patients with noninsulin-dependent diabetes.
• HHNK is differentiated from diabetic ketoacidosis (DKA) in that the magnitude of acidosis
and ketosis are less profound and often develop more insidiously. However, it should be
noted that up to one-half of patients with diabetic ketoacidosis also have hyperglycemic
hyperosmolarity.
EPIDEMIOLOGY
Incidence
• Lower incidence than DKA
• HHNK accounts for <1% of all primary admissions for diabetes mellitus (DM)
• Exact incidence is unknown due to a lack of population studies.
Prevalence
• Mean age of onset in the 7th decade
• Increased in elderly and institutionalized patients
Morbidity
Typically from the precipitating disease.
Mortality
Ranges from 10 to 20%; death is typically related to the precipitating cause.
• Noninsulin-dependent DM (baseline decreased insulin levels)
• Increased glucose levels
– Poor diabetes medication compliance
– Corticosteroids
– Sympathomimetics
– Cardiopulmonary bypass
– Hyperalimentation or total parenteral nutrition
• Altered thirst response or compromised access to free water
– Advanced age
– Institutionalized patients
– Sepsis
– Infections (urinary tract infections, pneumonia, sepsis)
– Diuretics
PATHOPHYSIOLOGY
• In noninsulin-dependent diabetics, increased blood glucose levels are further exacerbated by
decreased fluid intake, increased fluid loss, or impaired renal function. The kidneys excrete
glucose in the urine; however, this ability can become impaired in the setting of
hypovolemia causing a decrease in the glomerular filtration rate or renal dysfunction. Of
note, hypovolemia is further compounded by the osmotic diuresis that ensues as a result of
hyperglycemia.
• Gluconeogenesis. The body mounts a stress response to the inciting event with
counterregulatory hormones (glucagon, cortisol, growth hormone). The liver is stimulated
to increase glucose production and decrease utilization, further exacerbating hyperglycemia.
This occurs to a lesser extent than in DKA.
• Electrolytes. Total body deficits of potassium, sodium, chloride, phosphate, calcium, and
magnesium result.
– Potassium. Similar to DKA, patients may initially present with hyperkalemia due to
extracellular shifting of the ion, but are total body depleted. This is due to several causes:
Metabolic acidosis: H+ ions moves intracellularly via the Na+–H+ ion exchanger while
Na+ moves extracellularly. This reduces intracellular shifting of K+ via the Na+/K+
ATPase.
Decreased insulin levels: Decreases the Na+/K+ ATPase pump activity that moves
potassium intracellularly.
Osmotic diuresis: Potassium is excreted in the urine
Catabolism: Chronic states result in total body depletion
– Sodium. Depletion occurs due to osmotic diuresis. However because water losses may
exceed sodium losses, a hypovolemic hypernatremic state may be initially present.
• Delay elective procedures. The goal is to re-establish euvolemia and electrolyte levels as
much as possible before going to the operating room.
• Indication for emergency surgery may be the precipitating illness for HHNK coma and thus
full preoperative correction is not always possible. In this case, initiate measures to restore
euvolemia and replete electrolytes as the first priority, then correct hypoglycemia.
SYMPTOMS
Mental status changes
History
• Evaluate diabetes severity, prior episodes of HHNK coma, and comorbidities
• Determine the underlying/inciting cause
• Time of onset
Signs/Physical Exam
• Volume status
• Neurologic assessment
• Shock
• Polyuria
• Vomiting
TREATMENT HISTORY
• Potassium management (hyperkalemia versus hypokalemia); recall that total body stores are
decreased, but that extracellular shifting of potassium may lead to dangerously elevated
serum levels.
• Intubation for airway protection if the patient has altered mental status
MEDICATIONS
• Insulin administration
• Antibiotics if precipitating event is sepsis or infection
Labs/Studies
• Serum glucose
• HbgA1C (to evaluate glucose control over the past 3 months)
• Electrolytes (potassium, sodium)
• BUN/Cr
• Arterial blood gas
• Urine and serum ketones
• EKG may demonstrate abnormalities related to hyperkalemia or hypokalemia
• Neuropathy – Autonomic nervous system dysfunction may result in difficulties with
regulating blood pressure and temperature.
• Gastroparesis – Many consider patients with DM as a “full stomach” despite NPO status.
• Cardiovascular disease – Macrovascular disease of the coronary arteries increases morbidity
and mortality in diabetics.
• Renal insufficiency results from microvascular disease of renal vessels.
• Nonenzymatic glycosylation and formation of abnormal proteins may result in decreased
elastance and thus difficult intubation.
Delay elective procedures. In urgent or emergent procedures, reestablish euvolemia and
electrolyte levels as much as possible before going to the operating room.
CLASSIFICATIONS
Hyperglycemic crisis of DM include HHNK and DKA. These disorders are differentiated by the
magnitude of acidosis and lack of ketosis; however, they can overlap.
TREATMENT
Premedications
In emergent surgeries, treatment with volume resuscitation, insulin infusion, and electrolyte
replacement should be continued en route to the operating room.
• May not be possible to attain consent from the patient.
• Family members should be advised about the severity of their condition, emergent nature of
the surgery, and the increased risk of mortality.
INTRAOPERATIVE CARE
General endotracheal anesthesia is almost always chosen; patients with mental status changes
make poor candidates for sedation or regional blocks.
Monitors
• Arterial line may be useful for frequent lab checks as well as to monitor beat-to-beat BP in
patients that are hypovolemic.
• Foley catheter. Ins and outs should be carefully monitored
• Some consider CVP monitoring to be useful in guiding fluid administration.
• Endotracheal tube for airway protection is most often utilized.
• Patients are hypovolemic and may become unstable with induction medications. Consider
etomidate and/or ketamine, if appropriate. The risks of adrenocortical suppression with the
use of etomidate need to be considered, however.
• Induction agents may have effects on glucose homeostasis but are likely clinically
insignificant.
Maintenance
• Intensive care therapy should be continued in the operating room in the same manner.
• Labs
– Blood glucose
– Electrolytes
– If severe hypovolemia, 0.9% normal saline (NS) resuscitation.
– If mild hypovolemia, consider 0.45% NS if high/normal [Na+] and 0.9% NS if low [Na+].
• Insulin therapy
– Regular insulin 0.1 units/kg initial IV bolus
– Insulin infusion at 0.1 units/kg/hour
• Potassium replacement
– If the [K+] >5.3 mEq/L, continue insulin and monitor every 2 hours.
– Be cautious in patients with impaired renal function
• Normothermia. Hypothermia decreases the response to insulin.
Base the decision to extubate on mental status, volume status, and hemodynamic stability.
POSTOPERATIVE CARE
BED ACUITY
ICU admission is commonly indicated for altered mental status, hypovolemia, shock requiring
vasopressors, or if insulin infusions are still required.
• Endocrine consult may be advantageous
• Frequent blood glucose checks
• Electrolytes monitoring. Potassium moves intracellularly as the acidosis is corrected
COMPLICATIONS
• Inadequate resuscitation
• Hypoglycemia may result from excess insulin therapy.
• Overzealous potassium replacement can lead to cardiac arrhythmias.
• Pulmonary edema/heart failure from overzealous fluid administration.
• Cerebral edema or central pontine myelinosis from rapid correction of sodium imbalance.
REFERENCES
1. Hirsch I, et al. Perioperative management of surgical patients with diabetes mellitus.
2. Kitabchi A, et al. Hyperglycemic crises in adult patients with diabetes. Diabetes Care.
2006;29(12):2739–2748.
3. Milaskiewicz R, et al. Diabetes and anaesthesia: The past decade. Brit J of Anaesth.
1992;68:198–206.
4. Lorber D. Nonketotic hypertonicity in diabetes mellitus. Med Clin North Am.
1995;79(1):39–52.
5. Matz R. Management of the hyperosmolar hyperglycemic syndrome. Am Fam Physician.
1999;60(5):1468–1476.
• Hyperkalemia
• Hypokalemia
• Hypernatremia
CODES
ICD9
250.20 Diabetes with hyperosmolarity, type II or unspecified type, not stated as uncontrolled
ICD10
E11.01 Type 2 diabetes mellitus with hyperosmolarity with coma
CLINICAL PEARLS
• Pure HHNK differs from DKA in that the degree of hyperglycemia and dehydration is
greater, whereas the degree of acidosis, lipolysis, and ketosis is absent or minimal.
Additionally there is CNS depression.
• The mortality of HHNK is greater than DKA. Mortality is associated with the underlying
disease process, not hyperglycemia.
• Delay elective surgery until the patient is adequately volume and electrolyte repleted.
HYPERTENSION
BASICS
DESCRIPTION
According to the Joint National Committee’s 2003 report, hypertension is defined as a systolic
blood pressure (BP) >140 mm Hg or a diastolic BP >90 mm Hg.
EPIDEMIOLOGY
Incidence
• Affects ∼50 million people in the US (almost 25% of US adult population) and 1 billion
people worldwide.
• Individuals who are normotensive at age 55 years have a 90% lifetime risk of developing
hypertension.
Prevalence
Increases with age. About half of all adults between the ages of 60 and 69 years and three
quarters of all adults age >70 years have hypertension.
Morbidity
• A linear relationship exists between an increase in BP and risk of developing ischemic heart
disease and stroke.
• Randomized controlled trials have provided unequivocal proof that lowering BP with
regular medication dramatically reduces cardiovascular disability and death, and slows the
progression of chronic kidney disease
• Patients with isolated systolic hypertension also have a higher cardiovascular morbidity.
• There is increasing evidence that patients with labile and white coat hypertension are also at
increased risk of cardiac and vascular complications.
Mortality
Worldwide: ∼7.5 million deaths annually are attributable to hypertension.
• Essential (primary) hypertension describes high BP when no cause has been identified.
Associated factors include obesity, excess dietary sodium intake, reduced physical activity,
inadequate intake of fruits, vegetables and potassium, and excess alcohol intake.
• Secondary hypertension (<5%) is due to identifiable causes such as sleep apnea, drug-
induced or related causes, chronic kidney disease, primary aldosteronism, renovascular
disease, chronic steroid therapy, Cushing’s syndrome, pheochromocytoma, coarctation of
the aorta, thyroid, or parathyroid disease.
PATHOPHYSIOLOGY
• The pathogenesis of essential hypertension is not completely understood. Studies have
suggested that it may result from impaired sodium excretion by the kidneys, or an
overactive renin-angiotensin or sympathetic nervous system. During the early stages, an
increase in cardiac output and normal total peripheral resistance is seen. Over time, the
cardiac output returns to normal levels, but the total peripheral resistance increases and
intravascular volume decreases
• The relative intravascular volume depletion can become unmasked with sympatholysis from
anesthetic medications and neuraxial techniques.
• Perioperative anesthetic management aims to maintain hypertensives within a range of 10–
20% of preoperative values. However, increased vascular stiffness and decreased vascular
filling predispose patients to greater swings in BP. Thus, tight control may require the use of
antihypertensives, vasopressors, and invasive monitoring.
• There is conflicting evidence that mild-to-moderate preoperative hypertension in the
absence of target organ damage is an independent predictor of postoperative cardiac
complications of cardiac death, postoperative myocardial infarction (MI), heart failure, or
arrhythmias.
• Cardiac events in hypertensives occur at a higher frequency in the perioperative period for
cardiac surgery, carotid artery surgery, peripheral vascular surgery, abdominal aortic
surgery, and thoracoabdominal surgery.
• Severe hypertension or crisis in the perioperative period (diastolic BP >120 mm Hg) or
impending organ damage poses definite risks of cardiac complications such as myocardial
ischemia, MI, or stroke. Causes may include abrupt withdrawal of clonidine or beta-
blockers, interaction of monoamine oxidase inhibitors (MAO) with sympathomimetic
agents, pheochromocytoma, preeclampsia, or eclampsia.
• Preoperative BP medications should be continued in the preoperative as well as
perioperative period. ACE inhibitors and ARBs may cause profound and refractory
hypotension when taken on the morning of surgery; however there are no guidelines at this
time on how to manage.
SYMPTOMS
Usually asymptomatic
History
• Preoperative increases in BP due to anxiety or white coat syndrome can be distinguished
from previous clinic BP measurements.
• A “silent killer.” ∼30% of adults are unaware of their hypertension and may present to the
preoperative suite undiagnosed.
• Questioning should be directed at determining the severity, presence of target organ
damage, and associated comorbidities.
Signs/Physical Exam
• Vital signs, peripheral pulses, body mass index (BMI)
• Cardiac examination
• Auscultation for carotid, abdominal, or renal bruits and assessment for abdominal or renal
masses.
TREATMENT HISTORY
This may include adoption of healthy lifestyles that reduce, prevent or delay hypertension,
and increase the efficacy of antihypertensive medications. Lifestyle modifications include
adoption of dietary changes that are low in salt and rich in fruits and vegetables, limitation of
alcohol intake, regular exercise, and weight loss.
MEDICATIONS
• Drug type, recent changes, and compliance should be reviewed. Over 40% of patients with
hypertension do not take medications and 2/3rd are not optimally controlled. Furthermore,
most patients are on more than one antihypertensive.
• Diuretics. Thiazide-type diuretics are first-line treatment for most patients with
uncomplicated hypertension, either alone or in combination with other classes.
• Beta-blockers
• Calcium channel blockers
• Alpha-adrenergic blockers
• ACE inhibitors/angiotensin receptor blockers (ARBs)
• Central sympatholytics
• Direct vasodilators
• Hypertensive patients with diabetes mellitus (DM), chronic kidney disease, heart failure,
post-MI, high coronary disease risk, and recurrent stroke prevention are compelling
indications for treatment with a certain, specific class of antihypertensives.
Labs/Studies
• Renal function: CBC, electrolytes, BUN, creatinine, glucose, urinary albumin
• Cardiovascular function: Chest radiography, EKG, stress test or coronary angiography, as
appropriate
• Cerebrovascular function: Carotid artery duplex scan, as appropriate
• Cardiovascular, cerebrovascular, renovascular, and peripheral vascular disease
• Obesity, sleep apnea, DM
• Untreated hypertension can lead to target organ damage of the heart (LVH, angina, and
heart failure), brain (stroke or transient ischemic attack, dementia), chronic kidney disease,
peripheral arterial disease, and retinopathy.
• Preoperative diastolic blood pressure (DBP) <110 mm Hg. Studies have suggested that
patients can safely undergo elective surgery.
• Hypertensive urgency describes a severe elevation in BP without progressive end-organ
dysfunction. Preoperative DBP >110 mm Hg have been associated with an increased risk of
cardiac and vascular morbidity; thus elective surgery may be postponed until good
antihypertensive control has been achieved. However, there is increasing evidence that in
the absence of cardiac, vascular, or renal complications in this population, immediate
control of hypertension prior to surgery may be effective in preventing complications.
• Hypertensive emergencies describe a DBP >120 mm Hg AND accompanying end-organ
dysfunction. Surgery should be delayed for emergent treatment.
CLASSIFICATIONS
• BP readings are the average of two or more seated checks on each of two or more separate
office visits.
• Prehypertension: Systolic blood pressure (SBP) 120–139 mm Hg, DBP 80–89 mm Hg
• Stage 1: SBP 140–159 mm Hg, DBP 90–99 mm Hg
• Stage 2: SBP >160 mm Hg, DBP >100 mm Hg.
• Hypertensive urgency: Severe elevation without progressive end-organ dysfunction.
• Hypertensive crisis/emergency: SBP >180 mm Hg, DBP >120 mm Hg and accompanying
end-organ damage (hypertensive encephalopathy, intracerebral hemorrhage, subarachnoid
hemorrhage, acute stroke, unstable angina, acute MI, congestive heart failure, acute renal
dysfunction, and acute aortic dissection)
TREATMENT
Premedications
• In general, antihypertensive medications should be continued in the preoperative and
postoperative period. An increased risk of intraoperative bradycardia has been associated
with beta-blockers and intraoperative hypotension with calcium channel blockers, ACE
inhibitors, and ARBs on the morning of surgery.
• Anxiolytics such as midazolam are extremely useful to decrease the level of anxiety and
consequent increases in BP prior to surgery.
INTRAOPERATIVE CARE
• Dependent on the type and site of surgery, associated comorbidities, patient’s preference,
etc.
• Regional anesthesia may, however, obtund the sympathetic hypertensive response to
surgical stimuli. Hypotension may occur with neuraxial blocks, especially in the presence of
hypovolemia.
Monitors
• Standard ASA monitors are adequate in most patients.
• Invasive arterial line monitoring for continuous BP monitoring is indicated in patients with
uncontrolled hypertension, certain comorbidities, or surgical procedures.
• Other invasive hemodynamic monitoring may be indicated based upon comorbidities,
surgical procedure.
• Time of wide BP swings that can result in impaired myocardial oxygen supply or demand.
Consider frequent cycling and anticipate and treat perturberances.
• Choice of induction medication is less important than careful titration. Hypotension can
result from sympatholytic and/or direct vasodilatory effects combined with intravascular
volume depletion, and is commonly treated with a fast onset, short duration vasopressor.
• Hypertensive stress responses to airway manipulation may be decreased with the
prophylactic or therapeutic use of fentanyl, beta-blockers, or vasodilator drugs such as
nitroglycerine.
Maintenance
• None of the modern inhalational anesthetic agents have been shown to have any advantages
over the other.
• Hypertension is usually the result of light anesthesia, surgical stimulus, drug errors, hypoxia,
hypercarbia, or fluid overload. Unusual causes of sudden, unexpected, or severe
hypertension in the perioperative period include undiagnosed pheochromocytoma,
hyperthyroidism, malignant hyperthermia, intracranial hypertension, or other causes
mentioned above related to withdrawal of drugs like clonidine or interaction of MAO
inhibitors with sympathomimetic agents.
• Hypotension should be carefully avoided to maintain cerebral blood flow (CBF) as there is
likely a right shift in the cerebral autoregulation curve. Common causes of intraoperative
hypotension include hypovolemia, anesthetic drug overdose, or interaction with beta-
blockers, calcium channel blocker, ACE Inhibitors, or ARBs.
Anticipate a hypertensive response and be prepared to treat.
POSTOPERATIVE CARE
BED ACUITY
Uncontrolled hypertension requires a higher level of care and monitoring.
Resume antihypertensive medications as soon as possible after surgery. If oral intake is not
possible, the drug should be administered via the nasogastric tube or IV route (equivalent
doses, preferably same class).
COMPLICATIONS
• Hypertension may result from pain or a full bladder. Other causes include hypoxia,
hypercarbia, fluid overload, drugs, and cerebrovascular accident.
• Unexpected severe hypertension in the intraoperative or perioperative setting should lead to
suspicion of undiagnosed pheochromocytoma.
REFERENCES
1. The seventh report of the Joint National Committee on prevention, detection, evaluation,
and treatment of high blood pressure: The JNC 7 Report. JAMA. 2003;21(289):2560–2572.
2. mith I, Jackson I. Beta-blockers, calcium channel blockers, angiotensin converting enzyme
inhibitors and angiotensin receptor blockers: Should they be stopped or not before
ambulatory anaesthesia? Curr Opin Anesthesiol. 2010;23:687–690.
3. Fayad A, Yang H. Is peri-operative isolated systolic hypertension (ISH) a cardiac risk
factor? Curr Cardiol Rev. 2008;4:22–33.
• Mancia G. Blood pressure reduction and cardiovascular outcomes: Past, present, and future.
Am J Cardiol. 2007;100:3J–9J.
• Geriatric physiology
• ACE inhibitors and hypotension
CODES
ICD9
401.9 Unspecified essential hypertension
ICD10
I10 Essential (primary) hypertension
CLINICAL PEARLS
• Uncontrolled and untreated hypertension increases cardiac, vascular, cerebrovascular
morbidity and kidney disease progression. Chronic treatment and adequate control of
hypertension reduces these complications.
• Patients with hypertension are more prone to swings in BP perioperatively.
• Isolated systolic hypertension is associated with higher incidence of cardiac complications
and arrhythmia.
• Preoperative hypertension. Ensure correct BP readings: Patient seated, feet down, arms at
the heart level, cuff encircling at least 80% of arm’s width, and SBP measured at the
beginning of Korotkoff sounds and DBP measured at the disappearance of Korotkoff sounds.
• Chronic hypertension shifts the cerebral blood flow autoregulation curve to the right.
HYPERTHERMIA
BASICS
DESCRIPTION
• Hyperthermia is defined as an elevation of core body temperature above the normal diurnal
range of 36–37.5°C and is due to a failure of thermoregulation.
• It is not synonymous with fever, which is regulated at the level of the hypothalamus in the
setting of inflammation and cytokine release. Febrile patients are commonly encountered in
the ICU setting and present perioperatively (for surgery or have postoperative fever).
Postoperative fever includes the pneumonic: Wind (pulmonary causes such as aspiration,
pulmonary embolism, pneumonia), water (UTI), wound (surgical site infections), walking
(deep venous thrombosis), and “what did we do” (medications, blood product transfusions,
intravascular, urethral, nasal, and abdominal catheters). Postoperative fever includes the
pneumonic:
– Wind: Pulmonary causes such as aspiration, pulmonary embolism, pneumonia
– Water: Urinary tract infection
– Wound: Surgical site infection
– Walking: Deep venous thrombosis
– “What did we do:" Medications, blood product transfusions; intravascular urethral, nasal,
abdominal catheters
• Hyperthermia has perioperative relevance ranging from passive hyperthermia (excessive
heating, most common in infants and children) to drug reactions (malignant hyperthermia
[MH] neuroleptic malignant syndrome [NMS]) to increased incidence in laboring patients
who receive epidural anesthesia.
EPIDEMIOLOGY
Incidence
• NMS in patients taking neuroleptic drugs ranges from 0.02–3%
• Unexplained postoperative fever: Incidence remains ill-defined; however, studies suggest
that it is common and resolves within 48 hours without antibiotic treatment.
Morbidity/Mortality
• Heat stroke mortality: 21–63%
• MH: 1–17% (prior to introduction of dantrolene, as high as 70%)
• NMS mortality: 10–20%.
• Iatrogenic perioperative causes
– Conductive warming systems
– Fluid and blood warmers
– Warm operating rooms
• Drug reactions
– Malignant hyperthermia: Succinylcholine, volatile inhalational agents
– Neuroleptic drugs (NMS)
– Atropine
– Salicylates
– Lithium
– Sympathomimetics
– Serotonergic syndrome
• Fever (Wind, water, wound, walking, “what did we do")
– Urinary tract infections
– Abscesses
– Catheter-related infections
– Sepsis
– Meningitis
– Pneumonia
– Atelectasis
– Wound infections
• Endocrine
– Hyperthyroidism
– Thyroid storm
• Body temperature is maintained within a narrow range and is a balance between heat
production and heat dissipation. It is regulated by the thermoregulatory center located in
the anterior hypothalamus and varies over the course of the day.
– Heat production results from metabolic processes as well as heat absorption from the
environment.
– Heat loss is principally via evaporation to the environment (ineffective above a relative
humidity of 75%). Other methods of heat dissipation include radiation (emission of
infrared electromagnetic energy), conduction (direct transfer of heat to an adjacent cooler
object), and convection (direct transfer of heat to convective air currents). However, these
processes are inefficient when the environmental temperature exceeds skin temperature.
• Temperature elevation causes increased oxygen consumption and metabolic rate with
resultant tachypnea, hypercarbia, and tachycardia; as well as a reduced mixed venous
oxygen saturation. Thus, increased oxygen demand can aggravate preexisting cardiac or
pulmonary insufficiency. Above 37°C, each one degree increase corresponds to an ∼13%
increase in oxygen consumption. Above 42°C (108°F), oxidative phosphorylation is
uncoupled, making enzymes nonfunctional and thus putting the patients at risk for multiple
organ failure. Hepatocytes, vascular endothelium, and neural tissues are most sensitive to
these effects.
• Hyperthermia does not involve resetting the thermoregulatory centers; it remains
unchanged and can lead to uncontrolled increases in body temperature that can be rapidly
fatal.
• MH is a rare genetic disorder that is triggered by succinylcholine administration or exposure
to volatile inhaled anesthetic agents. It manifests as a hypermetabolic crisis with
unregulated release of calcium from myocyte sarcoplasmic reticulum. Despite the name
“malignant hyperthermia,” increased temperature is a late finding and proceeds
hypercarbia, tachycardia, acidosis, hyperkalemia, and possibly rhabdomyolysis
• NMS is an idiosyncratic reaction to antipsychotic agents, believed to be the result of central
dopamine receptor blockade. It presents as altered mental status, rigidity, fever, and
dysautonomia. It is more common with neuroleptic agents (haloperidol, droperidol,
fluphenazine); however, all classes of antidopaminergics can result in NMS (clonazpine,
olanzapine, metoclopramide, promethazine). Although it is not a dose-dependent
phenomenon, higher doses are a risk factor.
• Endocrine disorders. Hyperthyroidism and thyroid storm represent an abnormal increase in
basal metabolic rate with resultant heat products.
• Epidural analgesia for labor; patients are more likely to experience hyperthermia and overt
clinical fever. Believed to be due to placental and chorioamnio membrane inflammation;
however, the mechanism is not completely understood at this time. Because of its potential
for neonatal brain injury (cerebral palsy, encephalopathy, learning defects), it can lead to a
greater number of Cesarean sections. Additionally, heat transfer to the neonate may result
in unnecessary neonatal workup of sepsis.
• Fever is caused by exogenous or endogenous pyrogens. Exogenous pyrogens are mainly
microbes or their toxins (lipopolysaccharide endotoxin produced by gram-negative
bacteria). Endogenous pyrogens are mainly cytokines (IL-1, IL-6, TNF, ciliary neutrotrophic
factor). The interaction of pyrogens with hypothalamic circumventricular vascular
endothelium is the first step in raising the thermoregulatory set point to febrile levels.
– Immediate onset postoperative fever. Occurs in the operating room or a few hours after
surgery; they often resolve without therapy and are often unexplained (most often due to
trauma, infection, blood transfusion, or due to drugs ).
– Acute onset postoperative fever. First week after surgery and is commonly due to surgical
site infections, ventilator-associated pneumonia, aspiration, intravascular catheter
infections, UTI.
– Subacute onset postoperative fever. 1–4 weeks after surgery and includes fever from
antibiotic-associated diarrhea, febrile drug reactions, thrombophlebitis.
– Delayed onset postoperative fever. Greater than 4 weeks after surgery and includes
infections
• Monitoring of temperature intraoperatively can help avoid iatrogenic hyperthermia from
excessive warming techniques and assist with early detection of other causes.
• In patients with known history or familial history of MH, avoid triggering agents.
• Surgical site infections are reduced with aseptic technique; prophylactic antibiotics should
be considered.
• Central line placement should be performed with maximal barrier sterile technique.
• ICU bundles should be implemented to avoid ventilator-associated pneumonia, deep venous
thrombosis, and pulmonary embolism.
DIAGNOSIS
• History of heat exposure, infection, or the use of certain drugs that interfere with
thermoregulation.
• Vital signs: Increased temperature; pattern can be helpful. Sinus tachycardia, tachypnea,
widened pulse pressure, and hypotension. A temperature >41.5°C and can be observed in
severe infections of CNS hemorrhages. The most important causes of severe hyperthermia
(>110° F or 40°C) are heat stroke, MH, and NMS. Temperature-pulse dissociation (relative
bradycardia) is seen in typhoid fever, brucellosis, and leptospirosis.
• Physical exam should be performed to assess for infection. Chest auscultation may reveal
rhonchi or reduced sounds; Foley catheter may appear cloudy; wound, central line, and
peripheral IV sites may appear erythematous or purulent.
• Diagnostic procedures
– CBC, basal metabolic panel, electrolytes, BUN, Cr, CK enzymes, and liver enzymes
– PT, PTT, and INR because of the risk of DIC
– Urine for myoglobinuria
– Toxicological screening
– CXR may demonstrate pulmonary edema
– EKG may reveal sinus tachycardia
– Blood, urine, catheter (IV, central line), and sputum cultures
– Head CT and lumbar puncture to be performed if CNS etiologies are suspected.
Monitors
• Consider assessment of core temperatures (e.g., rectal).
• End-tidal CO2 monitor to detect MH
• Invasive monitoring as dictated by the patient’s clinical status: Arterial line and ABG, CVP,
mixed venous oxygen saturation
TREATMENT
• Depends on inciting cause

• Continuous core temperature monitoring with rectal or esophageal probes
• Cold water immersion is the most effective method of rapid cooling, but complicates
monitoring and access. Alternatives include application of ice to the axilla, groin, and neck;
however, may be poorly tolerated in awake patients. Cold oxygen, cold gastric lavage,
cooling blankets, mist of lukewarm water combined with large fans to circulate air may
augment evaporative cooling.
• Avoidance of alpha-adrenergic agents; vasoconstriction can decrease heat dissipation
• Shivering that occurs during cooling methods may be suppressed with meperidine,
clonidine, or benzodiazepines as appropriate.
• Acetaminophen for fever (infectious, blood products) and some causes of hyperthermia.
However, not effective in environmental hyperthermia. There is no role of antipyretic
agents in the management of heat stroke since the underlying mechanism does not involve a
change in hypothalamic set point.
• Heat stroke, NMS, and MH require ensuring an adequate airway, breathing, circulation;
initiation of rapid cooling and treatment of complications.
• MH and NMS require immediate discontinuation of triggering agents. MH requires treatment
with dantrolene, diuresis, and treatment of acidosis and hyperkalemia. 24-hour support is
available from consultants at MH Association of US. 1-800-MH-HYPER. NMS treatment is
controversial and use of dantrolene, bromocriptine, and amantadine is largely unsupported.
• Infection location and responsible organism should be sought out and treated with
antibiotic. Unexplained postoperative fevers without a source of infection should not be
treated empirically with antibiotics; often resolve within 48 hours without specific
therapeutic interventions.
• Central line infections require removal of access site.
FOLLOW-UP
Counseling after acute MH. Definitive diagnosis is made by susceptibility testing.
REFERENCES
1. Dinarello CA, Porat R. Pathophysiology and treatment of fever in adults: Up to date 2010. J
Endotoxin Res. 2004;10:201–222.
2. essler DI. Perioperative heat balance. Anesthesiology. 2000;92(2):578–596.
3. egal S. Labor epidural analgesia and maternal fever. Anesth Analg. 2010;111(6):1467–
1475.
4. Lee-Chiong TL, Stitt JT. Disorders of temperature regulation. Compr Ther.
1995;21(12):697–704.
ADDITIONAL READING
• Garibaldi RA, Brodine S, Matsumiya S, et al. Evidence for the noninfectious etiology of early
postoperative fever. Infect Control. 1985;6:273
• Insler SR, Sessler DI. Perioperative thermoregulation and temperature monitoring.
Anesthesiol Clin. 2006;24(4):823–837.
• Ventilator-associated pneumonia
• Hypothermia
CODES
ICD9
995.86 Malignant hyperthermia
ICD10
• T88.3XXA Malignant hyperthermia due to anesthesia, initial encounter
• T88.3XXD Malignant hyperthermia due to anesthesia, subs encntr
• T88.3XXS Malignant hyperthermia due to anesthesia, sequela
CLINICAL PEARLS
• Hyperthermia is defined as elevation of core body temperature above the normal diurnal
range of 36–37.5°C due to failure of thermoregulation.
• Temperature elevation is accompanied by an increase in oxygen consumption and metabolic
rate resulting in hyperpnea and tachycardia.
• Differential diagnosis is extensive and includes infectious, endocrine, CNS and toxic
etiologies.
• Management includes initiation of rapid cooling and treatment of complications.
HYPERTHYROIDISM
Joe C. Hong, MD
BASICS
DESCRIPTION
• Hyperthyroidism is an endocrine disorder that results in an excess of biologically active
thyroid hormones: Thyroxine (T4) and triiodothyronine (T3).
• Uncontrolled overt hyperthyroidism can lead to thyroid storm. This is a medical emergency
that presents with marked tachycardia, hyperthermia, weakness, and altered levels of
consciousness and can result in congestive heart failure (CHF) and shock (1).
EPIDEMIOLOGY
Incidence
• ∼1:1,000 women per year.
• ∼1:10,000 men per year.
Prevalence
General US population:
• Subclinical hyperthyroidism: ∼1%. Over the age of 55 years, it increases to 2%
• Overt hyperthyroidism: ∼0.2%
Morbidity
• Thyroid hormone increases bone resorption. Patients with hyperthyroidism have low bone
density and are at an increased risk of fracture.
• Incidence of atrial fibrillation is 2.5 times greater than in patients without hyperthyroidism
(2).
• Increased incidence of stroke.
Mortality
Increased risk is attributable to an increased incidence of cardiovascular disease.
• Female sex (prevalence ratio of 8:1)
• Smokers
• Elderly
• Positive family history
• Other autoimmune disorders
• Iodide repletion after iodide deprivation
PATHOPHYSIOLOGY
• Thyroid hormone functions in several capacities, including normal heart, liver, kidney, and
skeletal muscle metabolism, as well as cell differentiation and growth.
• T4 and T3 are produced by follicular cells in the thyroid gland in a classic negative feedback
system. Thyroid-releasing hormone (TRH; from the hypothalamus) stimulates the release of
thyroid-stimulating hormone (TSH; from the anterior pituitary) that in turn stimulates T3
and T4 release (from the thyroid gland). T3 and T4 feedback to inhibit synthesis and release
of TRH and TSH. Additionally, high levels of iodide ion can inhibit T4 synthesis and release.
• Hormone synthesis involves iodide uptake into the gland, iodination of thyroglobulin,
coupling of iodotyrosines to form T4 and T3, and release of thyroid hormone. T4 is
converted to T3 intracellularly, which binds to thyroid receptor proteins in the cell nucleus,
activates DNA transcription, and increases the rate of RNA synthesis, which ultimately
affects protein synthesis.
• The clinical manifestations of hyperthyroidism are the exaggerated expressions of the
physiologic activities of T3 and T4.
• Graves’ disease is an autoimmune disease whereby autoantibodies to TSH receptors bind to
and stimulate thyroid hormone production and secretion.
• Hashimoto’s thyroiditis is an autoimmune inflammation of the thyroid gland resulting in the
release of stored thyroid hormone. After inflammatory “burnout,” the patients become
hypothyroid.
• Toxic multinodular goiter develops when long-standing thyroid goiters become autonomous,
resulting in thyroid hormone production and secretion independent of TSH stimulation.
• Other less common causes include radiation thyroiditis, excessive replacement therapy, TSH-
producing pituitary adenomas, and ectopic sources of thyroid hormone (struma ovarii).
• Intraoperative risk is directly correlated to the severity of hyperthyroidism, and patients
scheduled for elective surgery should be made euthyroid prior to surgery.
• In patients requiring nonelective surgery, the avoidance of hyperthyroid crisis is the guiding
principle of management.
SYMPTOMS
• Symptoms are due to the supraphysiologic activity of T3 and T4.
• Alertness, emotional lability, nervousness, irritability, poor concentration
• Muscular weakness, fatigue
• Palpitations
• Voracious appetite, weight loss
• Hyperdefecation
• Heat intolerance
History
Focused on the multiple organ systems affected by the supraphysiologic activities of T3 and
T4: Neurological, cardiovascular, hematological, GI, metabolic, pulmonary, and
musculoskeletal systems.
Signs/Physical Exam
• Due to the supraphysiologic activity of T3 and T4.
• Hyperkinesia, rapid speech
• Proximal muscle (quadriceps) weakness, fine tremors
• Moist skin, abundant hair; onycholysis
• Lid lag, stare, chemosis, periorbital edema, proptosis
• Accentuated first heart sound, tachycardia, atrial fibrillation, widened pulse pressure,
dyspnea
MEDICATIONS
• Strategy should involve inhibition of TSH, TRH, peripheral conversion of T4 to the
biologically active T3, and the antagonism of beta-adrenergic activity.
• Propylthiouracil (PTU) and methimazole are thioamide derivatives that inhibit the synthesis
of thyroid hormones. PTU also has the added advantage of inhibiting the peripheral
conversion of T4 to T3 (3).
• Potassium iodide and glucocorticoids inhibit the release of thyroid hormones.
Glucocorticoids also inhibit peripheral conversion of T4 to T3 (3).
• Beta-blockers provide adrenergic antagonism by minimizing inotropism, chronotropism, and
the potential for arrhythmias (3).
• Medical control of hyperthyroidism may require several weeks.
Labs/Studies
• CBC: Anemia
• Coagulation panel: Thrombocytopenia and decreased vitamin K-dependent clotting factors.
• Chemistry panel: Hypercalcemia and hyperglycemia.
• EKG and appropriate cardiac evaluation based on history and physical exam.
• CT scan in patients with large goiter may be helpful in assessing airway anatomy.
• Cardiovascular: Increased risk of myocardial ischemia due to increased resting heart rate,
stroke volume, and cardiac output. Increase in beta-receptor sensitivity increases the
incidence of atrial fibrillation, premature ventricular contractions, and high-output CHF.
• Pulmonary: Weakness of respiratory muscles leading to a reduction in vital capacity and
lung compliance.
• GI: Impaired drug absorption secondary to rapid GI transit. Hyperdefecation and diarrhea
leads to hypokalemia and hypovolemia.
• Hematological: Anemia, thrombocytopenia, and decreased vitamin K-dependent factors.
• Metabolic: Hypercalcemia from increased bone resorption and impaired glucose tolerance
due to up-regulation of beta-adrenergic receptors.
• Musculoskeletal: Increased risk of osteopenia and fracture due to bone resorption.
Generalized weakness in skeletal muscles from metabolic derangements and the catabolic
state associated with severe hyperthyroidism.
• Thyroid storm is a medical emergency and must be treated prior to surgery.
• Signs and symptoms as well as concomitant organ dysfunction must be optimized prior to
elective surgery.
TREATMENT
Premedications
Patients usually have high anxiety. Appropriate use of anxiolytics/sedatives should be
balanced against the presence of airway compromise in patients with goiter.
INTRAOPERATIVE CARE
• Deep general endotracheal anesthesia for thyroidectomy.
• Anesthesia technique for nonthyroid surgery should be dictated by the type of surgery and
planned position, as well as surgeon/anaesthetist preference.
Monitors
• Invasive monitoring as dictated by planned surgery and patient comorbidities.
• EMG endotracheal tube per surgeon request for thyroid surgery.
• Large goiter can cause tracheal deviation, compression, and tracheomalacia. Preoperative
CT of the neck may help to delineate the severity of airway compromise. Awake fiberoptic
intubation should be considered if there is a high suspicion of airway compromise. Care
should be taken to blunt the adrenergic effect of awake intubation in these patients with
sensitized adrenergic tone.
• Induction drug should be chosen carefully based on comorbidities. Ketamine should be used
with care as this drug may increase adrenergic tone in these sensitized patients.
• Succinylcholine or nondepolarizing muscle relaxants with sympathomimetic effects or
histamine release should be used with caution.
• Patients with exophthalmos require careful application of ointment to the cornea and secure
taping of the eyelids.
Maintenance
• The avoidance of a thyroid crisis is the guiding principle in managing hyperthyroid patients.
• Maintenance of a deep level of surgical anesthesia is prudent.
• Medications that increase sympathetic tone should be avoided. Examples include
pancuronium, ephedrine, and meperidine.
• Anticholinergics for reversal of neuromuscular blockade may also increase sympathetic tone.
Careful attention must be paid to prevent an exaggerated sympathetic response.
Glycopyrrolate has less chronotropic effect than atropine and therefore may be the preferred
choice.
• After a thyroidectomy:
– Coughing/bucking on emergence should be minimized to decrease the likelihood of neck
hematoma formation. Preintubation tracheal lidocaine can provide airway analgesia.
– Communication with the surgeon regarding likelihood of recurrent laryngeal nerve injury
needs to take place prior to emergence and extubation.
POSTOPERATIVE CARE
BED ACUITY
Patients with poorly controlled hyperthyroidism and significant comorbidities should be
monitored in the ICU setting.
COMPLICATIONS
• Thyroid storm is a rare medical emergency that typically develops postoperatively in
patients with hyperthyroidism. Thyroid storm may be difficult to distinguish from
malignant hyperthermia, neuroleptic malignant syndrome, or pheochromocytoma. Mortality
may be as high as 20–30% (4). Management of thyroid storm involves:
– Oxygen, airway protection, hyperventilation, aggressive fluid replacement.
– Beta-adrenergic blockade, typically with a short-acting titratable beta-blocker like esmolol.
– PTU, methimazole, potassium iodide, corticosteroids.
– Cooling measures involving cool IV fluids, cooling blankets, nasogastric, or bladder
lavage.
– Plasmapheresis or peritoneal dialysis can remove excess thyroid hormones (5).
• Thyroidectomy
– Airway compromise (most common) from hematoma, airway edema, tracheomalacia,
hypocalcemia from hypoparathyroidism, and partial bilateral recurrent laryngeal nerve
injury. The RLN innervates all intrinsic laryngeal muscles except the cricothyroid (SLN).
Specifically, the RLN innervates a number of adductors, and a single abductor (posterior
cricoarytenoid muscles). Injury to the abductor component can result in unopposed
adduction (including from the SLN innervated cricothyroid). Complete transection will
result in the affected vocal cord lying in the midline (injury to the adductors and
abductors).
– Injury to the nearby carotid artery can result in massive bleeding and possible stroke
– Intraoperative carotid sinus irritation may lead to hemodynamic fluctuations and
bradyarrhythmias
– Occult pneumothorax can result from lower neck surgical dissection
REFERENCES
1. Singer PA, et al. Treatment guidelines for patients with hyperthyroidism and
hypothyroidism. Standards of care committee, American Thyroid Association. JAMA.
1995;273:808.
2. herman SI, et al. Clinical and socioeconomic predispositions to complicated thyrotoxicosis:
A predictable and preventable syndrome? Am J Med. 1996;101:192.
3. ooper DS. Antithyroid drugs. N Engl J Med. 2005;352:905.
4. ayak B, et al. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am.
2006;35:663.
5. etry J, et al. Plasmapheresis as effective treatment for thyrotoxic storm after sleeve
pneumonectomy. Ann Thorac Surg. 2004;77:1839.
ADDITIONAL READING
• Franklyn JA. The management of hyperthyroidism. N Engl J Med. 1994;330:1731.
• Graham GW, et al. Perioperative management of selected endocrine disorders. Int
Anesthesiol Clin. 2000;38:31.
• Hypothyroidism
• Vocal cord palsy
CODES
ICD9
• 242.90 Thyrotoxicosis without mention of goiter or other cause, and without mention of
thyrotoxic crisis or storm
• 242.91 Thyrotoxicosis without mention of goiter or other cause, with mention of thyrotoxic
crisis or storm
ICD10
• E05.80 Other thyrotoxicosis without thyrotoxic crisis or storm
• E05.90 Thyrotoxicosis, unsp without thyrotoxic crisis or storm
• E05.91 Thyrotoxicosis, unspecified with thyrotoxic crisis or storm
CLINICAL PEARLS
• Intraoperative risk is directly correlated to the severity of hyperthyroidism.
• Preoperative medical management involves inhibition of thyroid hormone synthesis, release,
and peripheral conversion. Commonly used medications include PTU, methimazole,
potassium iodide, glucocorticoids, and beta-adrenergic blockade.
• Careful airway management and possible awake fiberoptic intubation may be indicated in
patients with large goiter.
• The avoidance of thyroid crisis by maintaining a deep level of surgical anesthesia while
minimizing exposure to sympathomimetic medications is the guiding principle in managing
hyperthyroid patients.
• Postoperative complications are usually related to airway compromise. Causes include
hematoma, airway edema, tracheomalacia, and partial bilateral recurrent laryngeal nerve
injury.
• Thyroid storm is a medical emergency with high mortality. Decisive emergent management
is crucial.
HYPERTROPHIC CARDIOMYOPATHY
Adam M. Thaler, DO
BASICS
DESCRIPTION
• Hypertrophic cardiomyopathy (HCM) describes idiopathic, abnormal left ventricle
hypertrophy (LVH) (specifically an asymmetric septum).
• The obstructive variant, commonly referred to as hypertrophic obstructive cardiomyopathy
(HOCM) can impair LV ejection of blood to the systemic circulation.
EPIDEMIOLOGY
Prevalence
• In the US population: 1:500 people. It is the most common genetic cardiovascular disease
• Males > females
• Most commonly presents in the third decade of life, but it may present in persons of any
age.
Morbidity
Arrhythmias: Atrial fibrillation, atrial flutter, ventricular ectopy, ventricular tachycardia, and
ventricular fibrillation (one of the highest-risk groups for ventricular fibrillation)
Mortality
• Most common cause of sudden cardiac death (SCD)
• Annual mortality rates overall are ∼1% per year.
• Children with HCM have an SCD risk of up to 6% per year.
• Some adult subgroups 6% per year (2)
• In competitive athletes, there are <100 deaths a year (equates to about 1 death per 220,000
athletes).
Genetic predisposition. HCM is an autosomal dominant trait that causes mutations in
sarcomeric proteins. This results in structural abnormalities: A catenoid (curved surface with
the property of net zero curvature at all points) configuration of the septum, which results in
myocardial cell hypertrophy and disarray.
PATHOPHYSIOLOGY
• The hypertrophied myocardium exhibits
– Decreased lusitropy. Abnormalities of the cardiac microcirculation deplete energy stores
essential for the sequestration of calcium during diastole, resulting in subendocardial
ischemia. This causes persistent interaction of the contractile elements during diastole and
increased diastolic stiffness.
– Increased ejection fraction (EF) that is commonly >80% despite diastolic dysfunction and
decreased compliance.
– Increased myocardial oxygen demand. Similar to LVH and aortic stenosis (AS), there is
greater muscle mass.
– Decreased myocardial oxygen delivery. Hypertrophied muscle creates more resistance to
perfusion.
– Decreased wall tension. T = (R × ΔP)/H, where T = tension, R = radius, ΔP = pressure
gradient, and H = wall thickness
– However, over time, the thickened heart may become weak and ineffective causing
ventricular enlargement, systolic dysfunction (decreased EF), and dilated cardiomyopathy
(increased wall tension).
• Abnormal sympathetic stimulation: Heightened responsiveness of the heart to the excessive
production of catecholamines or the reduced neuronal uptake of norepinephrine might
exacerbate HCM.
• Abnormally thickened intramural coronary arteries: These do not dilate normally, which
leads to myocardial ischemia and, with time, can progress to myocardial wall fibrosis.
• Obstructive disease variant. Systolic anterior motion (SAM) of the anterior leaflet of the
mitral valve can result in dynamic left ventricular outflow tract (LVOT) obstruction when
the ventricle size decreases. Previously believed to result from high velocity flow and a
Venturi effect on the anterior leaflet of the mitral valve, but recent echocardiographic
evidence indicates that SAM is a low velocity phenomenon and that drag (the pushing force
of flow), not the Venturi effect, is the dominant hydrodynamic force on the mitral leaflets.
LVOT obstruction can be present at rest or can be induced with a Valsalva maneuver.
• Changes in electrical and muscular conduction and alterations of coronary perfusion
increase the incidence of atrial and ventricular arrhythmia and risk for SCD.
• Monitor and maintain normal sinus rhythm.
• In patients with HOCM, decrease “emptying” of the heart by:
– Maintaining adequate intravascular volume
– Maintaining appropriate systemic vascular resistance (SVR): Avoid vasodilators, provide
vasoconstriction
– Decreasing inotropy and chronotropy: Avoid inotropes and control sympathetic response
with adequate anxiolytics and narcotics.
SYMPTOMS
• Usually asymptomatic
• Dyspnea is seen in 90% of symptomatic patients; it results from the high LV filling pressures
(decreased compliance and causes pulmonary edema)
• Syncope from inadequate CO upon exertion
• Other: Fatigue, dizziness, palpitation, tachydysrhythmias, heart failure, and SCD
History
• Family history of cardiac disease or sudden death
• Commonly diagnosed after symptomatic exercising or during workup for diastolic or systolic
CHF or angina.
Signs/Physical Exam
• Systolic ejection crescendo–decrescendo murmur heard best between the apex and left
sternal border. Murmur/gradient increases with any decrease in preload (Valsalva, diuretics,
standing) or decrease in afterload (vasodilation).
• Double or triple apical impulse from forceful LA contraction against highly noncompliant
LV.
• Bisferiens carotid pulse due to obstruction
• Brockenbrough–Braunwald–Morrow. Describes an increase in peak-systolic gradient
combined with a decrease in pulse pressure after an extrasystolic beat.
TREATMENT HISTORY
• Prophylactic ICD or pacemaker (allows high dose beta-blockade)
• Septal myectomy. The removal of a small amount of cardiac muscle from the ventricular
septum. Performed when severe symptoms of CHF or outflow tract gradients are >50 mm
Hg.
• Nonsurgical percutaneous transluminal septal ablation. Alcohol is injected into septal
branches of the LAD causing therapeutic infarction within septal myocardium to decrease
hypertrophy and LVOT obstruction. Requires a permanent pacemaker 30% of the time.
MEDICATIONS
• Beta-blockers are first-line therapy. By decreasing the heart rate, diastole is prolonged
(increased time for passive ventricular filling, perfusion of the left ventricle, decreased
oxygen consumption). In patients with HOCM, they are useful by decreasing
contractility/inotropy.
• Calcium channel blockers (CCB) improve ventricular filling by increase LV compliance. In
patients with HOCM, they are useful by decreasing LVOT obstruction.
• Amiodarone for prophylaxis against arrhythmias
Labs/Studies
• EKG: Left ventricular hypertrophy
• Echocardiogram: Myocardial hypertrophy, EF >80% due to hypercontractile condition;
assessment of mitral valve and presence of SAM
• Catheterization: Increased LV end-diastolic pressures (LVEDP) and LV-aorta pressure
gradients between LV and aorta
• Definitive diagnosis: Endomyocardial biopsy showing myocardial fiber disarray and DNA
analysis
• Hypertension
• Pulmonary hypertension, congestion, pleural effusion
• Arrhythmias
Uncontrolled arrhythmias
CLASSIFICATIONS
Obstructive versus nonobstructive
• The obstructive variant has historically been known as idiopathic hypertrophic subaortic
stenosis (IHSS) and asymmetric septal hypertrophy (ASH). It is more commonly referred to
today as hypertrophic obstructive cardiomyopathy (HOCM).
• The nonobstructive variant (apical HCM) is also called Yamaguchi syndrome.
TREATMENT
Premedications
• Continue beta-blockers or CCB perioperatively
• Relieve anxiety
• Expansion of intravascular volume to minimize the adverse effects of positive pressure
ventilation (decreased preload in the presence of diastolic dysfunction) and to decrease
LVOT obstruction in patients with HOCM.
• Manage pacemaker/defibrillator appropriately
INTRAOPERATIVE CARE
• Dependent on type of surgery, patient comorbidities, and physical exam.
• In patients with HOCM, the use of spinal anesthesia is relatively contraindicated due to the
rapid decrease in SVR.
In the 3rd trimester, increases in inotropy, aortocaval compression, sympathetic stimulation,
and blood loss during delivery can result in cardiac decompensation. Regional, neuroaxial,
and general anesthesia have been safely administered for labor.
Monitors
• Additional monitoring depends on the surgery. Arterial line can help assess rapid
hemodynamic changes and the potential for hypotension and MI; may be placed
preoperatively. If the patient is at a high risk for decompensation, consider a pulmonary
artery catheter to monitor the right and LV function (may overestimate true volume status
as a result of reduced diastolic compliance).
• Transesophageal echocardiogram (TEE) may be indicated to evaluate myocardial function
and detect regional wall motion abnormalities.
Administration of volatile anesthetic or beta-blocker before laryngoscopy can blunt the
sympathetic response.
Maintenance
• Hypotension.
– Decreased coronary perfusion pressure can result in ischemia of the hypertrophic
myocardium.
– In patients with HOCM, decreases in SVR should be avoided. Volatile and IV agents can
decrease SVR; avoid excessive doses, consider concomitant alpha agonism (low dos
phenylephrine infusion).
– Avoid drugs with beta-activity (ephedrine, epinephrine) as they can increase myocardial
contractility and HR.
• Pain, awareness, and stimulation can increase the HR and contractility (increases oxygen
demand).
• Ventilation. Positive-pressure ventilation can significantly decrease preload. In patients with
HOCM, this can result in dynamic LVOT obstruction. Smaller tidal volumes or avoidance of
PEEP may be considered.
• Drugs. Caution with histamine-releasing medications or those that increase HR
(vancomycin, morphine, etc.). In patients with HOCM, vasodilators should be used
cautiously to treat hypertension as they can decrease SVR; alternatively, consider beta
blockade.
• Fluids. Prompt replacement of blood loss and titration of IV fluids is important; aggressive
replacement may result in pulmonary edema secondary to diastolic dysfunction.
• Arrhythmias. Immediate pharmacologic or electrical cardioversion
• Laparoscopy. Abdominal insufflation can cause severe hypotension and preload reduction;
insufflate slowly and maintain pressure <15 mm Hg.
All factors that stimulate sympathetic nervous system (SNS) such as pain, shivering, anxiety,
hypoxia, and hypercarbia should be avoided.
POSTOPERATIVE CARE
BED ACUITY
• Patients may benefit from ICU or telemetry given the high risk of cardiac complications; the
postoperative period is marked by increased myocardial oxygen demand, increased
catecholamine levels, hypoxia, hypercoagulability, and large fluid shifts. MI occurs more
frequently postoperatively.
• Consider supplemental oxygen (nasal cannula, face mask).
• Good analgesia can decrease SNS activity; consider PCA, epidural, or regional as
appropriate.
COMPLICATIONS
• In patients with HOCM, LV outflow tract obstruction from a variety of perioperative events
(hypovolemia, hypotension, increased inotropy) can cause acute decompensation.
• Arrhythmias
REFERENCES
1. Luckner G, et al. Systolic anterior motion of the mitral valve with left ventricular outflow
tract obstruction: Three cases of acute perioperative hypotension in noncardiac surgery.
Anesth Analg. 2005;100(6):1594–1598.
2. ingh KV, Shastri C, Raj V, et al. Anaesthetic management of a case of hypertrophic
obstructive cardiomyopathy for non cardiac surgery. Internet J Anesthesiol. 2007;12(2).
3. Thompson R, Liberthson R, Lowenstein E. Perioperative anesthetic risk of noncardiac
surgery in hypertrophy obstructive cardiomyopathy. JAMA. 1985;254(17):2419–2421.
ADDITIONAL READING
• Dilated cardiomyopathy
• Left ventricular end-diastolic pressures
• Ventricular hypertrophy
CODES
ICD9
• 425.11 Hypertrophic obstructive cardiomyopathy
• 425.18 Other hypertrophic cardiomyopathy
ICD10
• I42.1 Obstructive hypertrophic cardiomyopathy
• I42.2 Other hypertrophic cardiomyopathy
CLINICAL PEARLS
• SAM can be induced in an otherwise healthy patient who comes in with severe hemorrhage
and is administered epinephrine. The catecholamine surge causing a hypercontractile state
and the underfilled ventricle presents similarly to HOCM. Other causes of LVOT obstruction
include sepsis, excess SNS, pericardial tamponade, aortic valve replacement (AVR) for AS,
or mitral valve replacement (MVR).
• SAM may be an unrecognized cause of acute perioperative cardiovascular collapse. Acute
treatment includes volume infusion and vasopressors.
HYPOGLYCEMIA
BASICS
DESCRIPTION
• Hypoglycemia is defined as a serum glucose <70 mg/dL.
• Tight glucose control has been shown to improve outcomes in critically ill patients;
however, hypoglycemia is the most common complication of insulin therapy and has more
immediate and direct deleterious effects.
• Additionally, severely ill, elderly patients, and neonates have an increased susceptibility to
the deleterious effects of hypoglycemia (permanent neurologic damage and death).
EPIDEMIOLOGY
Incidence
• Rare in persons not treated for diabetes.
• Severe hypoglycemia (episodes per 100 patients/year)
– Type 1 diabetic: 11.5
– Type 2 diabetic treated with oral hypoglycemic agents: 0.05
– Type 2 diabetes treated with insulin: 11.8
– Elderly patients: 2
• Neonates: 1–5 per 1,000 live birth; higher incidence in large-for-gestational age, preterm,
and intrauterine growth restricted (IUGR) infants, as well as those born to diabetic mothers.
Morbidity
Increased when intensive insulin therapy (IIT) in the medical intensive care unit (ICU) is
implemented; particularly in patients with renal or hepatic failure.
• Iatrogenic hypoglycemia
– Overdose of insulin or other antidiabetic drug ingestion.
– Decreased exogenous glucose intake (missed meals/snack or after overnight fasting).
• Alcohol ingestion
• Side effect of certain drugs: Haloperidol, pentamidine, quinine, and nonselective beta-
blockers.
• Severe illness
• Tumors: Pancreatic islet cell adenoma or carcinoma, hepatoma, and sarcoma
• Adrenal insufficiency
• Autoimmune processes
• Increased sensitivity to insulin following exercise, weight loss, or due to insulin sensitizers.
• Renal failure: Decreased clearance of insulin
• Neonates
– Preterm delivery
– Transient hypoglycemia of the newborn
– IUGR
– Sepsis
– Hypothermia
– Birth asphyxia
– Inborn errors of metabolism
– Hepatic enzyme deficiencies
– Transplacental exposure to maternal hypoglycemic medications
• Elderly: Frail, polypharmacy, and multiple hospital admissions.
• Glucose is a principal energy substrate for the body; for the brain, it is the sole energy
substrate.
• Glucose is synthesized from gluconeogenesis (from the metabolism of pyruvate, lactate,
glycerol, and glucogenic amino acids) and glycogenolysis that results from the breakdown
of glycogen.
• In normal glucose homeostasis, blood glucose levels are tightly regulated by insulin,
glucagon, epinephrine, and cortisol. The liver is the principal storage site for glucose in the
form of glycogen.
• A decrease in blood glucose level will cause
– Drops in endogenous insulin production
– Release of epinephrine, glucagon, growth hormone, and cortisol that act as
counterregulatory hormones.
– An increase in hepatic glucose production
– A decrease in peripheral utilization of glucose
– Neurogenic and neuroglycopenic symptoms
• Diabetes
– Type 1, or insulin-dependent, diabetics have reduced or absent insulin secretion. In
addition, they have an impaired release of counterregulatory hormones such as glucagon
and epinephrine.
– In type 2 diabetes, patients are capable of generating and secreting insulin, but peripheral
tissues are resistant to its effects. There is a lower risk of hypoglycemia compared to type
1 diabetes, potentially due to the sustained ability to secrete counterregulatory hormones.
– Exogenous insulin administration and oral antihyperglycemic medications (e.g.,
sulfonylureas) can cause iatrogenic hypoglycemia.
• Neonatal hypoglycemia can cause seizure and permanent brain damage. The brain utilizes
glucose as the sole substrate of energy. In the rapidly growing neonatal brain, cerebral
consumption comprises nearly 90% of their total glucose consumption; however, neonates
are susceptible to hypoglycemia due to
– Inadequate hepatic glycogen reserve
– Immaturity of the liver in synthesizing glucose (hepatic gluconeogenesis).
– Relative hyperinsulinism in infants of diabetic mother
– Inherited disorders of metabolism
– Impaired release of counterregulatory hormones
• Evidence is suggesting that the benefits of tight glucose control may be outweighed by the
potential harm of hypoglycemia.
– The ACCORD trial revealed that intensive glucose control in patients with type 2 diabetes
mellitus (HBA1C <6%) is associated with increased mortality and no reduction in adverse
cardiovascular events.
– The NICE SUGAR study revealed that in the ICU patients treated with IIT had increased
mortality. IIT was defined as a blood glucose aim of 81–106 g/dL; the conventional group
was defined as a blood glucose aim of <180 g/dL.
– Several studies report that maintaining a stable glucose level is equally important to the
absolute glucose values. Fluctuations in glucose control lead to oxidative stress that cause
macrovascular complications.
• Cardiac surgical patients, particularly those requiring prolonged intensive care admissions,
are an exception; they show a clear benefit from strict glycemic control.
• Diabetics. Preoperative assessment of glucose control, type and dose of medications,
frequency of hypoglycemia, and current HBA1C level is needed.
• On the day before surgery
– Oral medications are usually dosed normally
– Long or intermediate-acting insulin can be taken in usual doses while on a normal diet.
Evening of night doses are normally decreased.
– If hypoglycemic while NPO, treat with 15–20 gm of glucose. Options include clear liquids,
in the form of sugary drinks and fruit juices, sodas, or electrolyte solutions.
– Blood sugar checks should be done frequently when NPO.
• On the morning of surgery
– In type 2 diabetics, oral medications and short-acting injectables should be withheld.
– Insulin pumps should be maintained at a basal rate and short-acting insulin should be
withheld.
– For morning cases, hold intermediate-acting insulin or give a percentage of the dose
calculated as below:
Fraction = [(dosing interval in hours) – (hours of fast during interval)]/(dosing interval
in hours)
– For cases later in the day, maintain a basal rate for patients on an insulin pump and for
patients on intermediate insulin, give a percentage of the dose based on the formula
above.
• In the recover room or hospital ward, resume oral hypoglycemic agents and insulin with
food.
• Hyperglycemia in the perioperative period. Correction doses of ultra short-acting insulin: 1–
4 U IV typically decreases blood sugar by 50 mg/dL.
DIAGNOSIS
• Signs and symptoms are the result of:
– Adrenergic excess; diaphoresis, tachycardia, palpitations, or tremulousness/shakiness.
– Neuroglycopenia; headache, confusion, mental sluggishness, seizures, or coma
• In anesthetized patients all symptoms may be masked; unexplained tachycardia can
sometimes present. Blood glucose monitoring is confirmatory.
• In awake patients
– Severe hypoglycemia: Requires the presence of another person to actively administer
carbohydrates, glucagon, or other treatments. It does not require documentation of the
plasma glucose level. Symptoms resolve after restoring normal blood glucose.
– Documented symptomatic hypoglycemia: The presence of hypoglycemic symptoms along
with a documented blood glucose <70 mg/dL.
– Asymptomatic hypoglycemia: Absence of hypoglycemic symptoms but documented blood
glucose <70 mg/dL.
– Probable symptomatic hypoglycemia: Presence of hypoglycemic symptoms with unknown
blood glucose level.
– Relative hypoglycemia: Presence of hypoglycemic symptoms but blood glucose level >70
mg/dL.
– Whipple’s triad: Hypoglycemic symptoms, symptoms relieved after glucose intake, and
documented low blood glucose level.
• Elderly patients display fewer hypoglycemic symptoms.
• Women respond less strongly to hypoglycemia than men.
• Seizure
• Vasovagal attack
• Cardiac arrhythmia
• Panic attack
TREATMENT
• Fully conscious patient

– Oral glucose (15–20 g), sucrose or sugar containing fluid, orange juice, or a piece of fruit.
– Ensure adequate subsequent food intake to prevent recurrence.
• Impaired consciousness
– Administer Dextrose 50% 25–50 mL IV until there is a return of consciousness or normal
blood glucose level. Then start a Dextrose 5% (D5W) or Dextrose 10% (D10W) infusion
and titrate to effect.
– In severe hypoglycemia, glucagon 1 mg IV may be administered. In patients without IV
access, glucagon IM or SQ may be given.
• Symptomatic infants
– D10W 2 mL/kg IV bolus, followed by an infusion rate of 6–8 mg/kg/min. To achieve this
rate:
D5W: IV rate (in mL/hr) = 8.4 × body weight (kg)
D10W: IV rate (in mL/hr) = 4.2 × body weight (kg)
• Anesthetized patient
– Administer Dextrose 50% 25–50 mL IV, followed by repeat testing and careful observation
with possible infusion. If glucose levels remain low, repeat the bolus and consider starting
an infusion.
FOLLOW-UP
• Anesthetic management should aim to minimize the stress response during the
intraoperative and postoperative period. Consider adequate pain relief and prophylaxis for
nausea and vomiting.
• Dexamethasone can elevate blood glucose for several hours, with a maximum blood glucose
noted 120 minutes after dosing.
• Autonomic neuropathy can cause swings in hemodynamic response during induction.
REFERENCES
1. Zammitt NN, Frier BM. Hypoglycemia in type 2 diabetes. Diabetes Care. 2005;28:2948–
2961.
2. ryer PE. Management of hyperglycemia in type 2 diabetes: A consensus algorithm for the
initiation and adjustment of therapy: A consensus statement from the American Diabetes
Association and the European Association for the Study of Diabetes. Diabetes Care.
2007;30(1):190–192.
3. Workgroup on Hypoglycemia, American Diabetes Association. Defining and reporting
hypoglycemia in diabetes: A report from the American Diabetes Association Workgroup on
Hypoglycemia. Diabetes Care. 2005;28(5):1245–1249.
4. Gabriely I, Shamoon H. Hypoglycemia in diabetes: Common, often unrecognized. Cleve
Clin J Med. 2004;71(4):335–342.
5. Wintergerst KA, Buckingham B, Gandrud L, et al. Association of hypoglycemia,
hyperglycemia, and glucose variability with morbidity and death in the pediatric intensive
care unit. Pediatrics. 2006;118(1):173–179.
6. NICE-SUGAR Study Investigators, Finfer S, Chittock DR, et al. Intensive versus
conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283–
1297.
7. Vann MA. Perioperative management of ambulatory surgical patients with DM. Curr Opin
Anaesthesiol. 2009;22(6):718–724.
ADDITIONAL READING
• Joshi GP, Chung F, Vann MA, et al.; Society for Ambulatory Anesthesia. Society for
Ambulatory Anesthesia consensus statement on perioperative blood glucose management in
diabetic patients undergoing ambulatory surgery. Anesth Analg. 2010;111(6):1378–1387.
• Moghissi ES, Korytkowski MT, Dinardo M, et al. American Association of Clinical
Endocrinologists and American Diabetes Association consensus statement on inpatient
glycemic control. Diabetes Care. 2009;32:1119–1131.
• The DCCT Research Group: Hypoglycemia in the Diabetes Control and Complications Trial.
Diabetes. 1997;46:271–286.
• Hyperglycemia
CODES
ICD9
251.2 Hypoglycemia, unspecified
ICD10
E16.2 Hypoglycemia, unspecified
CLINICAL PEARLS
• Hypoglycemia is the main obstacle in achieving good glycemic control in patients with
diabetes.
• Cardiac surgical patients benefit from strict glucose control, but the aim for most ICU
patients is a stable blood glucose <180 g/dL.
• Glucose is the sole energy substrate for the brain; furthermore, there are no stores to protect
against a decreased supply.
HYPOKALEMIA
BASICS
DESCRIPTION
• Hypokalemia is defined as a plasma potassium (K+) concentration <3.5 mEq/L (normal
3.5–5 mEq/L). Causes include K+ loss or intracellular shifting. Symptoms range from
arrhythmias to myalgias to respiratory depression.
• Hypokalemia may be a poor indicator of total body stores because of its asymmetric body
distribution. Ninety-eight percent of the body’s potassium is located intracellularly (75% in
muscle, 6% in red blood cells, and 5% in the liver). The remaining 2% is located in the
intravascular and extracellular compartments (2).
• Patients commonly present for surgery with low K+ levels, which is the most common
electrolyte abnormality in hospitalized patients. Anaesthetists must be able to determine
when and how a patient should be managed with such abnormalities.
• The majority of the body’s potassium stores are located intracellularly.
• The membrane resting potential is an electrochemical gradient that plays a role in transport,
signal transduction, myocardial pacemakers and contraction, and cell volume homeostasis.
Consequently, there are several mechanisms that serve to maintain intravascular
concentrations within a tight range.
– The Na+–K+–ATPase enzyme pump (embedded in the cell membrane) moves 3 Na+ ions
extracellularly and 2 K+ ions intracellularly. The exchange requires the expenditure of 1
adenosine triphosphate (ATP). The electrochemical gradient is manifested by an
intracellular concentration of 150 mEq/L (intravascular concentration is ∼3.5–5 mEq/L).
• Additional mechanisms: K+ concentrations between the two compartments are also affected
by pH, insulin, and catecholamines or sympathomimetics with beta-adrenergic receptor
activity.
– pH: The Na+–H+ ion exchange facilitates buffering against alkalemia or acidemia. In
alkalemia, H+ ions move extracellularly to offset the disturbance and Na+ moves
intracellularly. This increase in intracellular Na+ stimulates the Na+–K+–ATPase, which
results in a secondary intracellular shift of K+. Conversely, in acidemia, H+ ions move
intracellularly, in exchange for Na+ moving extracellularly. This reduces intracellular
shifting of K+ via the Na+–K+–ATPase (can result in hyperkalemia).
– Insulin: Activates the Na+–K+–ATPase in cells, causing an intracellular shift of K+.
– Beta-adrenergics: Activate adenylyl cyclase and increase cAMP levels, which then activate
protein kinase A. Results in activation of calcium-gated K+ channels as well as Na+–K+–
ATPase.
• K+ excretion: In addition to intracellular shifting, K+ levels are also regulated by the
kidneys (90%), the gastrointestinal (GI) tract, and sweat. Aldosterone, a mineralocorticoid,
lowers plasma K+ concentration at several levels in the renal tubule.
ANATOMY
• Although the resting membrane potential is maintained by the Na+–K+–ATPase, certain
cells exert their functional capacity via depolarization.
– Pacemaker cells spontaneously depolarize to produce an electrical signal that travels to
conduction cells and adjacent myocardial muscle cells in a domino-like fashion.
Repolarization (Phase 3) is primarily via potassium efflux.
– Myocardial muscle cells depolarize in response to adjacent pacemaker or muscle cells.
Electrical depolarization is coupled to mechanical contraction and blood being pumped.
Repolarization is mediated via potassium efflux; however, it is divided into an early
(Phase 1) and late (Phase 3) phase by an extended plateau.
– Nerve cells communicate and transmit their signal via electrical signaling that involves
changes in resting membrane potential. Repolarization occurs via potassium efflux.
• Hypokalemia is defined as a serum [K+] <3.5 mEq/L. This disturbance is the result of
either reduced total body stores or redistribution into the intracellular space.
• Reduced total body stores may result from reduced intake or increased excretion (renal or
extrarenal).
– Reduced intake: The minimum daily requirement is 40–50 mEq/day
– Increased renal excretion: Type I and II renal tubular acidosis, diuretic therapy, carbonic
anhydrase inhibitors, ureterosigmoidostomy, posthypercapnia, increased
mineralocorticoid activity (aldosterone), and hemodialysis
– Increased extrarenal excretion: Diarrhea, vomiting and nasogastric suction, increased
sweat loss, and laxative abuse
• Intracellular shifting can occur perioperatively via alkalemia, exogenous insulin
administration, and beta-adrenergics.
– Alkalemia: Hyperventilation results in hypocarbia, and can be caused perioperatively by
controlled mechanical ventilation (increased respiratory rate or tidal volume), stimulation,
or pain. Another cause is excessive bicarbonate administration.
– Exogenous insulin may be administered for glucose control. Hyperalimentation may
increase endogenous insulin release.
– Beta-adrenergics may be administered as catecholamines or sympathomimetics
(epinephrine, dobutamine, isoproterenol, and ephedrine). Nebulizers and inhalers for the
treatment of COPD or asthma. Thyrotoxicosis causes excessive beta-adrenergic
stimulation.
• Clinical manifestations of hypokalemia result from hyperpolarization of cell membranes, as
well as from prolongation of action potentials and refractory periods. Thus, it primarily
affects cardiac, skeletal muscle, GI, and renal systems.
– Cardiac: Dysrhythmias (premature atrial contractions, premature ventricular contractions,
AV block, ventricular tachycardia, ventricular fibrillation), conduction defects (increased
PR and QT intervals, reduced T wave amplitude, T wave inversion or U waves, and ST
segment depression), and potentiation of digitalis toxicity.
– Skeletal muscle: Weakness, paralysis, rhabdomyolysis, fasciculations, and tetany (typically
do not manifest until the serum [K+] is <3 mEq/L)
– GI: Ileus, constipation
– Renal: Metabolic alkalosis, nephrogenic diabetes insipidus, impaired urinary concentrating
abilities, increased NH3 production, and hypokalemic nephropathy.
• Acute changes are less well tolerated than chronic changes.
• Correlation between serum and total body K+ is not exact and may be difficult to
extrapolate. It is estimated that in chronic hypokalemia reduced plasma levels of 1 mEq/L
can equal a total body deficit of 200–400 mEq (1).
• Mild hypokalemia (3.0–3.5 mEq/L) does not typically require urgent correction (2).
• [K+] <3.0 mEq/L often requires K+ replacement. Of note, values greater than or equal to
2.6 mEq/L have not been shown to increase morbidity or mortality in patients undergoing
anesthesia.
• [K+] between 2.0 and 2.5 mEq/L are likely to cause arrhythmias and muscular weakness;
furthermore, it can potentiate the effects of neuromuscular blocking agents and can delay
recovery.
• Potassium replacement. Oral and IV preparations are available. Perioperative correction
often involves IV KCl preparations. The maximum recommended rate of infusion is 10–20
mEq/hour (peripheral IV: 10 mEq/hour; central line access 20 mEq/hour). Higher rates of
administration carry the risk of hyperkalemia or arrhythmias.
• Magnesium replacement should be concurrently performed.
• Delay or proceed? The decision to delay for further optimization versus proceeding depends
upon:
– Urgency of surgery. Urgent or emergent surgery may be performed with careful EKG
monitoring and avoidance of hyperventilation, alkalosis, and beta-adrenergics. K+
replacement should be undertaken. In the event that arrhythmias or EKG changes
manifest, boluses of 1 mEq may be administered while monitoring for resolution.
– Acute versus chronic onset. When patients present preoperatively with hypokalemia, a
determination of its onset should be attempted. Review old laboratory values.
– Clinical manifestations should be assessed
– EKG changes
– Need for perioperative hyperventilation. Intracranial surgical procedures may require
intracranial pressure optimization via hyperventilation (hypocarbia). Additionally, the use
of mannitol or furosemide to provide “brain relaxation” can further decrease potassium
levels (excreted by the kidneys). Attempts to correct potassium should be undertaken
prior to surgery. In the event that the patient’s clinical condition deteriorates, proceed as
discussed above for urgent/emergent surgery.
– Need for beta-adrenergic agents
REFERENCES
1. Lim S. Approach to hypokalemia. Acta Med Indones. 2007;39(1):56–64.
2. Katerinis I, Fumeaux Z. Hypokalemia: Diagnosis and treatment. Rev Med Suisse.
2007;3(101):579–582.
ADDITIONAL READING
• Lin SH, Halperin ML. Hypokalemia: A practical approach to diagnosis and its genetic basis.
Curr Med Chem. 2007;14(14):1551–1565.
• Hyperkalemia
• Cardiac action potential
• QT prolongation
CODES
ICD9
276.8 Hypopotassemia
ICD10
E87.6 Hypokalemia
CLINICAL PEARLS
• Hypokalemia is the most common perioperative electrolyte abnormality. May manifest as
arrhythmias, conduction disturbances, muscle weakness, potentiation of neuromuscular
blocking agents, and delayed awakening.
• Anaesthetists must determine whether to delay surgery in order to optimize plasma levels or
proceed. This clinical decision must factor in the urgency of surgery, the rate that
hypokalemia developed, and the manifestation of clinical signs or symptoms.
• Proceeding with surgery may require perioperative replacement; however, replenishment
must be done slowly and cautiously. Maximal IV repletion rate in most cases is 10–20
mEq/hour (peripheral IV is suggested as 10 mEq/hour; central line access as 20 mEq/hour).
• Small changes in plasma levels may actually represent significant total body deficits.
HYPONATREMIA
Adam Romanovsky, MD
BASICS
DESCRIPTION
• Hyponatremia describes a serum sodium (Na+) concentration <135 mmol/L (Exact value
depends on laboratory assay used.)
• In addition to being the most common electrolyte derangement, hyponatremia has been
associated with increased morbidity and mortality.
EPIDEMIOLOGY
Incidence
Hyponatremia is the most commonly encountered electrolyte disorder in hospitalized patients
Prevalence
• 1–2% in hospitalized patients
• 4.4% of postoperative patients
• Nearly 30% of critically ill patients
Morbidity
Hyponatremia is associated with prolonged durations of stay in the intensive care and
hospital, and associated with a higher rate of discharge to a long-term care facility.
Mortality
• Associated with an increased all-cause mortality in hospitalized patients
• It is an independent risk factor for death in cirrhosis, heart failure, and following acute
myocardial infarction.
Hypoosmolar Hyponatremia. Describes an increase in plasma water in excess of plasma
sodium.
• Increased endogenous antidiuretic hormone (ADH)
– Hypovolemic
Intravascular volume depletion.
GI losses (diarrhea, vomiting)
Skin losses (burns, sweat)
Renal losses (diuretics, cerebral salt wasting, ketonuria, bicarbonaturia)
Third spacing into a “nonfunctional” space (edema, tissue trauma)
Adrenal insufficiency (may also be euvolemic). Decreased aldosterone results in volume
contraction due to renal loss; ADH is released in response. Cortisol insufficiency also
stimulates ADH release.
– Hypervolemic
Decreased effective circulating volume (heart failure, cirrhosis, nephrotic syndrome). In
addition to increases in ADH, arterial underfilling is detected by baroreceptors in the
aortic arch, carotid sinus, and afferent renal arterioles that then activate the sympathetic
nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS) resulting in
avid sodium and water retention.
– Euvolemic
Syndrome of inappropriate ADH secretion (SIADH). Increased levels of ADH cause water
retention (decreased serum osmolality).
Reset osmostat. A type of SIADH where ADH release is stimulated by a lower osmolality
than would be expected in a normal patient. Seen in pregnancy and chronic
malnutrition.
Hypothyroidism. Mechanism is not completely understood. Possibly due to reduced
cardiac output or SIADH.
• Increased exogenous ADH (usually euvolemic)
– Desmopressin or vasopressin use
– Oxytocin infusion during the induction of labor or postpartum
• Appropriately suppressed ADH (usually euvolemic but may be hypervolemic)
– Insufficient solute to excrete excess free water. In beer drinker’s potomania, excessive
hypotonic fluid intake results in an overwhelmed capacity to excrete free water.
– Intake of hypotonic fluids
– Polydipsia
– Excessive hypotonic IV fluids
– Absorption of glycine or sorbitol solutions during hysteroscopy or trans-urethral resection
of the prostate (TURP) (may be associated with normal or elevated osmolality)
Hyperosmolar hyponatremia. May be referred to as redistributive hyponatremia because
water shifts from the intracellular to the extracellular compartment with a resultant dilution
of sodium. The total body water and total body sodium are unchanged.
• Mannitol. This effect is sometimes harnessed during increased intracranial pressure to
decrease cerebral volume. Similarly, for neurosurgical cases, mannitol may be administered
prior to opening the dura to decrease brain volume and protrusion.
• Hyperglycemia
• Maltose (IVIg)
• Pseudohyponatremia. The plasma is diluted by excessive proteins or lipids. The total body
water and total body sodium are unchanged.
– Hyperproteinemia
– Hyperlipidemia
• Antidiuretic hormone (ADH). Excessive exogenous or endogenous ADH prevents the
excretion of maximally dilute urine.
– ADH results in free water absorption as water moves passively down its concentration
gradient from the tubules to the hypertonic medullary interstitium via aquaporin-2
channels in the medullary collecting ducts.
– Endogenous ADH release from the posterior pituitary gland is normally stimulated by an
increase in serum osmolality thereby maintaining normal serum osmolality between 280
and 300 mOsm/kg. Sodium, along with its anion (mostly chloride or bicarbonate) account
for the vast majority of serum osmoles.
– ADH release may be enhanced despite a low serum osmolality in the following situations
(described above under etiology):
Decreased intravascular volume (in an attempt to maintain serum volume)
Decreased effective circulating fluid volume
SIADH and reset osmostat
– Exogenous ADH acts in the same way as endogenous ADH with resultant free water
absorption and hyponatremia.
– In polydipsia and beer drinker’s potomania, patients excrete maximally dilute urine;
however, their excessive intake of hypotonic fluid overwhelms the renal diluting capacity
resulting in hyponatremia.
• Neurological effects
– Hyponatremia increases free water movement into the intracellular space and cellular
edema. Because of the fixed space of the cranium, symptoms manifest from increased
intracranial volume and can result in herniation and death. When chronic, the cells are
able to compensate by moving solutes out and into the extracellular space (water moves
extracellularly as well); this decreases the pathological effects.
DIAGNOSIS
• The history and physical exam should be focused on searching for the underlying cause,
assessing volume status, and determining if the derangement is acute (present <48 hours)
or chronic (present >48 hours or if uncertain of time onset) causes
• History
– Fluid loss from diarrhea, burns, vomiting
– Cardiac, renal, and hepatic disorders
– Medications (desmopressin, thiazide diuretics, oxytocin, carbamazepine, SSRIs)
– IV fluids
– Surgical history
• Symptoms
– Mild and chronic cases are often asymptomatic
– Acute or more severe cases may have nausea, malaise, lethargy, headache, or seizures
• Signs/physical exam
– May have altered mental status or be obtunded
– Assessment of intravascular volume status: Jugular venous pressure, capillary refill,
edema, dry mucous membranes, hypotension, and tachycardia
• Laboratory investigations: Serum osmolality, urine osmolality, urine sodium
• Additional studies such as creatinine, urea, liver function panel, cortisol, and TSH can
further aid with the diagnosis.
• Measurement of serum osmolality and serum glucose will rule out hyperosmolar
hyponatremia.
– Hyperglycemia: Na+ is decreased by 1.6 mEq/L for every 100 mg that glucose exceeds
100 mg. True [Na+] = [Na+] + [1.6 (glucose−100)/100]
• Clinical exam to assess the volume status is important in differentiating between
hypervolemic, euvolemic, and hypovolemic hyponatremia.
• Patients with intravascular volume depletion and decreased effective circulating fluid
volume tend to avidly retain sodium and therefore have a low urine [Na+].
– Urine [Na+] is typically <20 mEq/L
– Fractional excretion of sodium (FENa) is a more accurate way to determine sodium
excretion.
– FENa = ([Na+]urine × Crplasma)/([Na+]plasma × Crurine) × 100; a FENa <1–2% is
consistent with avid sodium retention.
– An exception is when renal sodium loss leads to volume contraction (e.g., diuretics and
cerebral salt wasting).
[Na+]urine and FENa are usually >20 mEq/L and >2%, respectively.
In these circumstances, a FEurea <30% suggests avid renal reabsorption
– Because of high levels of ADH, urine osmolality will be high (>400 mOsm/L).
• Patients with hyponatremia from SIADH or exogenous ADH do not avidly retain sodium.
Typically, [Na+]urine is >20 mEq/L and FENa >2%.
– Urine osmolality is inappropriately high (exact value depends on degree of excess ADH
secretion/administration).
• Polydipsia and beer drinker’s potomania present with maximally dilute urine (<100
mOsm/L).
– These patients do not avidly retain sodium.
– FENa is typically >2% but [Na+]urine may be low due to high urine volumes.
TREATMENT
• Identify and manage acute symptomatic hyponatremia before proceeding with the
operation. In addition, when specific causes can be identified they should be treated
accordingly:
– Intravascular depletion from GI or renal losses, as well as insensible and third spacing,
should be repleted.
– Congestive heart failure: Volume overload should be treated with diuresis and/or
optimization of cardiac function (may require inotropic agents). Sodium and water
restriction are imperative.
– Volume overload states such as cirrhosis should be managed with water and sodium
restriction, diuresis, and treatment of underlying disorder.
– SIADH is managed with water restriction and management of the underlying disorder (see
SIADH chapter). Other possible therapies include demeclocycline or vasopressin
antagonists.
– Polydipsia is managed with water restriction
• Sodium correction. Prevent excessive rises in [Na+] in patients with documented chronic
hyponatremia (>48 hours).
– Maximum rate of change <0.5 mmol/L/hour (<10 mmol/L in 24 hours, <18 mmol/L in
48 hours)
– Rapid increases in [Na+] in chronic hyponatremia can lead to osmotic demyelination.
• Avoid intraoperative exacerbation of hyponatremia. Worsening hyponatremia may lead to
cerebral edema, seizures, and possibly death.
FOLLOW-UP
• Repeat serum electrolytes

• Consider medicine or nephrology consultation
REFERENCES
1. Bagshaw SM, Townsend DR, Mcdermid RC. Disorders of sodium and water balance in
hospitalized patients. Can J Anesth. 2009;56:151–167.
2. Wald R, Jaber BL, Price LL, et al. Impact of hospital-associated hyponatremia on selected
outcomes. Arch Intern Med. 2010;170(3):294–302.
3. Sterns R, Cappuccio J, Silver S, et al. Neurologic sequelae after treatment of severe
hyponatremia: A multicenter perspective. J Am Soc Nephrol. 1994;4:1522–1530.
4. Adrogué, HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581–1589.
• TURP syndrome
• Hypernatremia
• Urine osmolality
• Plasma osmolarity
• Hypothyroidism
• Syndrome of inappropriate antidiuretic hormone (SIADH)
CODES
ICD9
276.1 Hyposmolality and/or hyponatremia
ICD10
E87.1 Hypo-osmolality and hyponatremia
CLINICAL PEARLS
• Hyponatremia should not be ignored.
• To proceed or delay? Elective surgeries should be delayed for a [Na+] <130 mmol/L in
order to complete a full workup and begin treatment. Proceeding with urgent or emergent
surgeries must be done with caution while weighing the risk–benefit ratio of delay.
• Perioperatively, worsening of hyponatremia or a rapid rise of serum [Na+] in chronic
hyponatremia should be avoided.
HYPOTHERMIA
BASICS
DESCRIPTION
• Hypothermia refers to a subnormal core temperature (<37°C) and can be divided into three
subcategories:
– Mild hypothermia: 32–35°C
– Medium hypothermia: 28–32°C
– Severe hypothermia: <28°C
• Perioperative hypothermia occurs in three phases:
– An initial decrease in core temperature of 1–1.5°C in the first hour of anesthesia
– Slower linear decrease in heat due to heat loss outpacing metabolic heat production
– After 3–5 hours of anesthesia, a thermal plateau of core temperature
EPIDEMIOLOGY
Incidence
• Nearly all patients undergoing general anesthesia become mildly hypothermic (1–3°C
reduction in core body temperature).
– Varies between centers; reported to be as high as 70% (1)[B]
• Hypothermia is often undetected during spinal and epidural anesthesia due to reduced
monitoring of core temperature and inability of patients to feel cold.
Morbidity
• Mild hypothermia has been shown to increase blood loss by ∼16% and relative risk for
transfusion by 22% (2)[A].
• Mild hypothermia is associated with
– Myocardial ischemia (can be therapeutic in cardiopulmonary bypass), arrhythmias.
– Surgical wound infection
– Prolonged recovery from anesthesia
Mortality
No specific data available; cause of death is difficult to differentiate between hypothermia
related complications and preexisting comorbidities.
• Body morphology. Insulating properties of fat reduce core-to-peripheral temperature
gradient. Risk of hypothermia is inversely proportional to patient body fat percentage.
• Age extremes
– Infants and young children have a high surface area to mass ratio, allowing intraoperative
heat loss to easily exceed metabolic heat production.
– Geriatric patients have a lower metabolic rate, thus produce less metabolic heat.
• Size of incision
• Severe trauma (including burns)
• Chronic illness decreases metabolic heat production (e.g., cardiovascular disease).
• All general anesthetics cause a loss in core body temperature, mostly from reducing
thermoregulatory controls and promoting vasodilation.
• Heat loss can result from:
– Radiation. Describes the transfer of heat from one surface to another by emission of
photons. Heat from the patient radiates into the cool operating room air and accounts for
~90% of heat loss.
– Convection. Describes the carrying of heat from the core to the periphery.
Second largest contributor to heat loss (after radiation)
Dependent on peripheral blood flow and core-to-peripheral temperature difference
– Conduction. Adjacent tissue-to-tissue transfer of heat.
Slow
Dependent on tissue characteristics (insulation properties of tissue, diffusion coefficient)
and differences in surface temperatures.
– Evaporation. Derived from heat of vaporization of water (0.58 kcal/g)
Respiratory evaporative losses are small, usually <10% of basal metabolic rate.
Substantial heat loss occurs from evaporation through the surgical incision.
Skin-prep (especially alcohol-based) solutions contribute to evaporation heat loss (–0.2
to –0.7°C/m2 depending on solution).
– Cold intravenous fluids. The body warms cold fluids via conduction from blood and
tissues. IV fluid at room temperature decreases mean body temperature ∼0.25°C per liter.
– Irrigation. Irrigation fluid can reduce core body temperature by carrying heat way from
core organs (via conduction).
• Neurologic effects
– Cerebral metabolic rate of oxygen (CMRO2) decreases by 6–7% for every 1° decrease in
temperature.
– Delayed awakening from anesthesia
• Cardiac effects of hypothermia
– Heart rate and cardiac output gradually decrease
– Hypotension (particularly in severe hypothermia)
– Atrial and ventricular arrhythmias increase. Atrial fibrillation can occur secondary to
atrial distention. Ventricular fibrillation is an immediate hazard at core temperatures
<28°C.
– Prolonged asystole (most commonly occurs at core temperatures below 32°C)
– J-waves (Osborn waves), positive deflections at the end of the QRS complex, appear on
ECG (typically below 30°C). Clinically insignificant and disappear on rewarming.
– During cardiopulmonary bypass, hypothermia is utilized to decrease the myocardial
metabolic rate (decreases oxygen consumption during periods of decreased oxygen
supply). The perfusion pump is utilized to rapidly cool (and rewarm) the patient; it dwarfs
all other sources of heat transfer (e.g., radiation, convection). Afterdrop is a term used to
describe a rapid decrease in core temperature that can occur after discontinuation of
bypass. It is caused by a large core-to-peripheral temperature gradient and from
insufficient rewarming of peripheral tissues.
• Pulmonary effects of hypothermia
– Pulmonary vascular resistance (PVR) increases.
– Significant respiratory depression can occur with severe hypothermia.
– Reduced cough reflex and cold-induced bronchorrhea can lead to aspiration and difficulty
clearing secretions.
• Hepatic effects of hypothermia
– Enzyme activity (e.g., conjugation, detoxification) can decrease with a resultant decrease
in drug metabolism.
– Decreased synthesis of coagulation factors (in addition factors are also sensitive to
decreases in temperature).
• Hematologic effects of hypothermia
– Leukocyte and platelet counts commonly decrease secondary to splenic, hepatic, and
intravascular sequestration; this effect reverses with rewarming
– Hematocrit levels can increase secondary to volume contraction that results from osmotic
diuresis. Consequently, viscosity increases when temperatures drop below 27°C
• Metabolic effects
– Basal metabolic rate decreases 5–7% per 1°C; at 28°C it is decreased by 50%.
– Renal function decreases; a “cold diuresis" occurs secondary to depressed oxidative tubular
activity resulting in reduced sodium and water reabsorption.
– Insulin release as well as glucose uptake into cells are impaired, resulting in
hyperglycemia. This effect is reversed with rewarming.
• Therapeutic hypothermia
– Indicated for neuroprotection in procedures likely to cause cerebral ischemia (e.g.,
cardiopulmonary bypass, neurosurgery). Outcome studies have demonstrated increased
cerebral performance scores and greater survival after discharge, with no significant
difference in adverse events between hypo- and normothermic groups.
– Evidence indicates beneficial effect to inducing mild hypothermia within hours of
restoring circulation following cardiac arrest (3)[A].
– No significant benefit has been shown from the use of mild hypothermia in the treatment
of traumatic head injury (4)[A], stroke (5)[A], or in coronary artery bypass surgery (6)
[A].
• Preoperative (on ward, before premedication)
– Keep patient comfortably warm. Actively warm patient if hypothermic.
• Prior to induction
– Measure oral temperature, ask about thermal comfort level.
– Prewarm all patients for 20 minutes (forced air) to reduce the core-to-periphery
temperature gradient.
– Limit skin exposure.
– When possible, start anesthesia only when patient is normothermic.
DIAGNOSIS
• Oral measurements are adequate but typically 0.2–0.3°C below actual core temperature.
• Core temperature measurements through a Foley catheter can be inaccurate in cases of high
urine output.
• Core temperature <35°C.
– Gold standard is pulmonary artery measurement.
– Nasopharyngeal, urinary bladder (via Foley catheter), and esophageal measurements are
adequate, less invasive alternatives.
– Rectal temperature is acceptable in pediatrics, but measurements lag behind core
temperature readings in adults (1)[B].
TREATMENT
• There is currently no evidence-based gold standard for treating accidental hypothermia.

Intraoperative measures may include
– Measure patient temperature continuously
– Limit skin exposure. A single layer of cutaneous insulation (cotton blanket) can reduce
heat loss by 30% (1)[B].
– Active warming with a forced-air warming device can decrease heat loss from radiation as
well as rewarm the patient. Its use may not be feasible in trauma cases or where the skin
needs to be exposed.
– Warm intravenous fluids when administered at a rate >1 L/hour
– Warm irrigation fluids
– Operating room temperature ≥21°C
In anesthetized neonates, risk of hypothermia was roughly doubled when OR
temperature <23°C.
FOLLOW-UP
• Measure patient oral temperature in PACU every 15 minutes.

• Continue active warming until the patient is normothermic.
• Shivering. Can result in increased myocardial oxygen consumption up to 200–300%. For
shivering, meperidine 25 mg IV or clonidine 75 μg IV may be utilized (1)[B].
CLOSED CLAIMS DATA
• 54/3,000 total anesthesia claims secondary to burns.
• 64% of burns were due to IV fluid bags or bottles warmed in an oven prior to applying to
patient’s skin.
• 0 claims attributed to injuries due to forced-air warming (7).
REFERENCES
1. Torossian A. Thermal management during anaesthesia and thermoregulation standards for
the prevention of inadvertent perioperative hypothermia. Best Pract Res Clin Anaesthesiol.
2008;22(3):659–668.
2. Rajagopalan S, Mascha E, Na J, et al. The effects of mild perioperative hypothermia on
blood loss and transfusion requirement. Anesthesiology. 2008;108:71–77.
3. Arrich J, Holzer M, Herkner H, et al. Hypothermia for neuroprotection in adults after
cardiopulmonary resuscitation. Cochrane Database Syst Rev. 2010;8.
4. ydenham E, Roberts I, Alderson P. Hypothermia for traumatic head injury. Cochrane
Database Syst Rev. 2009;4:CD001048.
5. en Hertog HM, van der Worp HB, Tseng MC, et al. Cooling therapy for acute stroke.
6. ees K, Beranek-Stanley M, Burke M, et al. Hypothermia to reduce neurological damage
following coronary artery bypass surgery. Cochrane Database Syst Rev. 2009;1.
7. Cheney FW, Posner KL, Caplan RA, et al. Burns from warming devices in anesthesia.
ADDITIONAL READING
• Kelly FE, Nolan JP. The effects of mild induced hypothermia on the myocardium: A
systematic review. Anaesthesia. 2010;65:505–515.
• Rueler JB. Hypothermia: Pathophysiology, clinical settings, and management. Ann Intern
Med. 1978;89:519–527.
• Sessler DI. Mild perioperative hypothermia. N Engl J Med. 1997;336(24):1730–1737.
• Sessler DI. Perioperative heat balance. Anesthesiology. 2000;92:578–596.
CODES
ICD9
991.6 Hypothermia
ICD10
• T88.51XA Hypothermia following anesthesia, initial encounter
• T88.51XD Hypothermia following anesthesia, subsequent encounter
• T88.51XS Hypothermia following anesthesia, sequela
CLINICAL PEARLS
• The majority of heat loss in patients is due to a core-to-peripheral temperature gradient and
cutaneous radiation.
• Nearly all patients under general anesthesia undergo mild hypothermia. Those under
neuraxial anesthesia (spinal, epidural) are also at risk
• Mild hypothermia is associated with increased bleeding, greater susceptibility to infection,
and morbid cardiac events.
• Deep hypothermic circulatory arrest (DHCA) may be used concurrently with
cardiopulmonary bypass in complex cardiac and proximal thoracic aortic procedures. DHCA
is thought to increase ischemic tolerance and protect against injury to the CNS, viscera, and
kidneys.
HYPOTHYROIDISM
Joe C. Hong, MD
BASICS
DESCRIPTION
Hypothyroidism is a clinical state resulting from decreased circulating levels of the thyroid
hormones thyroxine (T4) and triiodothyronine (T3) or from peripheral hormone resistance.
EPIDEMIOLOGY
Incidence
• ∼4:1,000 women per year.
• ∼0.6:1,000 men per year.
Prevalence
• 1.9% of the female US population.
• 0.1% of the male US population.
• 6.9%–7.3% of patients age 55 or over.
• Women are 10 times more likely to be hypothyroid compared to men (1).
Morbidity
• Patients with hypothyroidism are at increased risk for atherosclerotic heart disease due to
increased incidence of hypercholesterolemia.
• Increased incidence of dementia and depression
Mortality
• Severe hypothyroidism may lead to coma and death if untreated.
• Increased incidence of suicide
• Female sex
• Elderly
• Positive family history
• History of autoimmune disorders
• History of treatment with radioactive iodine or antithyroid medications such as
propylthiouracil (PTU) or methimazole
• History of radiation to the neck
• History of thyroid surgery
PATHOPHYSIOLOGY
• Thyroid hormone functions in several capacities, including normal heart, liver, kidney, and
skeletal muscle metabolism, as well as cell differentiation and growth.
• T4 and T3 are produced by follicular cells in the thyroid gland in a classic negative feedback
system. Thyroid-releasing hormone (TRH; from the hypothalamus) stimulates the release of
thyroid-stimulating hormone (TSH; from the anterior pituitary), which in turn stimulates T3
and T4 release (from the thyroid gland). T3 and T4 inhibit synthesis and release of TRH and
TSH, via a feedback loop. Additionally, high levels of iodide ion can inhibit T4 synthesis
and release.
• Hormone synthesis involves iodide uptake into the gland, iodination of thyroglobulin,
coupling of iodotyrosines to form T4 and T3. T4 and T3 are released from the thyroid gland
into the bloodstream (20:1 ratio).
• When T4 enters target cells, it is converted to T3 (more potent). Both T4 and T3 bind to
thyroid receptor proteins within the cell nucleus and activate DNA transcription and
increase the rate of RNA synthesis, which ultimately affects protein synthesis.
• Hypothyroidism manifests as the lack of physiologic activities of T3 and T4. Primary
hypothyroidism (95% of cases) is defined by the inability of the thyroid gland to produce
thyroid hormones, while secondary hypothyroidism is defined as a functional thyroid gland
that is deprived of TSH (2).
• Determine the severity and tailor an anesthetic plan to the concomitant organ dysfunction.
• Mild or well controlled hypothyroidism likely poses no increased surgical risk.
SYMPTOMS
• General: Lethargy, decreased vigor, cold intolerance, diminished food intake, and weight
gain.
• Neurologic: Slow thinking.
• Integument: Dry skin, thickened hair, hair loss, broken nails.
• Gastrointestinal (GI): Constipation.
• Gynecologic: Menorrhagia, diminished libido.
History
• Focus on the multiple systems affected by the lack of physiologic activity of T3 and T4.
• Symptoms are insidious in onset and easily overlooked despite multisystem involvement.
• In patients with a history of Hashimoto’s thyroiditis, a careful review of associated
autoimmune diseases such as lupus erythematosus, rheumatoid arthritis, primary adrenal
insufficiency, and Sjögren’s syndrome is necessary.
Signs/Physical Exam
• Neurologic: Slow speech, mental slowing, depression.
• HEENT: Round puffy face, periorbital edema, hoarseness.
• Integument: Cold/thick/dry/scaling skin, dry/coarse/brittle hair, dry and longitudinally
ridged nails.
• Cardiovascular: Bradycardia, decreased stroke volume, narrow pulse pressure, cardiac
enlargement, pericardial effusion.
• GI: Ascites.
• Extremities: Ankle edema.
• In severe hypothyroidism or myxedema, there can be impaired mentation, coma, enlarged
tongue, decreased upper airway tissue tone, hypoventilation, CHF, hypothermia, and
hyponatremia secondary to SIADH.
MEDICATIONS
• Replacement therapy is typically with synthetic T4 (levothyroxine) which may take up to 2
weeks before symptomatic improvement is seen.
• Synthetic T3, which is the biologically active form of thyroid hormone, can be used to attain
a more acute response.
Labs/Studies
• Increased TSH for primary hypothyroidism; decreased TSH for secondary hypothyroidism.
• Decreased thyroid hormones T3 and T4.
• Decreased radioiodine uptake by the thyroid gland.
• Macrocytic anemia.
• Elevated serum cholesterol and CK level.
• Hypoglycemia, hyponatremia.
• Low voltage EKG.
• Degree of organ dysfunction is concomitant with the severity of hypothyroidism.
• Cardiac involvement includes pericardial effusion, QT prolongation, T-wave inversion, and
CHF; also, decreased cardiac output (stroke volume and heart rate), pulse pressure, and
blood volume hinders the heart’s ability to respond to circulatory stress.
• Pulmonary involvement includes decreased respiratory drive in response to hypoxemia and
hypercarbia, decreased maximal breathing capacity, and decreased diffusion capacity for
carbon monoxide.
• CNS involvement includes increased sensitivity to sedative medications and decreased level
of consciousness progressing to coma.
• Patients with signs and symptoms of severe hypothyroidism or myxedema should have
elective surgery postponed until after adequate replacement therapy.
• Patients with severe hypothyroidism or myxedema requiring emergent surgery require
immediate hormone replacement with T3, stress dose steroids, and intensive monitoring of
their response to therapy.
• In patients with coronary artery disease, care must be taken during thyroid replacement
therapy. Several studies have shown that replacement therapy may exacerbate angina and
even induce myocardial infarction.
• Most experts believe mild hypothyroidism poses no increased surgical risk (3).
TREATMENT
Premedications
• Carefully titrate sedatives and analgesics because hypothyroid patients may be more
sensitive to these medications.
• Aspiration prophylaxis should be considered because severe hypothyroidism or myxedema
may have a significant delay in gastric emptying.
INTRAOPERATIVE CARE
• General endotracheal anesthesia is indicated for thyroidectomy.
• Anesthesia technique for nonthyroid surgery should be dictated by the type of surgery,
planned position, as well as surgeon/anaesthetist preference.
• Patients with severe hypothyroidism or myxedema should be intubated and have their
ventilation controlled due to decreased respiratory response to hypoxemia and hypercarbia.
Monitors
• Invasive monitoring as dictated by the type of surgery, patient comorbidities, and severity of
hypothyroidism.
• Patients with severe hypothyroidism or myxedema are particularly susceptible to CHF.
Pulmonary artery catheter, peripheral arterial catheter, and transesophageal
echocardiography may be helpful to guide ionotropic support and fluid management.
• EMG endotracheal tube per surgeon request for thyroid surgery.
• Large goiter can cause tracheal deviation, compression, and tracheomalacia. In addition, the
frequently associated findings of obesity, large tongue, and decreased upper airway tone
among hypothyroid patients can make airway management difficult. Awake fiberoptic
intubation should be considered, if there is a high suspicion for airway compromise.
• Ketamine may be the induction agent of choice in patients with severe hypothyroidism or
myxedema due to its inotropism and ability to maintain sympathetic tone.
• Rapid or modified rapid sequence induction may be warranted in patients with significant
delay in gastric emptying.
Maintenance
• Mixed technique of a volatile agent, nitrous oxide, and short-acting opioid may be the
technique of choice. The presence of nitrous oxide and opioid will allow for a lower
concentration of the volatile agent, resulting in less cardiac depression and vasodilation.
• Controlled ventilation is necessary in patients with severe hypothyroidism or myxedema due
to impaired ventilatory response to hypercarbia and hypoxemia.
• Minimum alveolar concentration is unchanged in patients with hypothyroidism (4).
• Warming blanket and warm IV fluids should be used to minimize risk of hypothermia.
• For thyroidectomies, coughing/bucking on emergence should be minimized to decrease the
likelihood of neck hematoma formation. Preintubation tracheal lidocaine can provide
airway analgesia.
• Because of increased sensitivity to sedatives and analgesics, the use of non-narcotic
analgesics may help prevent delayed emergence.
• Complications:
– Delayed emergence due to increased sensitivity to sedatives and analgesics.
– Hypothermia.
– Postoperative dependence on mechanical ventilation.
– Thyroidectomy: Airway compromise such as hematoma, airway edema, tracheomalacia,
and bilateral recurrent laryngeal nerve injury. Massive bleeding and stroke may occur
when injury to the nearby carotid artery occurs. Carotid sinus irritation may lead to
hemodynamic fluctuations and bradyarrhythmias. Respiratory compromise from an occult
pneumothorax may result from lower neck surgical dissection.
POSTOPERATIVE CARE
BED ACUITY
Patients with severe hypothyroidism or myxedema should be monitored in the ICU
postoperatively.
COMPLICATIONS
For thyroid surgery, postoperative respiratory distress may be the result of a neck hematoma
or hypocalcemia causing laryngospasm and decreased upper airway tone. The latter may be
difficult to differentiate in the myxedematous patient that has decreased upper airway tone.
REFERENCES
1. Singer PA, et al.Treatment guidelines for patients with hyperthyroidism and
hypothyroidism. Standards of care committee, American thyroidassociation.
JAMA.1995;273:808.
2. anderpump MP, et al. The epidemiology of thyroid disorders in the community: A twenty-
year follow-up of the Whickham Survey. Clin Endocrinol. 1995;43:55.
3. arling PA. Thyroid disease. Br J Anaesth. 2000;85:15.
4. einberg AD, et al. Outcome of anesthesia and surgery in hypothyroid patients. Arch Intern
Med. 1983;143:893.
ADDITIONAL READING
• Graham GW, et al. Perioperative management of selected endocrine disorders. Int
Anesthesiol Clin. 2000;38:31.
• Kohl BA, Schwartz S. How to manage perioperative endocrine insufficiency. Anesthesiol
Clin. 2010;28:139.
• Thyroidectomy
• Hyperthyroidism
CODES
ICD9
244.9 Unspecified acquired hypothyroidism
ICD10
E03.9 Hypothyroidism, unspecified
CLINICAL PEARLS
• The overriding goal of management is determining the severity of the hypothyroidism and
designing an anesthetic plan tailored to the concomitant organ dysfunction.
• In patients with history of Hashimoto’s thyroiditis, a careful review of associated
autoimmune diseases is necessary.
• Most experts believe mild hypothyroidism poses no increased surgical risk and patients may
be able to proceed for surgery.
• Patients with severe hypothyroidism or myxedema must be medically optimized prior to
surgery. Replacement therapy with T4 or more acutely with T3 should be undertaken with
monitoring of symptomatic improvement.
• Careful airway management and possible awake fiberoptic intubation may be indicated in
patients with large goiter, large tongue, and/or decreased airway tone.
• Severely hypothyroid and myxedematous patients should have appropriate invasive
monitoring, induction with ketamine, and airway intubation with controlled ventilation.
Careful titration of short-acting opioid analgesics or the use of nonopioid analgesics may
help in minimizing the risk of delayed emergence.
HYPOXIA, INTRAOPERATIVELY
Suzanne Strom, MD
BASICS
DESCRIPTION
Intraoperative hypoxia is defined as arterial oxygen tension (PaO2) <60 mm Hg, which
correlates to a blood oxygen saturation (SpO2) <90%.
EPIDEMIOLOGY
Incidence
Transient intraoperative hypoxia has been shown to occur in 7% of patients who receive an
anesthetic for surgery.
Prevalence
• Hypoxia can occur during all stages of the anesthetic, particularly during induction and
emergence.
• It occurs most frequently in patients with American Society of Anesthesiology (ASA)
physical status classification III and IV.
Morbidity
Hypoxic brain injury, myocardial ischemia, stroke, renal injury
• Decreased fraction of inspired oxygen (FiO2) results from a failure to provide adequate
inspired O2. It can result from
– Pipeline O2 supply failure, empty tank, hypoxic gas mixture
– Higher altitude
• Inadequate alveolar ventilation or alveolar hypoventilation. The alveolar gas equation is as
follows: FA = [(Pbarometric – PH20)(FiO2)] –(PaCO2/0.8); increases in carbon dioxide in the
alveoli will decrease the FAO2 and, hence, PaO2.
– CNS depression. Respiratory depression from drugs, structural, or ischemic lesions
– Circuit or machine disconnection
– Obstruction. Upper airway, mucous plug, endotracheal tube (ETT) kink, herniated ETT
cuff
– Inadequate ventilator settings/parameters
• Venous admixture. Under normal conditions, there is a fixed physiologic shunt (∼5%) from
pleurohilar veins, bronchial veins, and Thebesian circulation.
• V/Q mismatch
– Dead space: Pulmonary embolism, profound hypotension, cardiac arrest
– Shunt: Bronchospasm, asthma, pneumonia, endobronchial intubation, pulmonary edema,
aspiration, inhibition of hypoxic pulmonary vasoconstriction (HPV), pneumothorax,
pleural effusion, hemothorax, acute lung injury (ALI), acute respiratory distress syndrome
(ARDS)
• Right-to-left anatomic shunts
– Atrial septal defects
– Ventricular septal defects
• Diffusion defects. Diffusion capacity depends on the thickness of the alveolar wall, the area
available for gas exchange, and the partial pressure difference of gas between the two sides.
– Thickened wall. Pulmonary fibrosis (chronic) or pulmonary edema (acute)
– Decreased equilibration time secondary to tachycardia
• Excessive metabolic O2 demand such as hyperthermia, hyperthyroidism, shivering, and
malignant hyperthermia (result in a decreased mixed venous oxygen saturation).
• Impaired tissue oxygen delivery/perfusion
– Myocardial infarction
– Congestive heart failure
– Shock
– Arrhythmias
– Cardiac tamponade
– Sepsis
– Arteriovenous malformation
• Aerobic metabolism. Each molecule of glucose can generate 36 ATP under normal cellular
metabolism and oxidative phosphorylation.
– C6H12O6 + 6O2 → 6CO2 + 6H2O + Energy
– The energy created is stored in the third phosphate bond on adenosine triphosphate
(ATP). ATP is utilized for muscle contraction, ion pumps, cellular secretion, and protein
synthesis: Energy + ADP + Phosphate → ATP
– ATP cannot be stored and must be continually formed requiring a constant supply of
substrates and O2.
• Anaerobic metabolism. When O2 is not available, anaerobic metabolism occurs in order to
manufacture ATP; however, it is inefficient (one glucose molecule yields 2 ATP) and
produces lactic acid. Progressive lactic acidosis impairs enzymatic function and ion
concentration gradients.
• Hypoxia is sensed in the carotid bodies (at the bifurcation of the common carotid arteries)
and the aortic bodies (surrounding the aortic arch). These peripheral sensors interact with
central respiratory centers via the glossopharyngeal nerves to produce reflex increases in
alveolar ventilation. Hypoxia receptor activity does not appreciably increase until the PaO2
decreases below 50 mm Hg, at which point the SpO2 is 80%.
• Compensatory mechanisms. When there is an imbalance of O2 supply to demand, the body
mobilizes its compensatory mechanisms to ensure adequate availability (e.g., increased O2
extraction and cardiac output).
• Signs of hypoxia. Early signs are the result of sympathetic system activation and include
tachycardia, hypertension, and an increased cardiac output. Late signs include myocardial
dysrhythmias, bradycardia, hypotension, and cardiac arrest.
• Deliver adequate supplemental FiO2
• Carefully monitor for signs of hypoventilation
DIAGNOSIS
• Verify all low SpO2 measurements.
– Ensure that the SpO2 rate correlates with the EKG tracing
– Verify accurate waveform
– Move pulse oximetry probe to different fingers, or an earlobe, nostril, or nasal ala.
• Check in-line FiO2 measurements.
• Assess for adequate ventilation
– If the patients is not intubated, listen for stridor, snoring, lack of air movement.
– If intubated, hand ventilate to assess pulmonary compliance and expand collapsed lung
segments.
Increased compliance: Consider cuff leak or deflation, supraglottic cuff, circuit leak
Decreased compliance: Consider bronchospasm, pneumothorax, mainstem intubation,
pulmonary edema; biting, secretions, or kinking of the ETT
– Auscultate the lungs to assess for
Bilateral breath sounds; rules out mainstem intubation, pneumothorax.
Wheezing; rules out bronchospasm, aspiration, pulmonary embolism
Crackles or rales; rules out pulmonary edema
– Check end-tidal CO2 (EtCO2) to verify intubation and evaluate capnograph pattern for
abnormalities such as obstruction.
• Portable chest x-ray should be obtained to ascertain atelectasis, infiltrates, or pneumothorax.
• Measure the arterial blood gas to evaluate the PaO2. The SpO2 is a non-invasive monitor
that may not accurately reflect the PaO2 in the setting of: Hypothermia, poor circulation,
electrocautery, motion, ambient lighting, carbon monoxide poisoning, methylene blue
administration, and cyanide poisoning. Additionally, PaO2 values can be utilized to
calculate the Alveolar to arterial gradient/ratio.
• Evaluating the Alveolar to arterial (A-a) gradient may help determine the cause.
Alternatively the a/A ratio can be utilized when increased FiO2 is being implemented.
• Oxygen administration may help differentiate between hypoventilation and V/Q mismatch.
In patients with:
– Low FiO2, hypoventilation, and V/Q mismatching, increasing the FiO2 will increase the
oxygen saturation.
– Large shunts (>25% of total cardiac output), the blood flow that returns from
unventilated alveoli or right-to-left anatomic shunts will be unchanged; it is not exposed
to the increased oxygen fraction.
TREATMENT
• Increase delivered FiO2 to 100% while evaluating reversible causes

• Atelectasis is the most common cause; recruitment maneuvers can be very effective:
– Increase tidal volumes (Vt) to 10–12 mL/kg
– Add positive end-expiratory pressure (PEEP)
– Recruitment maneuvers
– Alternatively, some patients with hypoxia have ALI or ARDS and management is based on
a lung protective ventilation strategy (LPVS) that minimize additional ventilator-
associated lung injury using lower Vt.
• Secretions: Suction the ETT, consider bronchoscopy
• Biting: Place a bite block, deepen anesthetic, administer neuromuscular blocking drugs.
• Bronchospasm: Administer aerosolized bronchodilators, deepen the anesthetic with volatile
agents or propofol
• Hypoventilation: Adjust minute ventilation. In patients that are not intubated, alleviate
possible upper airway obstruction (chin life, jaw thrust, oronasopharyngeal airway
insertion, suction oropharynx, apply positive pressure ventilation with a mask, or consider
LMA/ETT insertion).
• Pneumothorax: Needle decompression if hemodynamically unstable; if time permits, a chest
tube should be inserted
• Diffusion problems: If pulmonary edema, increase the surface area for diffusion by
increasing the transalveolar pressure (administration of continuous positive airway pressure
[CPAP] if not intubated, PEEP if intubated).
• Machine issue: If suspected, immediately convert to an Ambu bag while searching for the
cause (disconnect, internal issue); do not let the patient deteriorate while searching for the
cause
• Maintain adequate cardiac output and hemoglobin levels
• If hypoxia does not resolve with appropriate interventions, terminate surgery as soon as
possible
FOLLOW-UP
CLOSED CLAIMS DATA

• In the 1986 Closed Claims review, adverse outcomes associated with respiratory events
constitute the single largest class of injury (522 of 1,541 cases; 34%). Death or brain
damage occurred in 85% of cases. Most outcomes (72%) were considered preventable with
better monitoring. Inadequate ventilation (196; 38%) was one of the three mechanisms of
injury and accounted for 75% of the adverse respiratory events.
• In the 2000 review, which looked at the period of time after widespread introduction of
pulse oximetry and EtCO2 monitoring, the adverse outcomes associated with respiratory
events decreased significantly.
REFERENCES
1. Blum JM, Fetterman DM, Park PK, et al. A description of intraoperative ventilator
management and ventilation strategies in hypoxic patients. Anesth Anal.
2010;110(6):1616–1622.
2. are G, Kavanagh B. Hypoxemia during surgery: Learning from history, science, and current
practice. Can J Anesth/J Can Anesth. 2010;57:877–881.
3. Pedersen T, Moller AM, Hoyannisyan K. Pulse oximetry for perioperative monitoring.
• Ehrenfeld JM, Funk LM, Van Schalkwyk J, et al. The incidence of hypoxemia during surgery:
Evidence from two institutions. Can J Anesth. 2010;57.
• Hypoxia, postoperatively
• Carotid body
• Dead space
• Anaerobic metabolism
• Alveolar-arterial gradient and ratio
• Pneumothorax
CODES
ICD9
• 799.02 Hypoxemia
• 998.9 Unspecified complication of procedure, not elsewhere classified
ICD10
• R09.02 Hypoxemia
• T81.89XA Oth complications of procedures, NEC, init
CLINICAL PEARLS
• Always assume a low SpO2 is accurate until proven otherwise.
• Atelectasis is the most common cause of intraoperative hypoxia. Recruitment maneuvers
may need to be done regularly in intubated patients with decreased functional residual
capacity (FRC) such as obesity, pregnancy, laparoscopic procedures, and Trendelenburg
position. Similarly, recruitment maneuvers might be necessary in those with increased
closing capacity such as the elderly.
• Hypoxia should always be at the top of a differential diagnosis for abnormal cardiovascular
vital signs such as hypertension, tachycardia, and arrhythmia, as well as nausea and altered
mental status.
HYSTERECTOMY
BASICS
DESCRIPTION
General
• Hysterectomy is the surgical removal of the uterus and is the second most frequently
performed surgical operation in the US after Caesarean section.
• Emergent hysterectomy is performed in the immediate postpartum period for uncontrollable
hemorrhage from rupture, placenta accreta, and uterine atony.
• Elective hysterectomy is performed for several indications:
– Uterine fibroids (30%)
– Dysfunctional uterine bleeding (20%)
– Endometriosis and adenomyosis (20%)
– Genital prolapse (15%)
– Pelvic inflammatory disease
– Endometrial hyperplasia
– Cervical intraepithelial neoplasia, invasive uterine cancer, and ovarian cancers
• Types of hysterectomy
– Total hysterectomy. Surgical removal of the uterus including the cervix. This is the most
common type.
– Partial or supracervical hysterectomy. Upper portion of the uterus is removed leaving the
cervix intact.
– Total hysterectomy with bilateral salpingo-oophorectomy. In addition to the entire uterus
with the cervix, ovaries and fallopian tubes are also removed.
– Radical hysterectomy. Removal of the cervix, the uterus, the upper portion of the vagina,
and supporting tissues with pelvic lymph nodes. Usually done for cervical or endometrial
cancer.
• Surgical approaches (1)
– Abdominal hysterectomies
Indications: Multiple fibroids and/or the presence of abdominal adhesions from previous
abdominal surgeries
May have increased postoperative pain and impaired wound healing because of the
abdominal scar
– Vaginal hysterectomy
Indications: Uterine prolapse, dysfunctional uterine bleeding, and/or obese patients in
whom healing of an abdominal wound may be compromised.
– Advantages over abdominal hysterectomy: Shorter hospital stay, lower cost, and faster
recovery. Reduction in overall postoperative morbidity and period of convalescence.
– Laparoscopic-assisted vaginal hysterectomy (LAVH): Removal of the uterus through the
vaginal approach, with assistance from laparoscopic instruments inserted through small
incisions in the abdomen.
Advantages over abdominal hysterectomy: Decreased postoperative pain, faster
postoperative healing, and shorter hospital stay
Disadvantage of LAVH: Longer duration of surgery and increased risk of major
complications
– Total laparoscopic hysterectomy. Complete removal of the uterus by laparoscopy.
Accomplished with a morcellator, an instrument that cuts the uterus into small pieces and
can be removed from the abdominal cavity via the laparoscopic ports.
– Robotic–Da Vinci hysterectomy. Removal of the uterus using the laparoscopic instruments
remotely operated by the surgeon.
Position
• Abdominal hysterectomy: Supine
• Total laparoscopic and robotic hysterectomy: Supine with steep Trendelenburg
• Vaginal hysterectomy and LAVH: Lithotomy
Incision
• Abdominal: Vertical or transverse (Pfannenstiel) in the lower abdomen
• Vaginal: Small vaginal incision
• LAVH: Abdominal small incisions for trochars; small vaginal incision
• Total laparoscopic and robotic hysterectomy: Small abdominal incisions for trochars only
Approximate Time
• Abdominal hysterectomy: ∼1–3 hours
• Vaginal hysterectomy: ∼1–3 hours
• Laparoscopic hysterectomy, LAVH, and robotic hysterectomy: ∼2–6 hours
EBL Expected
• Elective hysterectomy: 200–600 mL
• Peripartum hysterectomy: 2,000–4,000 mL. Increased blood loss can be due to the larger
size of the uterus, more friable tissue, and dilated blood vessels in the uterus and pelvis (2).
Hospital Stay
• Abdominal hysterectomy: 3–5 days
• Vaginal, LAVH, laparoscopic, and robotic: 2–3 days
• Laparoscopic equipment
• Morcellator
• Robotic equipment
EPIDEMIOLOGY
Incidence
• 590,000 performed annually in the US.
– 66% via abdominal approach
– 22% via vaginal approach
– 12% via laparoscopic approach
• Peripartum hysterectomy: 4.1 cases per 10,000 births
Morbidity
• The overall hysterectomy-related morbidity rate is 6.1%.
• Higher with laparoscopic hysterectomies
Mortality
• For benign cases: 1–6 cases per 10,000
• Cancer related: 29.2 cases per 10,000
• Peripartum: 37.8 cases per 10,000, primarily due to bleeding
• Monitor intraoperative blood loss and maintain hemodynamic stability.
• Prevent nerve injuries:
– Femoral nerve damage can result from excessive abduction and external rotation of the
hip joint.
– Peroneal nerve injury can result from suspension of the legs in the stirrups for the
lithotomy position.
• Plan for good postoperative pain control and early ambulation to prevent DVT and
pulmonary embolism (PE).
SYMPTOMS
Anemia; pale or weak
History
• Indication
• Type of hysterectomy
• Continuous or profuse bleeding
• Assessment of comorbidities like hypertension, diabetes, pulmonary, and renal disease
• For cancer, chemotherapy or radiation
Signs/Physical Exam
Routine
MEDICATIONS
Iron
Labs/Studies
• CBC
• PT/PTT
• EKG if indicated
• Pregnancy testing for women of childbearing age
• Type and screen; if the patient is anemic, crossmatch packed red blood cells.
• Consider chemistry and chest x-ray if comorbidities indicate.
• Anemia from fibroids
• Tumor
• Postpartum hemorrhage
TREATMENT
Premedications
• Anxiolytics as appropriate
• Fluid bolus if the patient appears dehydrated (NPO status, bowel prep)
• Potential for transfusion
• Choice of anesthesia (general versus neuraxial with sedation) for vaginal and abdominal
hysterectomies.
• Epidural for postoperative pain management when abdominal performed
Third-generation cephalosporin; skin organisms
INTRAOPERATIVE CARE
• Dependent on the type of hysterectomy, patient’s condition, length of the procedure, and
patient’s requests.
• General anesthesia is the preferred technique for LAVH, total laparoscopic hysterectomy,
Robotic–Da Vinci hysterectomy, and radical abdominal hysterectomy.
• Neuraxial. Patients may be hypovolemic from bowel preparation, NPO status, or bleeding.
– Spinal anesthesia can provide surgical anesthesia for vaginal and simple abdominal
hysterectomies. It provides excellent muscle relaxation.
– Epidural catheters are commonly placed for postoperative analgesia in combination with
general anesthesia. It can also be used to provide surgical anesthesia for total abdominal
and vaginal hysterectomy, and the epidural can be used postoperatively for pain.
– Combined spinal epidural technique combines the benefits of both modalities.
Monitors
• Foley catheters aid with monitoring urinary output and detect injury to the urinary tract
(heme).
• Arterial line may be considered based on comorbidities: End-organ damage requiring beat-
to-beat BPs and frequent blood draws (hemoglobin, glucose).
• Central line access and pressures may be considered based on comorbidities or extensive
resection.
• General anesthesia is performed with an endotracheal tube. Induction may unmask
hypovolemia from bowel preparation and NPO status.
• Spinal anesthesia. Use a small needle, to minimize the incidence of spinal headache.
Typically, bupivacaine is utilized with a short (fentanyl) and/or long (morphine) acting
opioid.
Maintenance
• An oral gastric tube is placed to decompress the stomach in laparoscopic cases. May be
considered for abdominal cases as well to potentially decrease the risk of postoperative
nausea and vomiting.
• Temperature. Fluid warmers, blanket warmers, and airway humidifiers can be used to
prevent hypothermia.
• Fluids. Administration is based on NPO status, bowel prep, and blood loss. Ins and outs
should be carefully monitored. Abdominal incisions can have increased insensible losses
that should be accounted for and repleted as appropriate.
• Methylene blue dye. The surgeon may request IV administration to detect urinary tract
injury. Normally, it remains intravascularly and is excreted in the urine. In the event of
injury, the blue color will extravasate into the surgical field. May result in transient pulse
oximetry decrease.
• Positioning. Careful attention should be paid to the positioning and padding of extremities
against stirrups and the OR table to prevent nerve injuries.
• Standard extubation criteria apply
• Prophylactic antiemetics; patients have an increased risk, thus multimodal therapy should
be considered.
POSTOPERATIVE CARE
BED ACUITY
Floor bed is typically appropriate
ANALGESIA
• PCA is commonly utilized following general anesthesia.
• Transverse abdominis plane block with catheters allows for prolonged administration of
local anesthesia for postoperative pain control.
• Epidural catheters. Low-dose local anesthetic with opioid provides excellent pain relief;
reduces the amount of opioid requirement, and postoperative ileus (3).
COMPLICATIONS
• Excessive bleeding during surgery
• Postoperative hemorrhage
• Infection
• Injury to ureter, bladder, or other pelvic structures
• Bowel injury, though it is rare
• Blood clots in the veins lead to DVT or PE. Early ambulation reduces the risk of
thromboembolism, postoperative morbidity, duration of hospital stay, and hospital costs.
REFERENCES
1. Johnson, Barlow D, Lethaby A, et al. Surgical approach to hysterectomy for benign
gynecological disease. Cochrane Database Syst Rev. 2006;2:CD003677.
2. Wright JD, Devine P, Shah M, et al. Morbidity and mortality of peripartum hysterectomy.
Obstetric Gynecol. 2010;115(6):1187–1193.
3. Massicotte L, Chalaoui KD, Beaulieu D, et al. Comparison of spinal anesthesia with general
anesthesia on morphine requirement after abdominal hysterectomy. Acta Anaesthesiol
Scand. 2009;53(5):641–647.
4. Okin C, Guido RS, Meyn LA, et al. Vasopressin during abdominal hysterectomy: A
randomized controlled trial. Obstet Gynecol. 2001;97(6):867–872.
• Epidural
• Laparoscopy
• Placenta accreta
• Insensible fluid loss
• Uterine rupture
CLINICAL PEARLS
• Obstetric hemorrhage and postpartum hysterectomy may be decreased by arterial
embolization. In placenta accreta, endovascular interventions like prophylactic temporary
balloon occlusion or transcatheter embolization of the anterior division of the internal iliac
arteries can minimize postoperative hemorrhage AQ Please provide complete detail in ICD
code.
• Injection of vasopressin into the uterus during abdominal hysterectomy has been shown to
reduce blood loss by 40% without increasing morbidity (4). Vasopressin produces
vasospasm of uterine vasculature and uterine muscle contractions, thereby reducing blood
loss during the procedure.
• As an alternative to hysterectomy in cases of symptomatic fibroids, uterine artery
embolization may be performed.
I:E RATIO
Siamak Rahman, MD
BASICS
DESCRIPTION
• The I:E ratio describes the duration of inspiration to the duration of expiration.
– Each complete ventilator breath has an allotted time for inspiration time for inspiration (I-
time) before the ventilator must cycle into exhalation time (E-time).
– The sum of the I-time and E-time equals the allotted time per breath (total duration).
– The ventilator delivers a set number of breaths per minute, or ventilator frequency and
this determines the length of each breath. A frequency of 20 would result in 3
seconds/breath whereas a frequency of 10 would result in 6 seconds/breath.
• Programming the I:E ratio
– Generous I-time allows recruitment of collapsed lung segments.
– Adequate E-time avoids gas trapping.
• Inspiratory time. Describes the time over which the tidal volume is delivered (volume
control (VC) or the pressure is maintained (pressure control).
– Sufficient I-time is needed to allow distribution of the positive pressure inspiratory volume
and recruit collapsed lung segments (redistribution of gas from more compliant alveoli to
less compliant alveoli). Sustained elevations in airway pressure may recruit lung units
more effectively than transient increases. Additionally, sustained alveolar inflation
appears to decrease dead space, perhaps by facilitating the delivery of gas to well perfused
(less compliant) areas.
– Volume-controlled ventilation. As the I-time is increased, peak inspiratory pressures and
turbulence decrease; there is more time to deliver the set volume. Decreased peak
pressures also allow for improved venous return to the right atrium (and cardiac output)
particularly in volume-depleted patients.
Inspiratory pause. Following the tidal volume delivery, a pause may be programmed to
maintain inflation of the alveoli (optimize ventilation to perfusion). This pause occurs
during the programmed I-time: I:E = (inspiratory time + inspiratory pause
time):expiration
– Pressure-controlled ventilation (PCV). As the I-time is increased, larger tidal volumes and
decreased turbulence result; there is more time to recruit collapsed lung segments at a
given pressure.
• Expiratory time. Sufficient E-time is needed to allow alveoli to empty prior to the
subsequent positive pressure inspiratory breath.
• Selecting an I:E ratio is a balance between decreasing turbulence and peak pressures and
increasing tidal volumes against allowing enough time for exhalation and preserving
preload.
– Adults. Normal spontaneous ventilation usually ranges from 1:1.5 to 1:2.5.
– Children. The I:E ratio during normal spontaneous ventilation in young children is
typically 1:3.
• Inverse respiratory ventilation (IRV). In theory, prolongation of the inspiratory time can
maintain mean airway pressures (MAP) and tidal volume at lower levels of positive end-
expiratory pressure (PEEP) and peak alveolar pressure, provided that excessive end-
expiratory gas trapping does not occur.
• Hypoventilation and respiratory acidosis may occur if there is insufficient time for tidal
volume delivery or pressure limits are reached prematurely.
• Gas trapping occurs if there is insufficient time for alveoli to empty before the next breath.
This can result in progressive hyperinflation of alveoli and progressive rise in end-expiratory
pressure (known as auto-PEEP) with resultant barotrauma or cardiovascular compromise
due to high intrathoracic pressures. Situations where this may result include:
– Increased inspiratory time or inverse inspiratory time, compared to expiration
– Obstructive disease states such as asthma or chronic obstructive pulmonary disease
(COPD)
– High respiratory rates, resulting in a shortened absolute expiratory time. Has been
observed with high-frequency oscillatory ventilation (HFOV).
• Time cycling is used for pressure, volume, and dual controlled (VC with pressure limits)
modes. Either the I:E ratio or inspiratory time is set and flows are adjusted accordingly to
ensure that the set tidal volume is delivered.
• Volume-cycled. The flow is set and the inspiration ends when the set tidal volume has been
delivered.
• Hypoxemia not responding to increased FiO2. Inverse I:E ratio can facilitate redistribution of
the tidal volume from more compliant to less compliant alveoli. Under general anesthesia
this is well-tolerated, but in the awake or mildly sedated patient, this is poorly tolerated.
• Acute respiratory distress syndrome (ARDS). Inverse I:E ratios have been utilized to reduce
peak inspiratory pressures and barotrauma. Additionally, a long, sustained inspiration
reduces the mean airway pressure while increasing the PaO2 for a given FiO2. Despite the
benefits in gas exchange, the prolonged inspiratory duration relative to expiration is
uncomfortable for the alert patient, and paralysis may be required. However, the effects of
PCV with different I:E ratios on respiratory mechanics, gas exchange, and hemodynamics in
patients with adult respiratory distress syndrome have failed to show any short-term
beneficial effect of PCV or PCIRV (inverse ratio) over conventional VC with PEEP in patients
with ARDS (1).
EQUATIONS
See Table
GRAPHS/FIGURES
Measuring intrinsic PEEP: quantitative measurement of intrinsic PEEP can be obtained in an apneic patient by using the
expiratory pause hold control on the ventilator. This allows equilibration of pressures between the alveoli and the
ventilator allowing the total PEEP to be measured. The value for total PEEP can be read from the airway pressure dial or
the PEEP display.
Intrinsic PEEP = Total PEEP − Set PEEP
REFERENCES
1. Lessard MR, Guérot E, Lorino H, et al. Effects of pressure-controlled with different I:E ratios
versus volume-controlled ventilation on respiratory mechanics, gas exchange, and
hemodynamics in patients with adult respiratory distress syndrome. Anesthesiology.
1994;80(5):983–991.
2. Marcy TW, Marini JJ. Inverse ratio ventilation in ARDS. Rationale and implementation.
Chest. 1991;100(2):494–504.
• Pneumothorax
• Asthma
• Jet ventilation
CLINICAL PEARLS
• Normal, spontaneous ventilation follows an inspiratory to expiratory ratio of 1:2. During
mechanical ventilation, the I:E ratio is commonly set to this as well.
• In the ventilated patient, the inspiratory time may be increased to improve oxygenation or
decrease the peak inspiratory pressures; however it may result in auto-PEEPing,
barotrauma, or poor patient tolerance (sedated patients).
• Inspiratory pause time is an option in modes where a fixed tidal volume is set and delivered.
IGA DEFICIENCY
Sonia Vaida, MD
Chris A. Steel, MD
Berend Mets, MB, ChB, PhD, FRCA, FFASA
BASICS
DESCRIPTION
• IgA deficiency is defined as a decreased ability or inability to produce IgA antibodies.
• Most patients are asymptomatic. However, some patients are more prone to develop
recurrent upper respiratory tract infections, lower GI infections, and autoimmune disorders.
• Patients with an inability to produce IgA can develop IgA autoantibodies, and are thus at
risk for anaphylactic or anaphylactoid reactions when exposed to blood products that
contain IgA.
EPIDEMIOLOGY
Prevalence
• The most common primary immunodeficiency.
• 1:700 in people of European descent.
• Very low incidence in the Asian population.
Prevalence
• Up to 40% of patients with IgA deficiency can develop autoantibodies to IgA.
• In the general population, 1:1,200 have IgA deficiency and anti-IgA antibodies (1).
• In the general population, anaphylactic transfusion reactions from IgA deficiency occur in
1:20,000 to 1:47,000.
Morbidity
Possible severe anaphylactic or anaphylactoid reactions to blood or blood products.
Mortality
Very rare
• Mainly inherited as an autosomal dominant or autosomal recessive trait. However, it can
also be acquired (e.g., drug induced and secondary to viral infections).
• Patients with absolute IgA deficiency can develop antibodies to IgA and therefore are at risk
for severe allergic reactions when transfused with standard, IgA containing blood
components.
• IgA is a serum immunoglobulin and antibody predominantly found at mucosal surfaces with
an important role in immune protection.
• IgA deficiency results from an intrinsic B cell defect, which prevents their differentiation
into IgA producing cells (2). The defect seems to involve stem cells.
• Patients possess a higher risk of moderate to severe allergic manifestations (1).
• In patients with confirmed or suspected IgA deficiency, obtain IgA levels; if <0.05 mg/dL,
test for anti-IgA antibodies.
• Blood product options and methods
– Packed red blood cells (pRBCs).
IgA deficient units may be stored by the blood bank (deglycerolized allows for longer
storage times)
Alternatively, units can be washed to remove residual plasma (containing donor IgA
antibodies) and decrease the risk of anaphylaxis
– Fresh-frozen plasma (FFP) and cryoprecipitate are obtained from IgA-deficient blood
donors and can be kept frozen for 1 year or in the thawed state for 1–2 days.
– Platelets can be obtained from IgA-deficient blood donors or can be washed to remove
IgA; however, washing can impair platelet function.
– To avoid an allergic reaction, intravenous immunoglobulin G (IVIG) preparation treated
with solvent detergent has been utilized to pretreat patients with IgA deficiency and high
levels of IgA antibodies prior to transfusion.
• If anti-IgA antibodies are present, surgery is elective, and blood transfusion is expected, then
IgA-deficient blood and blood products should be obtained. Discuss the availability of IgA-
deficient blood and blood products with the blood bank pathologist.
• In a life-threatening situation, do not withhold blood or blood products based on an
unknown risk of a transfusion reaction (1). Ideally, IgA-deficient products should be
administered, if available. If not, pretreat with 200 mg hydrocortisone IV and 50 mg
diphenhydramine IV, and administer washed pRBCs or platelets. FFP or cryoprecipitate may
be administered after pretreating the patient and monitoring closely for signs of a reaction.
SYMPTOMS
• Most patients are asymptomatic and diagnosed coincidentally.
• May be identified among blood bank donors.
History
• Consider IgA deficiency in patients with a history of recurrent acute respiratory infections
(sinusitis, pneumonia, etc.)
• Determine how the patient was diagnosed with IgA deficiency.
• History of anaphylactic reactions associated with transfusion of blood; if so, determine if IgA
levels and IgA antibodies were identified.
Gravid patients with known IgA deficiency should have anti-IgA antibody levels checked and
the availability of specific blood products should be discussed with the blood bank
pathologist. If the patient has an increased risk for bleeding (e.g., placenta previa), a Cesarean
section should be scheduled and IgA-deficieny blood products should be available (3).
Signs/Physical Exam
Signs of bronchiectasis may be present in some patients with recurrent pneumonias.
TREATMENT HISTORY
• Patients with severe or frequent infections from IgA deficiency can be candidates for IVIG.
• The best way to avoid triggering a reaction is to simply avoid exposing patients with anti-
IgA antibodies to blood products with IgA.
• When this is unavoidable in an emergent situation, the patient should be pretreated as
previously mentioned and monitored closely for signs of a reaction.
MEDICATIONS
• No specific medication is available.
• Pulmonary, GI, or autoimmune disorders should be treated accordingly.
Labs/Studies
• IgA levels. Know your laboratory’s lower limit of IgA detection.
• Anti-IgA antibody presence.
• Pulmonary: Recurrent upper respiratory infections (bronchitis, pneumonia), otitis media,
asthma
• GI: Recurrent GI infections, chronic diarrhea.
• Autoimmune diseases: Celiac disease, Graves’s disease, systemic lupus erythematous,
rheumatoid arthritis
• Lymphoid malignancies
If anti-IgA antibodies are present, and there is a likelihood that blood or blood products will
be needed, delay elective surgery and obtain IgA-deficient products.
CLASSIFICATIONS
IgA1 and IgA2 subclasses
TREATMENT
Premedications
Diphenhydramine and corticosteroids can be administered in emergency situations if IgA
levels and/or anti-IgA antibody presence are unknown prior to transfusion of standard blood
products.
INTRAOPERATIVE CARE
No preference for a type of anesthesia.
Monitors
• Consider invasive monitors in a patient with anti-IgA antibodies and expected
bleeding/transfusion.
No preference
Maintenance
• No preference
• In general, when administering blood products, there should be vigilance for flushing,
wheezing, bronchospasm, hypotension, or other clinical signs of anaphylaxis.
• If an allergic reaction is suspected, stop the transfusion and administer hydrocortisone and
diphenhydramine.
• In patients with known IgA deficiency, consider autologous blood transfusion or cell salvage.
Also prepare the IgA-deficient or washed blood products prior to the case or as soon as
possible.
No preference
FOLLOW-UP
BED ACUITY
The reaction between IgA and anti-IgA antibodies would occur shortly after administration of
products containing IgA. If no significant reaction is noted, a delayed anaphylactic reaction is
unlikely.
• Should an anaphylactic reaction occur:
– Stop blood transfusion
– Administer IV fluids
– Maintain hemodynamic parameters with epinephrine in low doses (if needed)
– Type and cross match
– Perform a direct antiglobulin test and an IgA antibody test (if not already ordered).
• Blood product is considered IgA deficient if the serum IgA is <0.05 mg/dL.
COMPLICATIONS
• Possible anaphylactic reaction to blood or blood products
• Be prepared to treat anaphylaxis
• Epinephrine should be ready to administer
REFERENCES
1. andler SG. How I manage patients suspected of having had an IgA anaphylactic transfusion
reaction. Transfusion. 2006;46:10–13.
2. Yel L.Selective IgA deficiency. J Clin Immunol. 2010;30:10–16.
3. Steel C, Vaida S, Mets B. Massive blood transfusion in a patient with immunogobulin a
deficiency undergoing cesarean delivery. Anesth Analg. 2010;110:1088–1090.
ADDITIONAL READING
• Flickinger C, Petrone T, Church A. A review: American rare donor program.
Immunohematology. 2004;20:239–243.
• Gilstad CW. Anaphylactic transfusion reactions. Curr Opin Hematol. 2003;10:419–423.
• Anaphylaxis
CODES
ICD9
279.01 Selective IgA immunodeficiency
ICD10
D80.2 Selective deficiency of immunoglobulin A [IgA]
CLINICAL PEARLS
• Patients are advised to wear an identification bracelet.
• There is an IgA-deficient blood donor registry (consult American Rare Donor Registry).
• If testing for IgA is not available before urgent transfusion, do not withhold transfusion with
standard blood products.
INFECTIOUS DISEASE EXPOSURE IN THE HEALTHCARE
WORKER
Andrew L. Barker, MD
BASICS
DESCRIPTION
• Working in the healthcare setting necessitates a degree of exposure to infectious hazards
that is greater than non-healthcare-related jobs.
– Parenteral injury, inhalational exposure, and direct contact with bodily fluids are the
primary means of communication or exposure.
– The most common parenterally transmitted diseases are HIV, hepatitis B virus (HBV), and
hepatitis C virus (HCV).
– Universal precautions should be the standard. Additional precautions must be taken for
airborne pathogens such as tuberculosis, H1N1 influenza, and human papillomavirus
(HPV).
• Agents used in bioterrorism attacks have become increasingly more important for the
healthcare provider to be familiar with.
EPIDEMIOLOGY
Prevalence
• There are ~800,000 percutaneous injuries per year in the US. Most needlesticks occur in the
OR from suture needlesticks.
• HIV seroconversion after a needle stick from an HIV positive patient is 0.3%; in 2004, 57
healthcare workers reported contracting HIV in the workplace.
• Hepatitis B seroconversion after parenteral exposure can vary between 2% and 40% for the
nonimmunized. Since the introduction of the hepatitis B vaccination, infections have
decreased from 10,721 in 1983 to 384 in 1999 (a 96% reduction).
• Hepatitis C seroconversion after parenteral exposure is estimated at 1.3%.
• Tuberculosis infection among all healthcare workers has an incidence ranging from 3.6 to
5.4 workers per 100,000 from 1994 to 2000.
• HPV infection following inhalational exposure is unknown; most likely very rare.
Morbidity/Mortality
• HIV infects ∼5 million people worldwide annually. Roughly 900,000 cases of AIDS were
reported in the US in 2002. With appropriate antiretroviral therapy early in the disease
course, HIV patients have a life expectancy between 20 and 50 years. Without treatment,
however, the median life expectancy is estimated to be between 9 and 11 years from the
time of infection. The major cause of death is opportunistic infections in the later stages of
the disease.
• Hepatitis B causes asymptomatic disease in 60–65% of infected people, acute hepatitis in
20–25% of infected people, and chronic hepatitis in roughly 1% of people.
• Hepatitis C causes active liver disease in 75–80% of infected people, cirrhosis in 10–20% of
infected people, and liver cancer in 1–5% of cirrhosis patients.
• New, active tuberculosis infections affect 16,000 people per year in the US. Forty-five
percent of these infections occur in immigrants. In 10–50% of immunocompromised hosts,
the bacteria migrate to various organs and cause a disseminated disease. The major cause of
death is due to lung disease.
• Laryngeal papillomatosis does not cause a malignant disease, but frequently causes recurrent
papillomas that require multiple operations for treatment.
• Creutzfeldt–Jakob disease affects ∼1 in 1,000,000 people each year. It is uniformly fatal
and has an average duration of 7 months.
• Parenteral infections
– Wearing gloves has been shown to decrease the frequency of seroconversion from
needlestick injuries. Likewise, gloves prevent transmission of infection via open skin
wounds on the hands.
– Percutaneous injuries from smaller gauge needles have a lower incidence of
seroconversion than larger needles. This is likely due to the degree of tissue trauma
inflicted by the needle, as well as the viral load being transferred on the needle itself.
– Hollow bore needles have a higher rate of seroconversion than solid (suture) needles.
– Transmission from a patient with a high viral load has a higher incidence of
seroconversion than when a patient has a lower viral load.
• Inhalational infections
– Personal protective equipment like an N95 mask has been shown to reduce the
transmission of inhaled infections to healthcare workers.
– Negative pressure rooms prevent bacteria transmitted by the inhalational route from being
released into hallways and other rooms.
– When using a laser on HPV lesions, a suction device can be used to collect aerosolized
virions and is thought to reduce the risk of transmission of the virus.
• Prion diseases
– The only known risk factor for prion disease transmission is direct contact with infected
patient material. Creutzfeldt–Jakob disease is the most common prion disease worldwide,
and 85–90% of cases arise spontaneously rather than via an infectious route.
• Bioterrorism agents
– Anthrax, Yersinia pestis (plague), smallpox, and Clostridium botulinum are among the most
common agents used in bioterrorism.
– The most significant risk factor for infection with these agents is direct exposure. There
are no documented modifiable risk factors for these diseases other than standard universal
precautions.
• HIV is a retrovirus that infects human macrophages and CD4+ T-cells.
• Hepatitis B is a DNA virus that replicates primarily in hepatocytes.
• Hepatitis C is an RNA virus that also preferentially infects hepatocytes. The direct cytotoxic
effects on the hepatocyte are thought to be responsible for the bulk of the damage caused by
hepatitis C, in contrast to the immune-mediated cytotoxic effects of hepatitis B.
• Tuberculosis is caused by Mycobacterium tuberculosis. Tuberculosis typically leads to a latent
infection in the apical portions of the lung. However, an assortment of factors can cause the
bacteria to reactivate or disseminate into the blood stream, causing miliary tuberculosis.
The major cause of organ dysfunction is due to the caseating necrosis caused by the immune
response to the bacteria and surrounding structures.
• HPV can be disseminated into the healthcare environment via surgical lasering of infected
lesions. These virions can be inhaled into the respiratory tract and may (rarely) cause an
infection of laryngeal or other airway structures. Infection primarily causes laryngeal
papillomatosis, which can lead to hoarseness or airway obstructions. Treatment focuses on
removal of the papillomas with a laser.
• Influenza A is caused by the influenza virus. Symptoms include fever, myalgias, sore throat,
and pneumonia that may be fatal.
• Bacillus anthracis is a large spore-forming, Gram positive, rod-shaped bacteria that causes
anthrax. Anthrax’s prodrome consists of a fever, cough, and chest or abdominal pain. The
prodrome is typically 1–6 days in duration, but disease progression is imminent when the
fever acutely worsens. This is rapidly followed by hypoxia and possibly death.
• Smallpox virus is spread by the respiratory aerosol route or contact with infected bodily
fluids. It causes symptoms 7–17 days after infection, which first consist of fever, headache,
and/or backache. The characteristic rash starts on the mucosa of the oropharynx, face, and
extremities. The rash becomes vesicular and pustular in its later stages as it migrates toward
the trunk. Mortality is 30% or greater.
• Yersinia pestis is the causative agent of the plague. The bacteria have an array of mechanisms
to avoid host defenses while weakening the immune system. Depending on the route of
infection, symptoms can include pustules and ulcerations of the skin or hemorrhagic,
necrotizing pneumonia. Fulminant bacteremia with resultant disseminated intravascular
coagulation, hemorrhages, and thrombi are the major causes of death.
• Botulism is caused by Clostridium botulinum, a spore-forming, Gram-negative rod found in
inadequately sterilized canned foods. The neurotoxin produced by the bacteria prevents the
release of neurotransmitters, which results in paralysis. Without supportive care, mortality
is estimated at 60%. With supportive care, however, mortality is estimated at 5–10%.
• Creutzfeldt–Jakob disease and other spongiform encephalopathies are caused by prions.
Prions are proteins that have had a spontaneous conformational change in their tertiary
structure. This conformational change causes a chain reaction, which leads to massive
neural degeneration. The most common presenting symptom is dementia, which progresses
to a uniformly fatal encephalopathy.
• Universal precautions should be taken in all situations. Appropriate eye care, gloves, and
personal protective equipment should be made available in any location where healthcare
personnel may come into contact with infected patients or bodily fluids.
• Needleless IV tubing may reduce risk.
• One-handed needle recapping
• Hospital policies mandating appropriate isolation for high-risk patients should be in place.
There should be appropriate warning signs to alert all healthcare personnel of possible
exposure.
• The constellation of physical examination findings will differ based on the specific infectious
disease in question.
• All exposures need to be appropriately reported to employee health; after hours, the
emergency room or infectious disease on-call person usually has the capability of initiating
the workup and therapy as needed.
• Specific screening tests following exposure to various infectious diseases are dictated by the
route of injury.
• For percutaneous injuries, HIV, hepatitis B, and hepatitis C titers should be drawn as soon as
possible following the injury.
• Following initial titers, repeat screening should be performed at given intervals based on the
disease in question.
• For tuberculosis, PPD screening should be performed on an annual basis for all healthcare
providers.
Will vary depending on the specific infectious agent.
TREATMENT
• Healthcare workers who are exposed to HIV should be considered for a 4-week course of
treatment with a combination of zidovudine and lamivudine, lamivudine and stavudine, or
didanosine and stavudine. Resistant strains can occur.
• Hepatitis B exposures should be treated with prompt institution of the hepatitis B vaccine
series in individuals who have not already completed the series. In addition to the
vaccination series, hepatitis B immune globulin should be considered for patients who have
not completed the vaccination series OR who have an inadequate response to a completed
vaccine series.
• Hepatitis C exposures are not treated with immune globulin or antiviral agents (interferon,
with or without ribavirin). Only follow-up testing should be performed.
• Anthrax should be treated by a 60-day course of ciprofloxacin or doxycycline. If the bacteria
are known to be penicillin sensitive, however, the treatment should be a 60-day course of
penicillin G or amoxicillin.
• Smallpox has no definitive therapy. Secondary infections should be treated on an as needed
basis should they arise.
• Yersinia pestis is highly transmissible and requires respiratory/droplet isolation until at least
3 days of antibiotic therapy has been completed. Treatment can include a 10-day course of
streptomycin, gentamicin, doxycycline, or ciprofloxacin.
• Botulism should be treated with supportive care, which may include prolonged mechanical
ventilation. In addition, specific antitoxins are available based on bacterial serotype.
• There is no known cure or therapy for prion diseases such a Creutzfeldt–Jakob disease. The
only action currently known to be effective is to prevent further spread of disease by
limiting exposures of uninfected individuals.
FOLLOW-UP
Determined by the disease in question
REFERENCES
1. elay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol.
1999;53:283–314.
2. Centers for Disease Control and Prevention. Novel influenza A infections among healthcare
personnel – United States, April-May 2009. 2009;58(23):641–645.
3. Garden JM, O’Banion MK, Shelnitz LS, et al. Papillomavirus in the vapor of carbon dioxide
laser-treated verrucae. JAMA. 1988;259(8):1199–1202.
4. Centers for Disease Control and Prevention. Updated U.S. Public Health Service Guidelines
for the Management of Occupational Exposures to HBV, HCV, and HIV and
Recommendations for Postexposure Prophylaxis. 2001;50(RR11):1–42.
5. Fine A. New York State Department of Health. Summary of biological warfare agents.
2001.
6. Texas Department of State Health Services. Texas contaminated sharps injuries, 2008.
Available at:
http://www.dshs.state.tx.us/idcu/health/infection_control/bloodborne_pathogens/report/20
(accessed February 15, 2011.
• Hepatitis C
CODES
ICD9
V01.9 Contact with or exposure to unspecified communicable disease
ICD10
Z20.9 Contact w and exposure to unsp communicable disease
CLINICAL PEARLS
• Vigilance and prevention are the most effective ways to avoid transmission of diseases.
• Following exposure, certain diseases can be treated with postexposure prophylaxis in order
to decrease the rate of infection.
• The carrier rate among healthcare workers for methicillin-resistant Staphylococcus aureus
(MRSA) may be as high as 1 in 20 (approximately 2–3 times greater than the general
population). Only about 5% of those have symptoms. Healthcare workers may be 2–3 times
more likely to be a carrier of MRSA.
• Healthcare workers are considered to be at significant risk for acquiring or transmitting
hepatitis B, influenza, measles, mumps, rubella, and varicella. All of these are preventable
by vaccines. Immunocompromised healthcare workers are at a greater risk and the Centers
for Disease Control issue vaccination recommendations for this population.
INFRARENAL AAA REPAIR
E. Gail Shaffer, MD, MPH
Richard McAffee, MD
BASICS
DESCRIPTION
General
• Although endovascular aortic repair (EVAR) is gaining popularity, open repair of infrarenal
abdominal aortic aneurysms remains an important treatment option. Additionally, it may be
carried out after endovascular repair has been attempted and failed.
• The choice between open versus endovascular repair depends on many factors including
surgeon preference, patient preference, aneurysm characteristics (size, shape, and location),
and comorbidities.
• Following careful dissection and exposure of the aneurysm, the patient is heparinized. The
aortic cross-clamp is first placed distally (to prevent atheroembolic events) and then
proximally. For infrarenal AAAs, clamping usually occurs below the level of the renal
arteries; however, suprarenal clamping may be necessary in some situations.
• The graft is first sutured proximally, then a clamp is placed on the graft. The proximal aortic
clamp is removed, and the proximal suture line is examined for bleeding.
• The graft is then sutured distally to the aorta or iliacs, the graft clamp is removed and flow
is assessed. If there are no leaks, the distal clamps are removed.
• Reversal of heparin with protamine should be discussed with the surgeon.
Position
• Supine for transperitoneal approach
• Supine with left flank elevation for retroperitoneal approach
Incision
• Transperitoneal: Midline abdominal
• Retroperitoneal: Oblique incision along 10th rib extending toward umbilicus
Approximate Time
2–5 hours
EBL Expected
• Approximately 500 mL
• Ruptured AAAs have increased loss
Hospital Stay
• Open repair: 5–10 days
• Ruptured AAA: 10 days or greater
• Preparation for large volume blood loss may include cell salvage and rapid infuser
• Neuromonitoring is not typically used, but may be considered for extensive, “re-do” AAA
repairs, or for thoracic AAA repairs.
EPIDEMIOLOGY
Incidence
• Newly diagnosed: ∼200,000/year
• AAA repairs: 35,000–40,000/year; over 50% are performed via open repair
• Conversion to open from EVAR: ∼3%
Prevalence
• More prevalent with age, significant smoking history, hypertension (HTN), male gender,
family history, and connective tissue disease.
• Biggest predictors of risk of rupture are the diameter and rate of expansion.
Morbidity
Open repair has a higher morbidity and mortality than EVAR; however, this difference is not
significant when comparing long-term survival.
Mortality
Elective AAA repair 28-day mortality ranges from 3.3% to 27.1% in men and 3.8% to 54.3%
in women; 5 year mortality from 12.9% to 78.1% in men and 24.3% to 91.3% in women.
Age, congestive heat failure, cerebrovascular disease, and diabetes are independent risk
factors for 5-year mortality.
• Patients may present with multiple comorbid issues that need to be independently assessed
and optimized.
• Wide hemodynamic shifts can be seen with clamping and unclamping of the aorta; the
anesthesia provider must be in constant communication with the surgeon as well as
understand the physiological changes and treatment modalities at each stage.
SYMPTOMS
• Expanding AAA may present with pain
• Pulsatile mass may cause back and stomach pain
History
• Elicit history of cerebral, cardiac, renal, and peripheral vascular disease
Signs/Physical Exam
Palpable abdominal mass and bruits may or may not be present.
MEDICATIONS
• Beta-blockers can reduce cardiac morbidity and mortality (DECREASE study) and should be
continued perioperatively. Heart rate (HR) control and decreased contractility result in less
systolic pressure generated against the aneurysm wall.
• Statin’s pleiotropic effects can reduce postoperative cardiac, cerebral, and renal morbidity;
should be continued perioperatively.
Labs/Studies
• Electrolytes, BUN/Cr
• Hemoglobin/hematocrit
• Coagulation parameters (PT, INR, PTT)
• EKG (further cardiac workup is based on symptoms and EKG results).
• CXR if significant smoking history, chronic obstructive pulmonary disease (COPD)
• Cardiac evaluation may include stress testing and cardiac catheterization.
• COPD
TREATMENT
Premedications
• Anxiolytics as needed; anxiety may increase BP and the risk of AAA rupture.
• Beta-blockers have been shown to reduce morbidity and mortality in major vascular surgical
patients; titrate to a HR <80 bpm.
• Perioperative statin therapy initiation may be indicated.
• Cross-matched blood products should be in the room.
• Potential for blood transfusion
• Postoperative intubation in the ICU
Skin flora; first-generation cephalosporin such as cefazolin
INTRAOPERATIVE CARE
General endotracheal anesthesia +/– T8 epidural placement for postoperative analgesia.
Monitors
• 2 large-bore IVs
• Arterial line; consider preinduction placement
• Central venous catheter should be considered for pressure monitoring and inadequate PIV
access
• Pulmonary artery catheter for pulmonary artery pressure (PAP), MVO2, CO, SVR monitoring
based on comorbidities
• Foley catheter
• TEE depending on comorbidities
• A slow, controlled induction is necessary to ensure an adequate depth of anesthesia and
minimize hemodynamic changes. Hypotension can impair perfusion; HTN can result in
aneurysmal rupture (transluminal pressures, coughing, bucking, etc.).
• Epidural is advantageous for postoperative pain; it is often prudent to wait until after the
aorta is unclamped and hemodynamics have stabilized to bolus the epidural and begin an
infusion.
Maintenance
• Balanced volatile or IV techniques may be utilized.
• Cross-clamping of the aorta
– Preload: Variable increase (minimal to significant)
– Afterload is increased by the clamp. The more distal the clamp, the less increase in
afterload. Compensatory vasodilation above the clamp occurs. Patients with poor left
ventricular (LV) function may not be able to tolerate the increase in myocardial work and
oxygen consumption. Myocardial ischemia and “flash” pulmonary edema can result if not
properly anticipated. Treatment is with vasodilators at the time of clamping
(nitroprusside, nicardipine, propofol).
– HR: No change typically.
– Contractility will increase in a normal heart; in those with CAD or CHF, the heart may not
be able to compensate.
– Cardiac output: No change (or decreased in the setting of LV dysfunction).
– SVR distal to the clamp is increased to maintain perfusion; thus the administration of
vasodilators to decrease myocardial afterload may impair perfusion pressure. Distal tissue
hypoxia results in anaerobic metabolism with lactic acid production and the accumulation
of vasoactive metabolites (oxygen free radicals, cytokines, and prostaglandins).
• Unclamping of the aorta
– Preload decreases as vasodilated arterial beds fill with blood; volume loading should be
performed prior to unclamping.
– Afterload is abruptly decreased. Consider initiating phenylephrine or norepinephrine drip
a few minutes prior to anticipated release of cross-clamp or bolusing as needed.
– HR: May reflexively increase in response to hypotension
– Contractility: Washout of metabolites from distal ischemia may impair inotropy; consider
the use of inotropes.
– Cardiac output changes are variable; if adequately volume loaded, the abrupt drop in
afterload favors a high cardiac output; however, hypovolemia or ischemic metabolites
more often lead to a decreased cardiac output.
– PAP can increase from hypercarbia, acidosis, and ischemic metabolites.
– If hypotension cannot be medically managed, it may be necessary for the surgeon to
reclamp the aorta.
• Renal perfusion may be compromised. Renoprotective measures are limited to maintaining
adequate volume status, avoiding hypoxemia and hypoperfusion, and administering
mannitol and sodium bicarbonate.
• Maintain normothermia with active warming devices (forced air warmer, etc.) to counteract
anticipated heat loss from large incision, visceral exposure, skin open to room air, and
prolonged operative time.
• Volume replacement: May have large insensible losses. Significant blood loss may be
possible, especially with ruptured AAA.
• Standard extubation criteria; special attention to blood loss, hemodynamics, and
normothermia. Complicate surgeries or comorbid conditions may warrant leaving the
patient intubated postoperatively.
• Smooth extubation (avoid coughing and bucking).
• Control of HTN and tachycardia is important; consider beta-blockers and/or vasodilators
(bolus or drips).
• Postoperative neurologic exam should evaluate cerebral and peripheral ischemia.
POSTOPERATIVE CARE
BED ACUITY
• ICU bed for most patients
• Close control of BP to decrease bleeding from graft site, often requiring vasoactive infusions
ANALGESIA
• Patient may have significant pain.
• If an epidural catheter is present, ensure that the level of coverage, rate, and concentration
are adequate. Catheter removal may be performed after ensuring that the coagulation status
is normal.
COMPLICATIONS
• Cardiac complications such as myocardial ischemia or infarction, HTN (most common)
• Hemorrhage or coagulopathy
• Lower extremity or bowel ischemia
• Renal failure
• Respiratory failure
PROGNOSIS
• Incidence of reoperation is less with open repair compared to EVAR.
• Late graft complication with open repair is very low (less than 2.5%).
• 30-day mortality is higher compared to EVAR; however, no difference is observed at 12
months.
REFERENCES
1. Eliason JL, Clouse WD. Current management of infrarenal abdominal aortic aneurysms.
Surg Clin N Amer. 2007;87(5):1017–1033.
2. Mantha S, Ochroch EA, Roizen MF, et al. Anesthesia for vascular surgery. In: Barash PG,
Cullen BF, Stoelting RK, eds., Barash Clinical Anesthesia. 5th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2009:1122–1133.
3. Moulakakis KG, Dalainas I, Myloas S, et al. Conversion to open repair after endografting for
abdominal aortic aneurism: A review of causes, incidence, results, and surgical techniques
of reconstruction. J Endvasc Ther. 2010;17(6):694–702.
4. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality
and myocardial infarction in high-risk patients undergoing vascular surgery. New Engl J
Med. 1999;341(24):1789–1794.
• Abdominal aortic aneurysm (endovascular repair, EVAR)
CODES
ICD9
ICD10
CLINICAL PEARLS
• Open infrarenal AAA repair is a major vascular surgery that requires close collaboration
between the surgeons and anesthesia providers.
• Patient population with significant comorbidities; unless evidence exists otherwise, assume
all patients have vascular disease of the heart and cerebrum.
• Wide hemodynamic shifts from aortic cross-clamp and release need to be anticipated. In
discussion with the surgeon, these shifts can be minimized with pharmacologic intervention.
• Hemodynamic shifts from rapid blood loss are also possible – blood should be in the room
before incision and large bore IV access is essential.
INSENSIBLE FLUID LOSSES
Ashley Greene, DO
Mary E. McAlevy, MD
BASICS
DESCRIPTION
• Insensible fluid losses are defined as losses of fluid secondary to evaporation into the
environment. They are
– Difficult to measure and ascertain
– Involve estimates that are calculated from clinical experience
– Replaced with either crystalloid or colloid; controversy exists as to the preferred fluid.
Ultimately, the principal goal should be to optimize cardiac output.
• Common sources of insensible losses include
– Open wounds, in particular abdominal incisions and exposure
– Condensation in the breathing circuits
– Sweating
– Fever
– Hyperventilation
• Insensible losses differ from “third spacing” (transcellular movement of fluids) or temporary
sequestration (movement of fluid into functionless spaces). These can result from
inflammation, trauma, or damage to the normal integrity of the vascular barrier
• The current practices of managing insensible losses are hypotheses; interestingly enough,
there are no current studies that have proven that they are significant and need substantial
replacement.
• Perioperative fluid therapy of insensible losses are guided by the following assumptions:
– The preoperative patient is volume depleted as a result of fasting, continued physiologic
insensible loss, and urine output.
– Intraoperatively, insensible fluid loss to the environment increases with the size of the
surgical incision, amount of tissue exposed, and duration of exposure.
– Insensible fluid losses require replacement
Basal insensible loss. Mainly transdermal and estimated to be at most 0.5 mL/kg/hour
and may increase to 10 mL/kg/hour with major abdominal surgery.
Size of incision. Insensible loss increases proportionally in relation to the surface area
exposed to the environment.
Nonhumidified gases. Patients breathing nonhumidified gases have an increase in their
insensible losses. This is further accentuated if the patient is hyperventilated.
ANATOMY
• Abdomen
• Muscle
• Thorax
• Both hypovolemia and hypervolemia can have deleterious effects. In the perioperative
period, anesthesia providers rely on physical examination, vital signs and monitors, as well
as laboratory values to assess volume status and guide therapy.
• Hypovolemia. Decreases ventricular preload and hence stroke volume (Frank–Starling).
Initially, the body may be able to compensate by increasing the heart rate and systemic
vascular resistance. However, as hypovolemia progresses, the cardiac output can be
impaired and organ hypoperfusion and dysfunction can result. Outcome studies have also
shown that it can prolong hospital stay.
– History. NPO status, fever, diarrhea, vomiting. Intraoperative blood loss, size of incision.
– Physical exam. Dry mucus membranes, decreased skin turgor, decreased capillary refill,
sunken fontanelles in newborns, increased heart rate, decreased BP, decreased urine
output, and changes in mental status (awake patient)
– Laboratory values. Hemoconcentration, hypernatremia, and an increased BUN:Cr ratio
(>20:1)
– Invasive monitors. Arterial line, central venous monitoring, pulmonary artery catheters,
and transesophageal echocardiogram may be used in conjunction with, and to correlate,
the overall clinical picture.
• Hypervolemia. Can lead to pulmonary edema and increased myocardial oxygen demand
(increased preload and wall tension).
– History. Ins and outs
– Physical exam. Edema (likely pitting), wheezing, crackles on lung exam, increased urinary
output, jugular venous distention. In the awake patient, cough and dyspnea.
– Laboratory values. Hyponatremia, decreasing Hct levels (due to hemodilution), and
increased A-a gradient or decreased a/A ratio.
• Much of current practice on fluid management is based on algorithms that propose
replacement of
– Preoperative deficits (e.g., NPO status and bowel prep)
– Maintenance requirements
– Surgical losses
– Insensible fluid and third space losses
• Perioperative loss of fluid can be broken down into continuous loss (urine output and
insensible perspiration) and losses exclusively from trauma (mainly blood loss). In the
awake patient, continuous losses are replaced via the GI tract through the absorption of
colloid-free fluid and electrolytes. However in the “fasted” patient this mechanism may fail
and deficit replacement is performed by the anesthesia provider with crystalloid fluid.
• The principal goal of fluid management should be to optimize cardiac preload.
• Controversy and considerations
– Outcomes. Fluid management can have effects on nausea and vomiting, tissue perfusion,
pain, need for surgical revision, length of hospital stay and bowel motility, among other
things.
– Generous fluid resuscitation during laparoscopic procedures can decrease both
postoperative pain and the incidence of nausea and vomiting in patients prone to PONV.
– Errors with measurement. Insensible losses are difficult to accurately calculate, unlike
blood loss that can be visibly ascertained. It is often largely overestimated in clinical
practice, and many feel that it is negligible and should not be included in maintenance
requirements.
– Volume status. A clinical impression is based on several variables. At this time, direct
blood volume measurements are not available to the anesthesia provider.
– Colloid versus crystalloid. Many proponents still advocate that maintenance requirements
and preoperative deficits should be replaced with crystalloid solution while blood loss
should be replaced with colloid solution.
– Fluid restriction. “Optimizing does not mean maximizing.” Newer studies are challenging
the current “standard” views of fluid therapy. In fact, some experts advocate not replacing
perceived preoperative deficits, but instead fluid “restricted” strategies during the
perioperative period (especially during major elective GI procedures). This theory is based
on an increasing number of reports that demonstrate that excessive intravascular volume
can lead to an increase in morbidity and mortality. Overhydration can lead to pulmonary
edema, increased ICU duration, ileus, and abdominal compartment syndromes.
– Anesthetic drugs commonly result in decreased systemic vascular resistance and
vasodilation. This can unmask hypovolemia or relative hypovolemia (e.g., chronic
hypertensives with increased vascular tone, but decreased intravascular volume).
GRAPHS/FIGURES
See Table
REFERENCE
1. Chappell D, Jacob M, Hofmann-Kiefer K, et al. A rational approach to perioperative fluid
2. Joshi GP. Intraoperative fluid restriction improves outcomes after major elective
gastrointestinal surgery. Anesth Analg. 2005;101:601–605.
3. Matthias J, Daniel C, Markus R. The “third space” – Fact or fiction? Best Pract Res Clin
4. Gan TJ, et al. Goal-directed intraoperative fluid administration reduces length of hospital
stay after major surgery. Anesthesiology. 2002;97(4):820–826.
• Crystalloids
• Colloids
• Extracellular fluids
CLINICAL PEARLS
• Controversy exists on how to best manage insensible fluid losses in regard to
– How to accurately measure?
– Whether to replace with colloid versus crystalloid fluids
– Should a “restrictive” strategy be utilized? Studies have suggested that it may improve
outcome; however, the patient’s health, type of surgery, and outcome being measured
have not been standardized across these studies.
• At this time, the goal remains to maintain intravascular volume status, as both under and
over resuscitation can be hazardous.
• Goal-directed plasma volume expansion during the intraoperative period may be associated
with improved outcome:
– Reduction in hospital stay
– Earlier return of GI function
– Decreased postoperative complications.
INTERNATIONAL NORMALIZED RATIO (INR)
Jason Han Chua, MD
Anahat Dhillon, MD
BASICS
DESCRIPTION
• INR reports the international normalized ratio of prothrombin time (PT), which is a
measurement of the extrinsic and final common pathways of coagulation.
• The extrinsic pathway is triggered in vivo by tissue injury and the release of tissue factor.
• PT is performed in vitro by recalcification of patient blood in the presence of tissue factor;
PT is the time in seconds when fibrin clot forms (measured by visual, optical, or
electromechanical methods).
• Normal values for PT are usually between 12 and 15 seconds depending on the lab, hence
the need for a normalized ratio that is unitless.
• INR is the most frequently ordered test to monitor warfarin anticoagulation.
• Extrinsic pathway
– Initiated by tissue factor release via tissue injury.
– Rapidly proceeds to the final common pathway via factor VII and calcium.
• Common pathway
– Begins with assisted activation of factor X (by intrinsic or extrinsic pathway).
– Factor Xa converts prothrombin to thrombin, which in turn converts fibrinogen to fibrin
monomer, which crosslinks to form stable clot with calcium and factor XIII.
– Factor X also serves to initiate platelet-surface clotting activity, a vital component of the
clotting cascade (greatly accelerates overall clot formation).
• Role of thrombin
– Positive feedback via activation of cofactors V and VIII.
– Accelerates fibrin crosslinking via factor XIII activation.
– Stimulates platelet adhesion and aggregation.
– Releases tissue plasminogen activator from endothelium, facilitating clot resorption.
– Activates protein C (negative feedback via inactivation of factors Va and VIIIa).
ANATOMY
PT is sensitive to reduced activity of vitamin K-dependent factors (II, VII, IX, X, C, S), which
are produced in the liver.
• Prolongation of INR
– Warfarin; most common cause
– Vitamin K deficiency (malnutrition or prolonged use of antibiotics)
– Hepatic dysfunction. Mild dysfunction may lead solely to PT prolongation due to
predominant deficiency in factor VII; more severe dysfunction may prolong PT and
activated PTT (aPTT) due to a decrease in vitamin K-independent factors.
– Other deficiency or inhibition of factors II, V, VII, X, or fibrinogen
– Rarely, antiphospholipid antibodies can have antithrombin activity; it is usually associated
with a hypercoagulable state.
• Alternate assays include
– Chromogenic factor X
– Prothrombin-proconvertin time (not available in the US)
• Mixing study: INR abnormality in the absence of warfarin administration may be due to
factor deficiency or inhibition. Differentiation is accomplished via a mixing study, where
patient plasma is mixed 1:1 with pooled plasma.
– Deficiency: Normalization after dilution. Specific factor assays can reveal the specific
factor deficiency.
– Inhibition: Continued abnormality after dilution.
• Warfarin’s anticoagulation effect is mediated via inhibition of vitamin K-dependent gamma-
carboxylation of factors II, VII, IX, and X.
– Factors remain immunologically detectable, although biologically inactive.
– Full anticoagulation does not take place until preformed, normal factors are cleared,
which usually takes 36–72 hours.
– PT may be prolonged sooner due to the short half-life of factor VII (5–7 hours); recall,
however, that the intrinsic pathway does not require factor VII.
– Proteins C and S have shorter half lives than the other vitamin K-dependent factors, and
thus a theoretical risk exists for hypercoagulability early after initiation of warfarin
therapy. Skin necrosis has been described when used to treat protein C deficiency.
– Equilibration of factor levels usually occurs at least 1 week after initiation of therapy.
– Target INR varies depending on the patient’s indication for warfarin therapy, but is
typically between 2.0 and 3.0.
• Abnormal INR
– May be seen with first year warfarin therapy, age >65 years, hypertension, alcoholism,
liver disease, stroke, and history of GI bleeding.
– Patients with prolonged INR and any of the above risk factors undergoing major surgery
with significant expected blood loss may benefit from preoperative correction of INR (via
vitamin K in elective procedures or fresh frozen plasma in emergent procedures).
• When considering a neuraxial anesthetic technique in an anticoagulated patient, ASRA
consensus is to document a normal INR prior to placing the neuraxial block and an INR
<1.5 when removing an epidural catheter.
– Concern is for epidural hematoma, which may cause spinal cord compression with
devastating neurologic consequences.
– Regular neurologic checks should be performed for up to 24 hours following.
– The same concern may not exist for placement of peripheral nerve blocks, as epidural
hematoma is not a consideration.
EQUATIONS
• International sensitivity index (ISI) is determined for each reagent/instrument combination
depending on the performing lab.
• INR = (measured PT/control PT)ISI
GRAPHS/FIGURES
Coagulation cascade
Bold arrows: factor conversion;

Thin arrows: activation
Dashed arrows: inhibition
REFERENCES
1. nsell J, Hirsh J, Hylek E, et al. Pharmacology and management of the vitamin K
antagonists: American College of Chest Physicians Evidence-Based Clinical Practice
Guidelines (8th Edition). Chest. 2008;133:160S.
2. ensley FA, Martin DE, Gravlee GP. Coagulation management during and after
cardiopulmonary bypass. In A Practical Approach to Cardiac Anesthesia. Philadelphia, PA,
2008:497–498.
3. irsh J, Poller L. The international normalized ratio. A guide to understanding and
correcting its problems. Arch Intern Med. 1994;154:282.
4. Horlocker T, Wedel D, Benzon H. Regional anesthesia in the anticoagulated patient:
defining the risks (the second ASRA consensus conference on neuraxial anesthesia and
anticoagulation). Reg Anesth Pain Med. 2003;(28):172–197.
5. Zehnder JL, Clinical Use of Coagulation Tests, UpToDate. Hirsch J, Fuster V, Ansell J,
Halperin JL. AHA/ACC Scientific Statement: American Heart Association/American College
of Cardiology Foundation Guide to Warfarin Therapy. Circulation. 2005;107:1692–1711.
ADDITIONAL READING
• www.asra.com
• Prothrombin time (PT)
• Partial thromboplastin time (PTT)
• Cirrhosis
• Protein C
CLINICAL PEARLS
• Whole blood should be collected in citrated anticoagulant at the specific ratio of one part
citrate to nine parts blood. Most collection tubes have the correct fill level marked.
• Polycythemic patients require a smaller amount of anticoagulant due to relatively lower
volume of plasma in the sample. Lack of correction leads to artificially prolonged INR.
• Sample should be free of tissue fluids, IV solutions delivered through indwelling catheters,
and heparin.
• The American College of Chest Physicians and National Heart, Lung, and Blood Institute
suggested the following therapeutic ranges for warfarin therapy:
– 2.0–3.0 for prevention of venous thromboembolism, treatment of deep venous thrombosis
and pulmonary embolism, tissue heart valves, atrial fibrillation, and acute myocardial
infarction
– 2.5–3.5 for mechanical prosthetic valves
INTESTINAL OBSTRUCTION
Suzanne Strom, MD
BASICS
DESCRIPTION
• Patients with intestinal obstruction commonly present to the operating suite for exploratory
laparotomy or laparoscopy. However, they are considered a “full stomach” and pose an
increased risk when sedating or securing their airway. Hypoxia, respiratory failure, and
ARDS can result if stomach and/or intestinal contents trespass into the trachea.
EPIDEMIOLOGY
Incidence
• Small bowel obstruction is the most common cause of intestinal obstruction and comprises
60–80% of all obstructions.
• Perioperative aspiration. Despite the number of patients with “full stomach” and intestinal
obstruction, the incidence in the general population may be as low as 0.05% because of
provider vigilance.
Morbidity
• Approximately one-quarter of patients having surgery for obstruction will have some
complication. Rates increase when the patient has advanced age, comorbidities, a delay in
treatment, or previous abdominal surgery.
• Laparoscopic repair of lesions has decreased rates of morbidity and mortality.
Mortality
• Small bowel obstructions caused by adhesions carry a 5–10% risk of mortality. The risk rises
significantly in patients with large bowel obstruction from malignancy or bowel gangrene,
reaching 15–28%.
• Mortality from aspiration alone can be anywhere from 3% to 70%.
• Abdominal surgery that is complicated by aspiration pneumonitis has a mortality risk as
high as 75%.
• Intestinal obstructions are most often caused by:
– Adhesions secondary to previous surgery
– Inflammatory processes
– Endometriosis
• Risk factors for aspiration are
– GI dysfunction. Abnormal lower esophageal sphincter (LES) function, abnormal
esophageal motility, esophageal diverticulum or neoplasm, hiatal hernia, peptic ulcer,
gastritis, abdominal distension, intestinal or gastric outlet obstruction, abdominal trauma,
gastroesophageal reflux disease (GERD) abdominal infection, recent meal, obesity,
pregnancy, and presence of nasogastric (NG) tube (tube stents open the LES and prevents
full closure while not completely emptying the stomach contents).
– Airway dysfunction. Inadequate pharyngeal reflexes, weak cough, and recent extubation
(dysfunctional vocal cords, poor muscular coordination of hypopharynx, residual
sedation).
– Comorbidities. Extremes of age, altered mental status, pain, emergency operation, upper
abdominal or emergency abdominal surgery, and elevated intracranial pressure (ICP).
PATHOPHYSIOLOGY
• Third spacing. Patients with intestinal obstruction have considerable movement of
intravascular volume into the interstitial space because of the inflammatory response to
bowel distension and ischemia. It can result in significant hypovolemia.
• Aspiration. The increase in abdominal pressure can result in aspiration of stomach/bowel
contents when patients are sedated or during the period between induction and
endotracheal intubation.
– The three factors most important in determining the severity of a pulmonary insult in
aspiration are the volume, pH, and amount of particulate matter.
– The most severe pneumonitis can be caused with volumes >25 mL (or 0.3 mL/kg) and a
pH <2.5.
– Particulate matter can physically obstruct small airways and lead to ventilation/perfusion
mismatch, hypoxia, hemorrhagic edema, and even acute pulmonary hypertension.
• Pulmonary implications
– Functional residual capacity (FRC) is decreased with abdominal distension, the supine
position, and general anesthesia. Atelectasis results in an increased Alveolar-arterial
gradient.
– Impairment of normal diaphragmatic function and splinting from incisional pain can cause
continued respiratory embarrassment postoperatively. This is worsened by residual
anesthesia, IV anesthetics, and neuromuscular blockade.
– Vital capacity remains abnormal for at least 1 week following upper abdominal surgery;
aggressive pulmonary hygiene is encouraged.
• Anticipate the possibility that bowel obstruction has an increased risk for pulmonary
aspiration. Consider:
– NG tube placement and suctioning prior to induction
– Induction in the reverse Trendelenburg position
– Rapid sequence induction with cricoid pressure
– Suction equipment checked and ready
– Ability to quickly reposition the patient into Trendelenburg should aspiration occur
• Volume status should be assessed. Third spacing of fluids, vomiting, and NPO status can
result in a relative intravascular hypovolemia. Induction on anesthesia can result in
hemodynamic compromise or collapse.
SYMPTOMS
Determine if the patient has had nausea and vomiting.
History
Evaluate for NPO status, GERD, and other risk factors.
Signs/Physical Exam
• Evaluate abdomen
• Skin turgor, and mucous membranes for signs of hypovolemia.
TREATMENT HISTORY
• If the patient has had an NG tube placed, it is important to note its output.
• The patient may have had oral contrast for imaging of the lesion, which can add to the
increased gastric volume.
MEDICATIONS
Evaluate for the use of prokinetic agents, Histamine-2 (H2) blockers, proton-pump inhibitors,
as well as pain medicines.
Labs/Studies
• Review electrolytes for expected derangements and acid–base disorders.
• CBC should be ordered to evaluate for hemoconcentration. WBC should be followed since
the patient is at risk for sepsis.
Patients with obstruction often have poor nutrition, sepsis, hypovolemia, tachycardia, and
hypotension.
If the patient has not been adequately resuscitated (as evidenced by normalization of heart
rate and BP, return of urine output, and normalization of hemoconcentration and BUN/Cr
ratio), one should weigh the risks of proceeding with the benefits of fluid resuscitation prior
to induction.
CLASSIFICATIONS
Partial versus complete obstruction
TREATMENT
Premedications
• Reduce acidity of gastric contents. Nonparticular, clear antacids such as sodium bicitrate
increase the pH of fluids immediately while increasing gastric volume. However, they are
associated with only mild pulmonary changes if aspirated. H2 blocking agents such as
famotidine are effective at reducing the acidity and can also mildly decrease gastric fluid
volume (use may be limited due to onset time). By contrast, proton-pump inhibitors like
protonix are effective more rapidly, but still need to be administered 1 hour prior to
surgery.
• Consider reducing gastric volume with NG tube placement.
The severity of the associated conditions and risk of morbidity should be addressed.
INTRAOPERATIVE CARE
While it is possible to have adequate surgical exposure with neuraxial anesthesia, aspiration
risk and the possibility of hemodynamic instability often necessitate general anesthesia with a
cuffed endotracheal tube (also allows for positive pressure ventilation to compensate for
decreased lung compliance)
Monitors
• Standard ASA monitors should be used.
• CVC or arterial line placement may be necessary if the patient is hemodynamically unstable.
• Goals include avoiding aspiration while maintaining hemodynamic stability.
• Rapid sequence induction (RSI). Should proceed with cricoid pressure and rapid
administration of sedative/hypnotic and neuromuscular blockade. Avoidance of mask
ventilation can decrease insufflation of the stomach. Cricoid pressure (Sellick maneuver)
should be applied and not released until the cuff is inflated and tube placement has been
verified by capnography and auscultation.
• Awake intubation should be considered in difficult airways (RSI is contraindicated).
Maintenance
• Choice of anesthetic is only limited by concerns about nitrous oxide (N2O) administration.
This may lead to increased intraluminal volume and pressure, which can cause bowel
ischemia and difficulty with abdominal closure. Use should be avoided or minimized until
closure of the abdominal fascia is complete.
• Fluid resuscitation should continue in the intraoperative period. Additionally, there is the
potential for significant insensible fluid losses and third spacing.
• Monitor for electrolytes and acid–base status, as appropriate.
• Ventilator settings. Increased peak inspiratory pressures may be seen with decreased
pulmonary compliance from the underlying pathology as well as retractors and positioning.
Consider adjusting volumes, respiratory rate, I:E ratios, and mode (volume versus pressure)
to optimize pressures and decrease the risk of barotrauma, hypoxia, or hypercarbia.
Increases in atelectasis may be offset or decreased with PEEP.
• Muscle relaxation should be administered and monitored to aid with exposure and closing.
• Temperature. Large bowel incisions may present difficulty with maintaining normothermia.
Ensure that patients are covered and warming techniques considered for the upper and
lower body; fluids are warmed; irrigation is warmed; and consider warming the room.
• In any patient with known intestinal obstruction or “full stomach,” an attempt should also
be made to suction the esophageal and gastric material before emergence from anesthesia.
• In addition, extubation should occur only after swallowing, adequate strength, and the
ability to follow commands has been clearly demonstrated.
• Delayed awakening might occur due to metabolic causes. Patients with acidosis,
hemodynamic instability, and ventilation/perfusion mismatch can result in failure to meet
extubation criteria.
POSTOPERATIVE CARE
BED ACUITY
Depending on the severity of the pathology, patients should be monitored appropriately.
• Analgesia
– Postoperative opioids should be carefully administered to prevent excessive sedation and
subsequent aspiration during recovery.
– Placement of a regional or neuraxial block in the postoperative period can prevent
splinting and sedation, as well as improve deep breathing techniques. Ensure that the
patient has been properly resuscitated and does not have a coagulopathy.
• Electrolytes and CBC as appropriate
• Antibiotics as appropriate
COMPLICATIONS
• The most common concerns are
– Aspiration pneumonia and respiratory failure
– Cardiovascular instability from acidosis and hypovolemia.
REFERENCES
1. El-Orbany M, Connolly LA. Rapid sequence induction and intubation: Current controversy.
Anesth Analg. 2010;110(5):1318–1325.
2. g A, Smith G. Gastroesophageal reflux and aspiration of gastric contents in anesthetic
practice. Anesth Analg. 2001;93:494–513.
3. Olsson GL, Hallen B, Hambraeus-Jonzon K. Aspiration during anaesthesia: A computer-
aided study of 185,358 anaesthetics. Acta Anaesthesiol Scand. 1986;30:84.
• Aspiration
CODES
ICD9
560.9 Unspecified (Intestinal obstruction)
ICD10
K56.60 Unspecified intestinal obstruction
CLINICAL PEARLS
• The three factors most important in determining the severity of a pulmonary insult in
aspiration are the volume, pH, and amount of particulate matter.
• Unrecognized or “silent” regurgitation can occur, as well as subsequent aspiration that is
subclinical.
INTRACRANIAL HYPERTENSION
Shreyas Bhavsar, DO
BASICS
DESCRIPTION
• Intracranial pressure (ICP) is the pressure exerted on the dura by the contents of the cranial
vault; normal ICP is <15 mm Hg.
• Intracranial hypertension (ICH) is a neurological emergency that, if left untreated, can cause
brain herniation, irreversible neuronal damage, compromised cerebral blood flow (CBF),
and eventually death.
• Treatment includes medical management and possibly surgery (resection of the mass lesion
or a decompressive craniectomy for cases refractory to medical management). These
procedures are performed to improve brain tissue oxygenation and CBF.
• The cranium is comprised of
– Brain matter
– Cerebrospinal fluid (CSF)
– Blood; both arterial and venous
– A noncompliant intracranial vault with only a small reserve for additional volume
(provided by the intervertebral spaces).
• Monroe–Kellie hypothesis: The intracranial volume is in dynamic equilibrium; the increase
in one component volume will cause a decrease in volume of the other components in order
to prevent increases in ICP.
• Cerebral perfusion pressure (CPP) = MAP–ICP, where MAP is mean arterial pressure and
ICP is intracranial pressure
– Normal cerebral autoregulation maintains CPP between 50 and 150 mm Hg (see
Equation).
– If the CPP is <50 mm Hg or >150 mm Hg, then CBF directly follows changes in
perfusion pressure.
– PaO2: Severe hypoxia causes cerebral vasodilation. A PaO2 <50 mm Hg drastically
increases CBF.
– PaCO2: CBF is directly proportional to changes in PaCO2. Between a PaCO2 of 20 and 80
mm Hg, blood flow changes ∼1–2 mL/100 g/min per mm Hg of PaCO2.
– Cerebral metabolic rate of oxygen (CMRO2): Cerebral metabolic activity is directly
coupled to increases or decreases in CBF.
ANATOMY
• Intracranial volume is comprised of
– Brain tissue: 80%
– CSF: 8–12%
– Intracerebral blood
• Radiological images of brain with high ICP will reveal a midline shift and effaced basal
cisterns.
• Once maximum capacitance is achieved, additional volume will quickly increase the ICP.
• Anatomical factors that increase ICP
– Brain tissue: Tumors, edema (ischemic stroke, cerebral contusion), trauma (epidural
hematoma, subdural hematoma, cerebral contusion), psuedomotor cerebri
– CSF: Hydrocephalus
– Blood: Hypoxia, hypercarbia, obstruction of venous return from head position, Valsalva
maneuvers or increased intrathoracic pressures (coughing, gagging, excessive PEEP),
seizures, severe hypertension, hypotension (vasodilation to maintain CBF can increase
cerebral blood volume)
• Clinical signs of increased ICP
– Headache
– Nausea/vomiting
– Periodic or irregular breathing
– Decreased mental status (obtunded, comatose)
– Papilledema
– Cushing response: Severe hypertension, bradycardia, and irregular respirations
• This response indicates severe brain herniation. ICP leads to compression of intracerebral
vessels and cerebral ischemia. Reflexively, the body activates hemostatic mechanisms to
maintain cerebral perfusion by increasing the systemic BP (mainly systolic and hence
widening the pulse pressure). Likely, the carotid baroreceptors sense the increased pressure
and, in turn, activate the vagal response to slow the heart rate.
• Perioperative goals include maintaining the CPP by:
– Mean arterial pressure (MAP): Increase or maintain
– ICP: Decrease or prevent increases
• Monitors
– Standard ASA monitors, with special attention to capnography
– Arterial line for continuous BP monitoring and blood gas sampling (PaO2, PaCO2,
glucose).
– Fluid intake and output with a Foley catheter and possibly a central venous catheter
– Continuous ICP monitoring
– Nerve stimulator to help determine depth of neuromuscular blockade
– EEG may be needed during barbiturate coma to determine depth of sedation, evaluate for
seizures, and to help establish cerebral electrical silence.
• Induction and airway management
– Head of bed (HOB) at 30°. Facilitates cerebral venous drainage and decreases intracerebral
blood volume. However, it may hinder brain tissue oxygenation.
– Intubation and controlled ventilation can facilitate (or avoid) hypoventilation.
– Rapid sequence intubation (RSI) should be used in emergent conditions. The benefits of
quickly securing the airway and controlling respiratory parameters (avoiding hypoxia,
hypercarbia) outweigh the small and transient increase in ICP from succinylcholine.
However, if the patient is not adequately anesthetized or only partial muscle relaxation
has occurred, ICP can increase during direct laryngoscopy and intubation.
• Maintenance is typically via a combined technique to minimize any further increases in ICP.
– Volatile anesthetics decrease CMRO2 in a dose-dependent manner, dilate cerebral blood
vessels, and increase CBF (uncoupling).
– Nitrous oxide causes mild cerebral vasodilation. Its effects are generally mild especially
when used with other IV agents.
– Propofol decreases CBF and CMRO2 and has some anticonvulsant properties.
– Opioids have little direct effect on CBF, CMRO2, and ICP. Respiratory depression may
cause changes in PaCO2.
– Muscle relaxation has no direct effect on the brain.
– Succinylcholine can potentially increase ICP but that effect can be attenuated with a
defasciculating dose of a nondepolarizing neuromuscular blocker and adequate induction
agent.
– Head flexion and rotation can impede venous outflow from the brain and should be
avoided.
– Hyperventilation: Adjusting the PaCO2 to 30–35 mm Hg is one of the fastest techniques to
decrease ICP. Decreases in the PaCO2 alkalinize the CSF and cause cerebral
vasoconstriction. This phenomenon, however, fades with time as the CSF readjusts to a
normal pH (vasoconstrictive effects typically last 11–20 hours). Avoid excessive
hyperventilation (PaCO2 <25 mm Hg), as it can contribute to cerebral ischemia.
– Maintain a CPP >60 mm Hg. With increased ICP, cerebral perfusion is maintained by
systemic hypertension and sympathetic hyperactivity. To that extent, caution is advised in
treating hypertension as it may result in cerebral ischemia (hypotension is an independent
risk factor for poor outcomes). At the same time, the risk of persistent systemic
hypertension includes cerebral edema and intracranial hemorrhage. Furthermore, cerebral
autoregulation can be compromised in areas of brain injury and complicates the
management of systemic hypertension. If treatment is undertaken, short-acting titratable
drugs (beta-blockers, propofol) can be used to lower the BP and avoid increases in ICP.
Avoid drugs such as nifedipine, nitroglycerine, or nitroprusside as they can induce
cerebral vasodilation and worsen ICP.
– Mannitol is a hyperosmolar agent that is commonly used to lower ICP (effect is dose-
dependent). IV bolus doses of 0.25–1 g/kg can begin to decrease the ICP in 1–5 minutes
(peak effect of 20–60 minutes, duration up to 6 hours). Redosing may be required for
continued clinical effect. Advantages include its free radical scavenging properties and
reduction in CSF production. Adverse effects include hypotension (initial vasodilatory
response), exacerbation of congestive heart failure (initial intravascular osmotic effect),
electrolyte abnormalities (later diuresis), and cerebral edema (areas of compromised
blood-brain barrier, or rebound from prolonged administration). Mannitol is, thus,
contraindicated in hypovolemic and hypotensive patients.
– Hypertonic saline creates an osmotic gradient for interstitial intracerebral fluid to shift
intravascularly. This reduces overall brain volume and decreases ICP. This has a more
pronounced effect compared to mannitol and can be used in a hypovolemic and/or
hypotensive patient needing intravascular volume expansion. Potential adverse effects
include hyperchloremic metabolic acidosis, platelet dysfunction, prolonged coagulation
parameters, and central pontine myelinolysis.
– Furosemide: A loop diuretic that may decrease the production of CSF; less effective than
hypertonic saline and mannitol.
– Sedation and analgesia: Pain and agitation can increase ICP and should be addressed.
Benzodiazepines can decrease CMRO2 and CBF without effects on the ICP; beware of
hypotension or hypercarbia.
– Avoid seizures: Consider antiepileptics to avoid significant increases in CMRO2, CBF, and
ICP.
– Avoid hyperglycemia: Associated with poor neurological outcomes. The optimal target
glucose range is uncertain but generally maintained below 220 mg/dL.
– Corticosteroids decrease vasogenic edema from primary and metastatic tumors; a common
regimen is dexamethasone 4 mg IV every 6 hours. Steroids can increase serum glucose
levels and if left uncontrolled can lead to hyperglycemia.
– Barbiturate coma has not been shown to improve outcomes but can be considered in
refractory, elevated ICP. Proposed mechanisms: a coupled reduction in CBF with
decreased CMRO2 and arterial vasoconstriction (decreases CBF). Disadvantages include
the loss of neurological exam and hypotension.
– CSF drainage: Removal of CSF is a quick and reliable method to lower the ICP. The most
common method is through a ventriculostomy that has the advantage of being both a
therapeutic and diagnostic maneuver. Disadvantages include a risk of infection,
hemorrhage, and difficulty in placement with diffuse cerebral edema or slit-like ventricles.
Fiberoptic monitoring devices can be placed in the subarachnoid space, epidural space, or
brain parenchyma. They are easier to place but cannot remove volume and cannot be
recalibrated. An external ventricular device can be placed for temporary measures, while
ventricular shunts are placed for chronic ICP management (i.e., hydrocephalus).
– Avoid hyperthermia: Increases in temperature can elevate the CMRO2 and hence CBF.
Outcome studies have demonstrated worsened neurologic injury in traumatic brain injury.
Treatment includes antipyretics, cooling blankets, and treatment of infectious causes.
– Hypothermia: Controversial with no studies showing improved neurological outcomes. It
may be considered in cases of severe refractory ICH maximized on medical management.
• Extubation and emergence
– Extubation criteria are the same as with any surgical procedure (confirm that neurological
issues are stable or resolved); if extubation is not possible, consider appropriate sedation.
Avoid bucking/straining/coughing that can worsen ICP or cause cerebral hemorrhage.
Consider IV lidocaine to attenuate the gag reflex to suctioning/extubation. Rapid
awakening is also important to conduct a neurological assessment postoperatively.
EQUATION
CPP = MAP - ICP; where CPP is cerebral perfusion pressure, MAP is mean arterial pressure,
and ICP is intracranial pressure.
GRAPHS/FIGURES
FIGURE 1. Increases in intracranial volume begin to increase the intracranial pressure within the fixed/rigid cranial vault
after compensatory mechanisms have been exhausted.
REFERENCE
1. ershad EM, Humphreis WE, Suarez JI. Intracranial hypertension. Semin Neurol.
2008;28(5):690–702.
2. Jantzen JP. Prevention and treatment of intracranial hypertension. Best Pract Res Clin
Anaesthesiol. 2007;21(4):517–538.
3. Rangel-Castilla L, Gopinath S, Robertson CS. Management of intracranial hypertension.
Neurol Clin. 2008;26(2):521–541.
4. Wolfe TJ, Torbey MT. Management of intracranial pressure. Curr Neurol Neurosci Rep.
2009;9(6):477–485.
• Cerebral metabolic rate
CODES
ICD9
348.2 Benign intracranial hypertension
ICD10
G93.2 Benign intracranial hypertension
CLINICAL PEARLS
• Treatment of ICH includes medical and surgical means.
• Medical treatment
– HOB at 30°
– Secure airway and ensure normal oxygenation (PaO2 >60 mm Hg)
– Hyperventilate to a PaCO2 of 30–35 mm Hg
– Maintain CPP >60 mm Hg
– Mannitol 0.5–1.0 g/kg IV bolus
– Consider hypertonic saline, antiepileptics, steroids, barbiturate coma
– Diuretics
– Avoid factors that aggravate ICP
• Surgical treatment is often undertaken if the ICP increases suddenly or is refractory to
medical management.
– CSF drainage via ventriculostomy
– Decompressive craniectomy
INTRAOPERATIVE MYOCARDIAL ISCHEMIA
Alan P. Zaggy, MD
BASICS
DESCRIPTION
• Intraoperative myocardial ischemia can occur when there is an oxygen supply and demand
imbalance. This can lead to such perioperative events as:
– Congestive heart failure (CHF)
– Arrhythmias
– Myocardial infarction (MI)
– Cardiogenic shock and end-organ damage
– Death
• A thorough preoperative cardiac evaluation can identify the severity (and presence) of
disease in patients with diagnosed or suspected coronary artery disease (CAD). History and
physical exam, combined with laboratory, EKG, and stress testing (stress EKG,
echocardiography, nuclear scans), can confirm or refute myocardium at risk for ischemia.
EPIDEMIOLOGY
Incidence
• CAD, the primary contributing factor to myocardial ischemia, affects over 11 million
Americans.
• The incidence of perioperative myocardial ischemia is unknown as its detection is largely a
function of monitoring technique (simple or multilead EKGs with or without computer ST
segment analytic enhancement, pulmonary artery catheter, TEE, etc.) and the skill of the
monitoring personnel.
Prevalence
CAD in the general population increases with age.
• Age 15–44 years: 4 per 1,000
• Age >65 years: 80 per 1,000
Morbidity
Myocardial ischemia can lead to infarction, arrhythmias, heart failure.
Mortality
Perioperative MI remains the leading cause of postoperative death in the elderly (1)[C].
• Preoperative risk factors:
– Increasing age
– Previous MI
– Angina
– Arrhythmias
– Hypertension
– Diabetes mellitus
– Peripheral vascular disease
– Hypercholesterolemia
– Cigarette smoking
• Perioperative risk factors:
– Hypertension
– Hypotension
– Hypoxia
– Hemodilution
– Tachycardia
– Increased cardiac work/tension
• Ischemia can result from a decrease in oxygen supply or an increase in oxygen demand.
• Decreased myocardial oxygen supply is the result of a decrease in coronary blood flow or
blood oxygen content:
– Decreased coronary artery perfusion pressure can result from decreased diastolic blood
pressure or increased left ventricular end-diastolic pressure. CPP = DBP - LVEDP, where
CPP is coronary perfusion pressure, DBP is diastolic blood pressure, and LVEDP is left
ventricular end-diastolic pressure.
– Coronary artery stenosis (fixed) or vasospasm (variable) obstructs coronary blood flow.
Distal to the stenosis, the vessel becomes maximally dilated over time to maintain blood
flow. However, it lacks the ability to further compensate for decreases in blood flow.
– Thromboembolic phenomenon. Stasis, inflammation, and tachycardia can dislodge clots
and block coronary arteries, decreasing coronary blood flow.
– Tachycardia decreases diastolic time, and, thus, the duration that the LV is perfused.
During systole, LV intracardiac pressures exceed CPP; thus, blood flow only occurs during
diastole.
– Decreased blood oxygen-carrying capacity can result from red blood cell loss/anemia,
decreased oxygen saturation, or hypoxemia.
• Increased myocardial oxygen demand occurs when there is an increase in cardiac work:
– Tachycardia increases the number of times that the myocardium depolarizes and
repolarizes as well as mechanically contracts and relaxes.
– Increased contractility. Mechanical contraction follows myocyte depolarization and
involves the energy consuming process of sarcomere shortening.
– Increased ventricular wall tension can occur with
Increased afterload (pressure work): Increased systemic (or pulmonary) vascular
resistance, intraventricular pressures and radius, as well as hyperviscosity, and
decreased aortic compliance
Increased preload (volume work)
– Ventricular hypertrophy. The increased muscle mass requires a greater amount of energy
for each contraction. Additionally, the “watershed” subendocardium is more likely to
become ischemic during times of decreased supply or increased demand.
• Optimize myocardial oxygen supply
– Maintain mean arterial pressures. General anesthesia with volatile or IV medications as
well as neuraxial blocks can decrease BP. Consider the use of nitrous oxide to allow
decreased doses, low-dose vasopressor infusions, and fluid and/or blood administration, as
appropriate.
– Decrease LVEDP. Consider enhancing inotropy to improve emptying as well as decreasing
preload
– Decrease the risk for thromboembolic phenomenon.
Discuss with the surgeon and primary care doctor/cardiologist the perioperative
management of platelet inhibitors or other anticoagulants in patients currently on
medications or at high-risk for cardiac events.
The pleiotropic effects of statins have been shown to improve endothelial function,
enhance the stability of atherosclerotic plaques, decrease oxidative stress and
inflammation, and inhibit the thrombogenic response. Certain patient populations may
benefit from de novo preoperative administration; additionally, abrupt withdrawal in
patients taking statins has been associated with an increase in myocardial events.
– Decrease the heart rate with beta-blockers, calcium channel blockers, and opioids.
Additionally, avoid increases in heart rate from drugs with sympathetic or vagolytic
properties as well as hypotension (reflex). Anticipate increases during laryngoscopy,
incision, surgical stimulation, and extubation.
– Optimize blood oxygen content with adequate hemoglobin levels and oxygen partial
pressure. Consider transfusing blood, increasing the FIO2, adjusting ventilator settings
(respiratory rate, tidal volumes), and administering positive end-expiratory pressure
(PEEP).
• Decrease myocardial oxygen demand
– As above, decrease the heart rate and anticipate inciting medications or events that can
cause tachycardia.
– Decrease inotropy, if appropriate, by removing sympathetic stimulation, administering
beta-blockers, and avoiding drugs with positive inotropy. However, decreases in ejection
fraction/stroke volume can increase the LVEDP (thus decreasing the CPP) as well as
forward flow.
– Decrease preload. Consider diuretics, venodilators, fluid restriction, and enhancing
forward flow with inotropy, as appropriate.
– Decrease afterload. Maneuvers to decrease systemic vascular resistance may jeopardize the
mean arterial pressure and should be done cautiously.
DIAGNOSIS
• Vital signs: Tachycardia, hypotension, hypertension, cardiac arrest
• EKG. The standard lead monitoring (3 lead: I, II, III) is relatively insensitive, but can be
altered by placing the left shoulder lead at the cardiac apex yielding a 3 lead: I, II, modified
V5 that allows for ischemic monitoring of the inferior (II) and lateral (V5) LV walls (the
areas most vulnerable to ischemia). Diagnostic mode with computer ST segment analytic
enhancement is more robust when used with a 5 lead system. Intraoperative 12-lead EKG is
generally cumbersome and impractical. However, it may be considered when ischemia is
suspected.
– ST segment depression or elevation
– T wave changes
– Arrhythmias
– Conduction changes
• Pulmonary artery catheters may demonstrate increases in LVEDP or PCWP, reflecting a
change in ventricular compliance during ischemic states, or acute mitral insufficiency from
papillary muscle ischemia. The etiology of these changes should be determined to
distinguish them from false positives. Additionally, decreases in cardiac output and mixed
venous oxygen saturation can also suggest ischemia.
• Transesophageal echocardiogram (TEE). New regional wall-motion hypokinesis, dyskinesis;
systolic thinning/thickening abnormalities; new papillary muscle dysfunction/mitral
insufficiency.
• False positive ST-segment changes may result from
– Mitral valve prolapse
– Pressure overload of the LV in young hypertensive patients can lead to false positive ST-
segment changes (2)[B].
– Left bundle branch block
– Wolff–Parkinson–White syndrome
– Right bundle branch block
– Digitalis, tricyclic antidepressants, diuretics
– Artificial pacemakers
• Arrhythmias may be seen with sympathetic agents, metabolic abnormalities, drug toxicities
TREATMENT
• Many of the treatment maneuvers are similar to preventative actions, but can differ in the
degree of aggressiveness, level of invasive monitoring, as well as the possible need for
discontinuing the surgery and intraoperative or postoperative cardiology evaluation.
Additionally, because the heart is the pump for its own blood supply, decreasing oxygen
consumption may come at the cost of decreasing the oxygen supply; this requires careful
titration and optimization.
• Decrease the heart rate with beta-blockers and remove inciting stimuli in order to increase
oxygen supply and decrease demand. Beta-blockers need to be titrated appropriately to
avoid undesired decreases in inotropy.
• Decrease inotropy with myocardial depressants (beta-blockers, volatile anesthetics) in order
to decrease myocardial work (3)[B] while maintaining an appropriate forward flow/stroke
volume.
• Optimize the BP to balance coronary perfusion with myocardial tension (afterload).
– Mean arterial pressures can be increased with vasopressors (alpha-agonists such as
phenylephrine, norepinephrine, or vasopressin). High-dose dopamine and epinephrine
have predominantly alpha-effects, but may be accompanied by tachycardia. Consider
removing medications that decrease the systemic vascular resistance (e.g., volatiles, IV
medications, and epidural infusions).
– Decrease afterload with nitrovasodilators, volatile agents, calcium channel blockers.
• Decrease preload with venodilators such as nitroglycerin (immediate) or diuretics such as
furosemide (onset 20–30 minutes). Additionally, decreasing the LVEDV/LVEDP can
optimize the CPP.
• Increase blood oxygen content
– Blood transfusion can increase the hemoglobin level, but is associated with metabolic
abnormalities, immune reactions, increased viscosity, and worsened outcomes in critically
ill patients.
– Increase oxygen delivery
– Optimize ventilation/perfusion (tidal volumes, respiratory rate, PEE)
• Discontinue or abbreviate the surgical procedure, if appropriate.
• Cardiology evaluation may be performed intraoperatively or in the recovery room.
FOLLOW-UP
• EKG. Attain a 12-lead EKG and place the patient on continuous monitoring.
• Cardiac enzymes should be drawn to evaluate for myocardial damage. Troponin (most
cardiac-specific peaks at 12 hours), CK-MB (relatively cardiac-specific peaks at 10–24
hours), LDH (least cardiac-specific peaks at 72 hours).
• Cardiology consultation to oversee dynamic cardiac stress or angiographic evaluation, acute
interventional management (4)[A] (5)[B], and ongoing risk factors (6)[A].
REFERENCES
1. Djokovic JL, Hendley-Whyte J. Prediction of outcome of surgery and anesthesia in patients
over 80. JAMA. 1979;242:2301.
2. roelicher VF, Yanowitz FG, Thompson AJ, et al. The correlation of coronary angiography
and the electrocardiographic response to maximal treadmill testing in 76 asymptomatic
men. Circulation. 1973;48:597.
3. emmotsu S, Hashimoto Y, Shimosato S. Inotropic effects of isoflurane on mechanics of
contraction in isolated cat papillary muscles from normal and failing hearts. Anesthesiology.
1973;39:470.
4. Singh S, Bahekar A, Molnar J, et al. Adjunctive low molecular weight heparin during
fibrinolytic therapy in acute ST-segment elevation myocardial infarction: A meta-analysis
of randomized control trials. Clin Cardiol. 2009;32:358–364.
5. Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852
patients with acute myocardial infarction: Randomized placebo-controlled trial. Lancet.
2005;366:1622–1632.
6. Russell CL, Conn VS, Jantarakupt P. Older adult medication compliance: Integrated review
of randomized controlled trials. Am J Health Behav. 2006;30:636–650.
• 12 Lead EKG
CODES
ICD9
414.8 Other specified forms of chronic ischemic heart disease
ICD10
I25.89 Other forms of chronic ischemic heart disease
CLINICAL PEARLS
• Largely preventable with diligent hemodynamic monitoring and close attention to
maintaining baseline hemodynamics and physiologic conditions in the face of surgical
interventions.
• Accurate EKG lead placement – especially leads II, V5 – is a cornerstone of myocardial
ischemia detection.
• Treatment should consist largely of restoration of baseline hemodynamic and physiologic
conditions.
INTRAOPERATIVE TRANSESOPHAGEAL ECHOCARDIOGRAM
(TEE)
Nanhi Mitter, MD
Mary Brady, MD, FASE
BASICS
DESCRIPTION
• TEE was first developed by cardiologists in the 1970s. It was used as a tool to measure left
ventricular performance.
• An M-mode transthoracic probe was originally used for epicardial imaging in patients
undergoing coronary artery bypass grafting (CABG). Disadvantages of this included:
– Interruptions in the surgery because it was manipulated by the surgeons
– An inability to reproduce the images.
• The first TEE probe was made of a wire and a vinyl esophageal stethoscope catheter.
Modifications have continued; now probes are capable of:
– Doppler technology, including color flow Doppler (CFD)
– M-mode, 2D, and 3D
• The National Board of Echocardiography provides two main types of perioperative TEE
certification:
– Advanced certification (since 2004)
– Basic certification (since 2009)
• Doppler technology provides measurement of the velocity of red blood cells traveling within
the heart.
• The simplified Bernoulli equation provides an estimation of the pressure gradient between 2
chambers of the heart. This equation utilizes the velocity measured by Doppler technology.
Δp = 4 (v2)
– Specifically, the simplified Bernoulli equation can be used to estimate the right ventricle
systolic pressure (RVSP) by measuring the velocity of the tricuspid regurgitation jet:
RSVP (PASP) = 4vTR2 + RAP; were PASP is pulmonary artery systolic pressure and RAP
is right atrial pressure.
– Another example of the utility of the simplified Bernoulli equation is in the evaluation of
the gradient across a potentially stenotic AV. The pressure gradient between the LVOT and
the AV can be estimated by measuring the velocity in the aorta.
– Color Doppler technology provides estimation of blood flow direction. Blood flowing
toward the transducer is depicted as red; blood flowing away from the transducer is
depicted as blue.
– BART: This mnemonic helps to remember the direction of blood flow in relation to the
TEE probe: Blue Away, Red Towards
ANATOMY
A comprehensive examination can be performed based on the images outlined by Shanewise
et al. These 20 images will allow a complete intraoperative examination. If adequate time is
not available for a complete examination (i.e., in emergency situations), an abbreviated
examination can be performed in order to obtain information from the 8 images listed below.
• Chamber dimension: Abnormal chamber size can be associated with pathologic conditions.
For example, increased left atrial size is seen in severe mitral regurgitation.
• LV function: There are many measurements of LV function including Simpson’s method of
discs, stroke volume, fractional area change, strain technology and tissue Doppler velocity.
One of the simplest ways to determine a rough estimate of EF is by estimating endocardial
thickening and excursion in the transgastric (TG), left ventricle (LV), midpapillary, sagittal
views (SAX). This view is also helpful in evaluating ischemia as it represents perfusion from
the 3 main coronary arteries.
• Volume status: Gross LV filling can be estimated by using end-diastolic LV chamber size
most often evaluated at the TG LV mid pap SAX view.
• Valvular evaluation: A complete evaluation requires baseline knowledge of normal valve
anatomy so as to diagnose abnormal anatomy by 2D Echo. This is corroborated with
Doppler (CFD or Spectral) across the valve. Utilization of 2D echo and Doppler technology
allows a detailed examination to evaluate the following (structure and function) in a native
and/or prosthetic valve (e.g., the presence/absence of normal washing jets or abnormal
perivalvular leaks).
• Aortic evaluation: The evaluation of the aorta should include interrogation for plaque,
dissection, aneurysms, and thrombus from the root to the descending thoracic aorta (with
the exception of the distal ascending and arch which cannot be imaged well due to
interposition of left main stem bronchus as air prevents ultrasound penetration at that site).
• Additional utility: Pleural effusions, pericardial effusions, and intracardiac masses can also
be evaluated. Central venous pressure can also be estimated using the IVC diameter (ratio
between inspiration and expiration). Specific signs of tamponade physiology from
pericardial effusion include RA diastolic collapse and decreased RV filling.
• Congenital: TEE is an invaluable tool in imaging cardiac anatomy in adult patients after
complex congenital reconstruction who may be presenting for cardiac surgery as an adult.
According to the 2010 ASA/SCA Guidelines, the indications can be classified by setting:
• Cardiac
– “For adult patients without contraindications, TEE should be used in all open heart (e.g.,
valvular procedures) and thoracic aortic surgical procedures and should be considered in
coronary artery bypass graft surgeries.”
• Noncardiac
– “TEE may be used when the nature of the planned surgery or the patient’s known or
suspected cardiovascular pathology might result in severe hemodynamic, pulmonary, or
neurologic compromise.”
– “If equipment and expertise are available, TEE should be used when unexplained life-
threatening circulatory instability persists despite corrective therapy.”
• ICU
– “For critical care patients, TEE should be used when diagnostic information that is
expected to alter management cannot be obtained by transthoracic echocardiography or
other modalities in a timely manner.”
– Three causes of hypotension that TEE is useful to manage:
Hypovolemia
Ischemia (best view: TG LV mid pap SAX)
Tamponade
– Regional wall abnormalities can be assessed:
Normal: >30%
Hypokinetic: <30%
Akinetic: No movement
Dyskinetic: Paradoxical systolic movement
• Contraindications (ultimately, these are based on one’s clinical judgment)
– Absolute
Previous esophageal surgery
Stricture
Tracheoesophageal fistula
Esophageal trauma
Zenker’s diverticulum
Colonic interposition
– Relative
Barrett’s esophagus
Hiatal hernia
Large descending aortic aneurysm
Unilateral vocal cord paralysis
Esophageal varices
Postradiation therapy
Previous bariatric surgery
• Complications are rare, but include:
– Esophageal perforation
– Esophageal injury
– Hematoma
– Laryngeal palsy
– Dysphagia
– Dental injury
– Death
• Artifacts
– There are many types of well-known ultrasound artifacts. The details of these can be found
in the references.
REFERENCES
1. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2003 guideline update
for the clinical application for echocardiography: Summary article: A report of the
American College of Cardiology/American Heart Association task force on practice
guidelines (ACC/AHA/ASE committee to update the 1997 guidelines for clinical
application of echocardiography). J Am Coll Cardiol. 2003;42:954–970.
2. Hilberath JN, Oakes DA, Shernan, et al. Safety of Tranesophageal Echocardiography. J Am
Soc Echocardiogr. 2010;23:1115–1127.
3. Nishimura RA, Miller FA Jr, Callahan MJ, et al. Doppler echocardiography: Theory,
instrumentation, technique, and application. Mayo Clin Proc. 1985;60(5):321–343.
4. Oka Y. The evolution of intraoperative transesophageal echocardiography. Mt Sinai J Med.
2002;69:18–20.
5. Quiñones MA, Otto CM, Stoddard M, et al. Doppler Quantification Task Force of the
Nomenclature and Standards Committee of the American Society of Echocardiography
Recommendations for quantification of Doppler echocardiography: A report from the
Doppler Quantification Task Force of the Nomenclature and Standards Committee of the
American Society of Echocardiography. J Am Soc Echocardiogr. 2002;15(2):167–184.
6. Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA Guidelines for performing a
comprehensive intraoperative multi-plane transesophageal echocardiography examination:
Recommendations of the American Society of Echocardiography and the Society of
Cardiovascular Anesthesiologists task force for certification in perioperative
transesophageal echocardiography. Anesth Analg. 1999;89:870–884.
7. Thys DM, Abel MD, Brooker RF, et al. Practice Guidelines for Perioperative TEE: An
Updated Report by the American Society of Anesthesiologists (ASA) and the Society of
Cardiovascular Anesthesiologists (SCA) Task Force on TEE. Anesthesiology. 2010;112:1084–
1096.
8. www.echoboards.org
• Aortic stenosis
• Pericardial tamponade
CLINICAL PEARLS
• It is important to note that the ASA/SCA perioperative guidelines specifically state that
“proficiency…is of paramount importance due to risk of adverse outcomes resulting from
incorrect interpretation.”
INTRARENAL ACUTE KIDNEY INJURY
Andaleeb Abrar Ahmed, MBBS, MD, MPH
Jill Eckert, DO
BASICS
DESCRIPTION
• Acute renal failure (ARF), also known as acute kidney injury (AKI), is a common syndrome
characterized by a rapid decline in glomerular filtration rate (GFR), accompanied by
azotemia with, or without, oliguria. It is divided into three categories:
– Prerenal. Impaired blood flow to the kidney
– Intrarenal. Disease processes involving renal parenchymal tissue (may also result from
prerenal causes).
– Postrenal. Impaired movement of urine out of the kidneys.
• Prevention and management of intrarenal ARF involves careful preoperative assessment,
avoidance of nephrotoxic agents, maintenance of normovolemia, and close perioperative
monitoring.
EPIDEMIOLOGY
Prevalence
• 1% of all patients undergoing general surgery develop postoperative AKI.
• 1%–7% of patients with perioperative AKI require renal replacement therapy.
• 35–40% cases of AKI can be attributed to intrarenal causes.
Prevalence
• 5–7% of hospital admissions and 30% of intensive care unit (ICU) admissions carry a
diagnosis of AKI.
• Acute tubular necrosis (ATN) accounts for 85% of intrinsic AKI.
• Contrast-induced nephropathy (CIN) is the 3rd most common cause of AKI in hospitalized
patients.
Morbidity
AKI is also associated with prolonged length of hospital stay and increased healthcare cost
(1).
Mortality
• Postoperative AKI worsens long-term survival in patients with normal baseline renal
function (1).
• AKI after noncardiac surgery is an independent predictor of hospital mortality.
• AKI in the critical care setting has a mortality of 50% or higher.
• Causes of intrinsic AKI can be conceptually divided into four categories
– Acute tubular necrosis
Ischemia from hypotension or shock
Nephrotoxic agents. Exogenous agents including NSAIDs, radiocontrast agents,
angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists,
antimicrobials such as aminoglycosides, amphotericin B, antiretrovirals. Endogenous
agents such as rhabdomyolysis.
– Tubulointerstitial disease
Allergic interstitial nephritis (AIN) from antimicrobials (penicillin, cephalosporin,
sulphonamide), NSAIDS, proton pump inhibitors, anticonvulsants (phenytoin, valproate)
Infection (bilateral pyelonephritis)
Infiltration (leukemia, sarcoidosis, lymphoma, myeloma, uric acid)
– Diseases of large renal vessels
Renal artery obstruction (atherosclerotic plaque, thrombosis, emboli, vasculitis,
cholesterol embolization)
Renal vein thrombosis, or compression
– Diseases of the glomeruli and microcirculation
Glomerulonephritis
Vasculitis, collagen vascular disease
Microangiopathic disorder (hemolytic uremic syndrome, thrombotic thrombocytopenic
purpura, preeclampsia)
Malignant hypertension (HTN)
• Patient risk factors include
– Comorbidities (heart failure, liver failure, diabetes, chronic kidney disease)
– Advanced age
– Sepsis
– Preoperative renal insufficiency
– Prolonged hypovolemia
– High ASA score status (3,4)
• Surgical/procedure related factors include
– Emergent surgery
– Intra-abdominal surgery
– Cardiac surgery
– Vascular surgery
– Aortic cross-clamping or occlusion of the inferior vena cava (IVC)
– Intra-aortic balloon counterpulsation
– Organ transplantation
• Three-phase sequence
– Initiation: Characterized by an acute decrease in GFR and increase in creatinine (Cr) and
BUN.
– Maintenance: Demonstrates a sustained severe reduction in GFR; variable length of time
(1–2 weeks); BUN and Cr continue to rise.
– Recovery: Characterized by an increase in urine volume and by a gradual decrease in
BUN, Cr to preinjury levels.
• GFR. An acute decline in GFR is a hallmark of AKI. Proposed mechanisms include
– Reduced glomerular filtration pressure due to renal autoregulatory disruption.
– Back-leak of glomerular filtrate due to disruption of normal tubular epithelium.
– Luminal obstruction due to epithelial cell sloughing.
• Histopathology. Microvascular inflammation, apoptosis, and endothelial cell dysfunction
play a major role in the pathophysiology of AKI. Proximal tubular epithelium demonstrates
obliteration from necrotic cells that lack a nucleus. However, the basement membrane
remains intact, so tubular epithelium regeneration is possible.
• Any anesthetic technique causing a reduction in BP will decrease GFR, renal blood flow, and
urine formation. Carefully titrated neuraxial anesthesia that achieves a sympathetic block to
the T4 to T10 level may be beneficial in diminishing the renal vasoconstrictive response
from sympathoadrenal stimulation. However, hypotension secondary to neuraxial
anesthesia may impair renal perfusion.
• Except for aiding diuresis, loop diuretics, and mannitol have no role in preventing or
treating ARF.
• Whenever possible, low or iso-osmolar, nonionic contrast media should be considered.
• History
– ATN: Exposure to nephrotoxic agents; recent surgery, hemorrhage, or hypotension; history
of chronic renal insufficiency; evidence of sepsis, or pyelonephritis; history suggestive of
rhabdomyolysis (trauma, drug abuse, seizure, urine color), tumor lysis syndrome (recent
chemotherapy), myeloma (bone pain), or hemolysis (recent blood transfusion).
– AIN: Recent drug use, fever, rash, or arthralgia.
– Malignant HTN: Headache, neurological dysfunction, heart failure, papilledema.
– Atheroembolism: Vascular procedure, atrial fibrillation, thrombolysis, or anticoagulation.
– Glomerulonephritis/vasculitis: Edema, sinusitis, hematuria, hemoptysis, HTN, recent
infection, and rash.
• Symptoms are usually absent, mild, or nonspecific in the early stages of ARF.
• Urine analyses (U/A)
– Muddy brown casts and tubular epithelial cells: ATN
– White cell casts/eosinophiluria: Pyelonephritis, interstitial nephritis, cholesterol emboli
– Red blood cell (RBC) casts: Glomerulonephritis
– Crystalluria: Drug toxicity, tumor lysis syndrome
– Brown waxy casts: Chronic renal failure
– Bacteria: Pyelonephritis
– Proteinuria: Glomerulonephritis, thrombotic microangiopathy, cholesterol emboli,
nephrotic syndrome, vasculitis, AIN, malignant HTN, and renal vein/artery thrombosis.
– Hematuria: Glomerulonephritis, renal vein/artery thromboses, vasculitis.
• Serum creatinine (Cr), BUN, urine indices
– Serum BUN/Cr ratio >20:1, likely prerenal; <20:1, likely ATN (4).
– Urine sodium (mEq/L): <20, likely prerenal; >40 likely ATN (4)
– Fractional excretion of sodium (FENa) (%): FENa = [(UNa × PCr)/(PNa × UCr)] × 100,
where U = urine, P = plasma, Na = sodium, Cr = creatinine. If FENa <1%, likely
prerenal; if FENa >2%, likely intrarenal (4)
– Fractional excretion of urea (FEurea) (%): FEurea = [(Uurea × PCr)/(PBUN × UCr) × 100.
FEurea <35% is suggestive of prerenal etiology.
– Urine osmolality (mOsmol/kg): >500, likely to be prerenal; <400, likely ATN (4).
– Urine/Plasma creatinine (UCr/PCr): >40, likely prerenal; <20, likely ATN.
• Assessment of GFR
– Creatinine clearance (ml/min) is commonly used to estimate GFR.
– Creatinine clearance = (UCr × Uv)/PCr, × 1440, where Uv is 24-hour urine volume in mL.
– GFR is estimated using the Modification of Diet in Renal Disease (MDRD), or Cockcroft–
Gaut equation.
• Renal ultrasound: To assess kidney size, renal parenchyma and rule out urinary obstruction
• Serum electrolytes, arterial blood gas (ABG), CBC, EKG
• Prerenal acute kidney failure
• Postrenal acute kidney failure
TREATMENT
• Nephrology consultation may be needed for management of dyselectrolytemia, severe

azotemia, or refractory volume overload. Hemodialysis (HD), continuous renal replacement
therapy, and ultrafiltration may be considered.
• Early goal-directed resuscitation for sepsis
• Protein restricted, low potassium diet
• CIN: N acetyl cysteine (600 mg PO BID), IV NaHCO3
• Metabolic acidosis: Bicarbonate
• Malignant HTN and preeclampsia: BP control
• Uremic bleeding: Desmopressin
• “Renal dose” dopamine and fenoldopam is unlikely to be beneficial.
FOLLOW-UP
• Complications of ARF include death, arrhythmias, volume overload, hyperkalemia,

metabolic acidosis, infection, pericarditis, platelet dysfunction, bleeding, anemia, and long-
term renal replacement therapy.
• ICU may be required for closer hemodynamic monitoring.
REFERENCES
1. orthwick E, Ferguson A. Perioperative acute kidney injury: Risk factors, recognition,
management, and outcomes. BMJ. 2010;341:c3365.
2. ehta RL, Kellum JA, Shah SV, et al. Acute kidney injury network: Report of an initiative to
improve outcomes in acute kidney injury. Crit Care. 2007;11:R31.
3. Bentley ML, Corwin HL, Dasta J. Drug-induced acute kidney injury in the critically ill
adult: Recognition and prevention strategies. Crit Care Med. 2010;38(6 Suppl):S169–174.
4. Esson ML, Schrier RW. Diagnosis and treatment of acute tubular necrosis. Ann Intern Med.
2002;137(9):744–752.
• Prerenal acute kidney failure
• Postrenal acute kidney failure
CODES
ICD9
584.9 Acute kidney failure, unspecified
ICD10
N17.9 Acute kidney failure, unspecified
CLINICAL PEARLS
Patients with ARF should have nonemergent surgery delayed until improvement has
occurred. If necessary to proceed:
• Nephrotoxic drug exposure should be avoided in the perioperative period (e.g.,
aminoglycosides and ketorolac).
• Volume status. Maintain normal volume status and consider placement of invasive monitors
to aid with management (e.g., arterial line, central line, or pulmonary artery catheter).
Diuretics should be avoided until adequate intravascular volume has been achieved.
• Renally cleared drugs can have a prolonged duration of action (e.g., benzodiazepines).
Additionally, active metabolites of morphine (morphine-6-glucuronide) and meperidine may
accumulate, causing prolonged activity. Fentanyl and hydromorphone may be better
alternatives.
• Muscle relaxants. Succinylcholine should be avoided in patients with hyperkalemia or
unknown potassium levels. Cisatracurium and atracurium have organ-independent
clearance and should be considered. Additionally, hyperkalemia may increase the effects of
depolarizing muscular blockers and opposes the action of nondepolarizing muscular
blockers.
• Antibiotics. Adjust according to the estimated GFR.
• Labs. Frequent electrolytes and ABGs should be considered.
• Avoid potassium containing solutions such as lactated Ringer’s. Packed red blood cells
contain ∼4 mEq/unit and can increase with storage time (caution with multiple or older
units).
• Postoperative mechanical ventilation and ICU admission may be required.
INTUBATION/EXTUBATION CRITERIA
BASICS
DESCRIPTION
• In the US, 1–3 million patients annually require intubation and mechanical ventilation
outside of the OR. This decision typically stems from the need to maintain airway patency,
protection against aspiration, or provide oxygenation and ventilation for pathologic
pulmonary processes.
– In the OR, intubation is typically dependent on the surgical procedure and patient
comorbidities; apnea or respiratory depression is drug-induced.
• The decision to extubate is of considerable consequence, as delayed extubation is associated
with increased duration of mechanical ventilation and increased mortality. Criteria include
subjective, as well as objective parameters.
– However, because intubation is typically performed to facilitate the surgical procedure,
extubation criteria centers around adequate reversal of neuromuscular blocking drugs and
the return of airway reflexes from perioperative medications.
• Normal breathing is described as negative pressure ventilation. The diaphragm and chest
wall generate negative intrapleural pressures by moving caudally and with chest wall
expansion, respectively. Air movement, with resultant lung expansion, results from the
creation of a pressure gradient from the oropharynx to the alveoli.
• Mechanical ventilation, on the other hand, is described as positive pressure ventilation
(PPV), and has effects on the pulmonary and cardiovascular system.
• Pulmonary effects of mechanical ventilation may include
– Improvement in oxygenation, lung compliance, and V/Q matching
– Increased functional residual capacity (FRC) with resultant decreases in shunt and
improved oxygenation.
– Decreased work of breathing (WOB)
– Improved respiratory acidosis
• Cardiovascular effects of mechanical ventilation may include
– Improve cardiac function in patients with cardiac dysfunction by improving arterial
content of oxygen to the coronaries.
– Decreased ventricular afterload from increased intrathoracic pressures
ANATOMY
• The larynx is a cartilaginous skeleton with ligaments and muscle. There are nine cartilages
including the thyroid, cricoid, epiglottis, arytenoids (paired), corniculate (paired), and
cuneiform (paired).
• Sensory innervation
– Nose mucous membrane: Ophthalmic branch (V1) and the maxillary branch (V2) of the
trigeminal nerve
– Hard and soft palate: Palatine nerves from the trigeminal nerve
– Anterior 2/3rd of tongue: Lingual nerve; a branch of the mandibular branch (V3) of the
trigeminal
– Posterior 1/3rd of tongue: Glossopharyngeal nerve (CN IX)
– Sensation of taste: Anterior 2/3rd by the facial nerve (CN VII), posterior 1/3rd by the
glossopharyngeal nerve
– Below the epiglottis to above the vocal cords: Internal branch of the superior laryngeal
nerve (SLN), a branch of the vagus (CN X)
– Below the vocal cords: Recurrent laryngeal nerve (RLN), a branch of the vagus nerve
• Motor innervation
– Cricothyroid muscle (vocal cord adductors): External branch of the SLN.
– All other muscles of the larynx: RLN (posterior cricoarytenoid muscle is an abductor, the
remaining muscles are all vocal cord adductors).
• Blood supply is via branches of the thyroid arteries. The external carotid artery gives rise to
the superior thyroid artery that branches to the cricothyroid artery. During cricothyrotomy,
it is best to stay midline to avoid these vessels.
• Intubation complications include airway trauma, physiologic responses like hypertension,
tachycardia, increased ocular pressures, arrhythmias, aspiration, and tube malposition.
• Mechanical ventilation (PPV) complications include
– Decreased cardiac output (CO) from diminished venous return; increased intrathoracic
pressure decreases end-diastolic volume and stroke volume of both ventricles.
– Increased pulmonary vascular resistance (PVR) resulting in increased right ventricular
load; this may limit left ventricular distensibility and CO.
• Extubation complications include hypertension, tachycardia, arrhythmias, coughing, breath
holding, laryngospasm, airway obstruction, aspiration, increased ocular pressure, sore
throat tracheomalacia, and laryngotracheal stenosis.
• Vocal cord dysfunction may require intubation to maintain a patent airway
– Bilateral paralysis of the SLN: Hoarseness and easy tiring of voice. No airway compromise.
– Bilateral partial transection: The abductor portion is more prone to injury and results in
unopposed adduction. The vocal cords meet in the midline and cause complete airway
obstruction.
– Bilateral paralysis of the vagus nerve: Affects both SLN and RLN with resultant flaccid,
midpositioned vocal cords. Airway control is not a problem, but phonation is affected
significantly (neuromuscular blocking drugs).
• General intubation criteria (any 1 of the following):
– Cardiac or respiratory arrest
– Loss of consciousness
– Hemodynamic instability <70 mm Hg
– PaO2 <45 mg despite supplemental oxygen
• Objective intubation indications (≥2 of the following, in the context of respiratory distress):
– Respiratory rate (RR) >35/min or <6/min
– Oxygen desaturation <90% despite adequate supplemental oxygen
– Tidal volume (VT) <5 mL/kg
– Vital capacity <15 mL/kg
– SBP <90 mm Hg
– pH <7.20 and decreased from onset
– PaCO2 >50 mm Hg
– Alveolar-arterial gradient (A-a gradient) >350 mm Hg on 100% O2
• Intubation indications in the intensive care unit (ICU)
– Airway patency
– Aspiration protection
– Tracheobronchial toilet
– Route for airway pressure therapy
– Neurological: central loss of ventilatory drive, spinal cord injury, brain injury, Guillain–
Barré syndrome (GBS), phrenic nerve injury
– Chest wall: flail chest, rib fractures
• Intubation indications in the OR settings
– Airway control
– Unobstructed leak-free airway for prolonged ventilation
– Thoracoabdominal surgery
– Head and neck surgery
– Risk of aspiration
– Positioning (prone, lateral decubitus)
– Resuscitation of the moribund patient
– Preemptive utility if feared that ventilation/intubation may later become impossible.
• Weaning from extubation should be considered as early as possible in both the ICU and the
OR. In the ICU, the majority are successfully weaned on first attempt (physicians frequently
underestimate the ability of patients to be successfully weaned). In the ICU, the initial
weaning is a two-step process and begins with assessment of readiness to wean, followed by
suitability to extubate.
• Readiness to wean
– Clinical assessment for an intact cough reflex, absence of excessive tracheobronchial
secretions, and resolution of acute phase of disease causing the intubation
– Objective assessment with a rapid shallow breathing index (RSBI). It is calculated as
RR/VT. A value of <100–105 breaths/min/L predicts successful spontaneous breathing
test (SBT) with a sensitivity of 0.97 and specificity of 0.65.
• Suitability to extubate can be assessed objectively with the SBT. The initial SBT should last
for 30 minutes and consists of T-tube breathing or low levels of PS (5–8 cm H2O) with or
without 5 cm H2O PEEP while making assessments of
– Adequate mentation
– Stable cardiovascular status (heart rate (HR) ≤140 bpm, SBP 90–160 mm Hg, minimal or
no vasopressors)
– Stable metabolic status
– Adequate oxygenation
SaO2 >90% on fraction of inspired oxygen (FiO2) ≤40% or PaO2/FiO2 ≥150 mm,
PEEP ≤8 cm H20
– Adequate ventilation
RR ≤35 breath/min
Mean inspiratory pressure (MIP) ≤20–25 cm H2O
VT >5 mL/kg
Vital capacity >10 mL/kg
• Failed SBT criteria include
– RR >35 breaths/minute for >5 minutes
– SaO2 <90% for >30 seconds or PaO2 ≤50–60 mm Hg on FiO2 ≥50%
– PaCO2 >50 mm Hg
– HR >140 bpm
– SBP >180 or <90 mm Hg
– pH <7.32
– Increased WOB, cyanosis
– Agitation, anxiety
– Depressed mental status
– Cardiac arrhythmias
• Causes of failed SBTs include
– Psychological dysfunction (anxiety, agitation, delirium)
– Infections
– Electrolyte abnormalities
– Respiratory load (COPD, asthma, pulmonary edema, infiltrates, secretions, edema)
– Cardiac load (ischemia, increased metabolic demand, CHF, anemia)
– Nutrition (deconditioning, malnutrition, obesity)
– Neuromuscular disease (depressed central drive, GBS, myasthenia gravis)
– Endocrine (hypothyroidism, hyper/hypoglycemia, adrenal insufficiency)
• Pressure support ventilation (PSV) as a weaning mode after a failed SBT has strong support
in the literature. The literature does not support the use of synchronized intermittent
mandatory ventilation (SIMV) alone for weaning. Little data exists for the use of SIMV/PSV
combined.
• Noninvasive ventilation may shorten the duration of intubation in patients with hypercapnic
respiratory failure. However, in hypoxic respiratory failure, it could be used with caution in
the event of extubation failure.
• Cuff-leak test involves deflating the cuff or occluding the ETT, and observing if the patient
can breathe around the tube.
– Failed leak test does not mean failed extubation, but that if extubation is performed, they
may require close monitoring.
– A positive leak test does not guarantee successful extubation.
• Reasons not to extubate, even when the patient meets extubation criteria include unstable C-
spine, inability to protect airway, likely to return to the OR, and potentially difficult
reintubation.
• Tracheostomy may be required in patients who fail extubation, as prolonged intubation may
cause airway edema and injury.
– Advantages include decreased WOB, comfort, patient communication, and pulmonary
hygiene.
– Disadvantages include risk of tracheal stenosis, infection, and procedure related
complications.
• Extubation criteria in the OR has unique challenges of its own
– Adequate oxygenation
– Adequate ventilation
– Full reversal of neuromuscular blockage (5 second head lift, train-of-four, sustained
tetany)
– Hemodynamic stability
– Mental status intact
– Return of reflexes (cough, gag)
– Adequate acid–base status
– Normothermia
– Adequate pain control
– Stable metabolic status
– Adequate volume status
– Electrolytes
• Potential difficult extubations postoperatively include
– History of a difficult intubation
– Sleep apnea
– Airway edema
– Postsurgical complications from thyroid surgery (RLN injury risk), diagnostic
laryngoscopy, uvulopalatoplasty, carotid endarterectomy (hematoma, nerve palsies),
cervical spine procedures, and maxillofacial surgery.
EQUATIONS
RSBI = RR/tidal volume (VT)
REFERENCES
1. oles JM, Bion J, Connors A, et al. Weaning from mechanical ventilation. Eur Respir J.
2007;29(5):1033–1056.
2. acIntyre NR, Cook DJ, Ely EW Jr, et al. Evidence-based guidelines for weaning and
discontinuing ventilatory support: A collective task force facilitated by the American
College of Chest Physicians; the American Association for Respiratory Care; and the
American College of Critical Care Medicine. Chest. 2001;120(6 Suppl):375S–395S.
3. ongnecker DE, Brown DL, Newman MF, et al. Anesthesiology, 1st edn. New York: McGraw
Hill, 2008, Chapter 83.
ADDITIONAL READING
• Miller RD, Fleisher LA, et al. Miller’s Anesthesia, 6th edn. Philadelphia: Elsevier Churchill
Livingstone, 2005, Chapter 75.
• Tracheostomy
CLINICAL PEARLS
• The incidence of unplanned extubation ranges from 0.3% to 16%, 83% of which are
initiated by the patient. Almost half of patients who self-extubate do not require
reintubation.
• SBTs do not guarantee that the patient will remain extubated, especially if the airway is
unstable or the patient is unable to clear secretions.
• If intubation was difficult, airway edema should be suspected.
JET VENTILATION
Huafeng Wei, MD, PhD
BASICS
DESCRIPTION
• Method of ventilation that is characterized as an open system, with high frequency, and low
tidal volumes.
• Inspiration is characterized as positive pressure, jet pulsed breaths delivered via a jet nozzle.
Exhalation occurs passively and around the jet nozzle; there is no dedicated expiratory limb.
• Jet ventilation may be performed supraglottically, infraglottically, or transtracheally.
Furthermore, it can be delivered manually or by automatic devices.
• Anesthesia providers utilize jet ventilation when the operative field needs to be shared or
still; or in the formidable “cannot ventilate, cannot intubate” difficult airway.
• Distinguishing and desirable features of jet ventilation include an open system, high
frequency, and low tidal volumes.
– Open system for inspiration and exhalation. The internal diameter (ID) of the jet nozzle is
small and does not “seal” the airway (unlike the endotracheal tube (ETT) cuff).
Furthermore, there is no dedicated expiratory limb (unlike controlled mechanical
ventilation (CMV)); instead air egresses out and around the nozzle. Additionally, the jet
pulsed inspiratory breaths entrain air via the Venturi effect (high speed pulses generate
negative pressures on the gas flow edge that drags air or oxygen from the opening
environment into the airway).
– High frequency (>60 breaths/minute). Results in “auto-PEEP” (positive end-expiratory
pressure) from air trapping and subsequent alveolar opening; without this effect, the low
tidal volumes generated would not be able to insufflate alveoli and optimize V/Q
matching. Thus, this is a desired effect that increases airway pressures (Paw) and PaO2, but
at the risk of hypercapnia and barotrauma.
– Low tidal volumes. Correspond to low peak airway pressures (PIP) and intrathoracic
pressures, with resultant increases in venous return.
• Components of jet ventilation include a gas source, jet valve, and jet nozzle.
– Gas source: Oxygen or oxygen mixed with air from either a wall source or cylinder.
– Jet valve: Electronically or manually controlled valve to generate jet pulses when it opens
and closes. Gas passes intermittently through the valve to produce jet pulses at different
frequency.
– Jet nozzle: Any tubing with an ID around 2 mm to deliver jet pulses from the jet valve.
These are usually disposable compliant tubes at various lengths (e.g., 14G or 16G
angiocatheter, transtracheal jet catheter, Cook tube exchanger, and soft suction catheter).
• Working parameters and settings include respiratory frequency, driving pressure, inspiration
time, FiO2, and humidification.
– Respiratory frequency: 15–150 breaths/minute. As frequency is increased, exhalation time
is reduced and can result in physiologically beneficial auto-PEEPing. Air build-up, due to
insufficient time for exhalation, results in alveolar opening with consequent improvements
in V/Q matching and oxygenation. High frequencies result in reduced chest wall
excursions, thereby providing a more “still” surgical field. However, the shorter exhalation
times combined with the smaller tidal volumes compared to CMV results in less CO2
elimination (hypercarbia) and greater dead space ventilation (inefficient ventilation).
– Driving pressure refers to the pressure applied to the jet valve. In adults, settings usually
start at ~20–25 Psi, with a maximum of 50 Psi. Driving pressure is a major determinant of
tidal volume; increases result in higher tidal volumes and minute ventilation.
– Inspiration time is typically set at 30–40%. It dictates the time spent in insufflation versus
exhalation. By increasing this value, tidal volumes and oxygenation (due to reduced
exhalation time and auto-PEEPing) are increased
– FiO2: Is set at 100% and is the oxygen concentration at the jet nozzle. The actual FiO2 is
significantly less in the alveoli due to Venturi effects and the open system (Figure 1)
FIGURE 1. Venturi effect entrains room air at the level of the jet nozzle.
– Humidification: For prolonged use of jet ventilation, gas from jet pulses should be
humidified to avoid airway mucus membrane damage or formation of airway mucus clot
and airway obstruction.
• Monitoring during jet ventilation is limited because it is an open system. The following
cannot be accurately monitored or measured.
– FiO2. Decreases along the axis of the airway towards alveoli due to air entrance from
Venturi effects. The entrained air from the surrounding opening system mixes with and
dilutes the injected oxygen from the jet valve. This decreases the actual oxygen at the
alveolar gas exchange site.
– Partial pressure of end-tidal of carbon dioxide (PetCO2). Varies along the axis of the
airway due to the opening system.
– Airway pressure. Increases along the axis of the airway due to air trapping, especially at
high frequency.
– Tidal volume. Primarily depends on the driving pressure.
ANATOMY
Approaches of jet ventilation include supraglottic, infraglottic, and transtracheal.
• Supraglottic jet ventilation (SJV). Jet nozzle is positioned above the vocal cords with the air
aimed toward the glottic opening. Non-invasive and may have less incidence of barotrauma
compared to other approaches; additionally, faster to set up. Can be utilized in “cannot
intubate, cannot ventilate” and difficult airway scenarios as well as in upper GI endoscopy
cases. Also applicable to when the jet ventilator is attached to an LMA adaptor.
• Infraglottic jet ventilation. Jet nozzle is positioned below the vocal cords. Has less ambient
air entrainment (from Venturi effect) and possibly sore throat than supraglottic access.
Utilized when sharing the airway; additionally, also applicable to when the jet ventilator is
attached to an ETT adaptor
• Transtracheal jet ventilation (TTJV). Jet nozzle is attached to cricothyroidotomy access.
Invasive and higher risk of barotrauma (up to 10% in emergent airway access). Utilized in
“cannot ventilate, cannot intubate” scenarios; however, must be avoided in complete upper
airway obstruction to prevent barotrauma.
• Barotrauma occurs when pressure builds up in a closed tissue pocket, similar to when a
balloon is constantly blown up until it eventually ruptures. The high-pressure system can
result in injuries including pneumothorax, pneumomediastinum, and subcutaneous
emphysema. Avoid jet ventilation in known barotrauma or where there is upper airway
obstruction that would preclude gas egress/exhalation. Additionally, some suggested
preventative measures include
– Begin to learn and use jet ventilation in elective cases rather than during emergent TTJV
– Keep the airway system open and avoid pressure building up in a closed tissue pocket
– Consider using noninvasive jet ventilation (supraglottic)
– Implement low driving pressures (<25 Psi), low frequency (<120 breaths/minute)
• Hypercapnia. Worsened with high-frequency jet ventilation, particularly in obese patients,
reduced chest wall compliance, or COPD with increased baseline CO2 levels. Consider
switching to CMV periodically to check PetCO2 to avoid hypercapnia or hypocapnia. Can
check ABG if arterial line is available. May be treated by increasing tidal volumes (increase
driving pressure or inspiratory time, or decrease respiratory rate).
• Insufficient oxygenation can result from insufficient alveolar expansion (insufficient
ventilation). Seen more commonly in patients with baseline pulmonary disease. May be
prevented by increased FiO2, driving pressure, or inspiratory time. Adding ambient oxygen
can increase the delivered FiO2.
• Inadequate humidification may result in necrotizing tracheobronchitis and mucus clot-
mediated airway obstruction. Use humidification methods if available especially for
prolonged use of jet ventilation. (Current clinical studies do not identify an agreed upon
time point).
• With its three features of open system, high frequency, and small tidal volumes, jet
ventilation is often utilized to support respiration and perform mechanical ventilation in
certain clinical scenarios.
• Open systems
– “Cannot ventilate, cannot intubate” emergent airway. Included in the ASA difficult airway
algorithm. TTJV is comparatively faster, easier to perform, and more often used than
emergent tracheostomy. A cricothyroidotomy is performed with either a commercially
available cricothyroidotomy needle or a 14G or 16G angio catheter.
– GI endoscopy; SJV via a nasal airway allows oxygenation and ventilation without
intubating or other airway devices that are invasive or preclude endoscopy.
– Difficult airway management. Allows oxygenation while a definitive airway is attained, as
during the process of tracheal intubation under direct laryngoscopy or a fiberoptic
bronchoscopy.
– ENT cases with an open airway such as rigid bronchoscopy, vocal cord, or other upper
airway surgeries. During surgical procedures of the upper respiratory tract, surgeons and
anesthesia providers must share the airway, and the use of an ETT may obscure access to
the surgical site; conversely, surgical instruments can preclude tight sealing of the airway.
High-frequency jet ventilation (HFJV) is used to continuously or intermittently provide
oxygenation and ventilation.
– Thoracic or pulmonary cases such as one lung ventilation, bronchofiberoptic examination
or resection of airway tumors, tracheal resection, bronchopleural fistulas
• High frequency to provide oxygenation with minimal diaphragm movement
– Electrophysiology procedures such as atrial fibrillation or atrial flutter ablations. Less
movement allows for more precise mapping and ablation. May reduce the operating time
relatively.
– Shock wave lithotripsy. CMV or SV via an LMA can result in significant respiratory
movement and is akin to hitting a “moving target.” Jet ventilation may be implemented at
high frequency and therefore minimize the diaphragm movement and provide optimistic
environment for lithotripsy.
• Low tidal volume and low intrathoracic pressure. Serves to minimize interference with
venous return and may improve hemodynamic in patients with hypovolemia or shock. HFJV
(RR at 100/min) seems to be better than CMV to maintain BP and cardiac output during
hypovolemia in animal studies. Synchronization of the heart rate with breathing using the R
wave of the EKG to trigger jet ventilation has been shown to improve cardiac function in
animal studies.
• Total IV anesthetic technique is utilized to maintain general anesthesia when utilized in this
capacity. A balanced technique utilizing sedatives, opioids, or muscle relaxants may be
utilized depending on the case specifics and the needs.
REFERENCES
1. ourgain JL, Desruennes E, Fischler M, et al. Transtracheal high frequency jet ventilation for
endoscopic airway surgery: A multicenter study. Br J Anaesth. 2001;87(6):870–875.
2. hra G, Gockner G, Kashanipour A, et al. High-frequency jet ventilation in European and
North American institutions: Developments and clinical practice. Eur J Anaesthesiol.
2000;17(7):418–430.
3. Wei HF. A new tracheal tube and methods to facilitate and placement in emergency airway
management. Resuscitation. 2006;70:438–444.
4. ezaie-Majd A, Bigenzahn W, Denk D, et al. Superimposed high-frequency jet ventilation
(SHFJV) for endoscopic laryngotracheal surgery in more than 1500 patients. Br J Anaesth.
2006; 96:650–659.
5. Peng J, Ye J, Zhao Y, Liang J, Huang H, Wei H, Peng S. Supraglottic jet ventilation in
difficult airway management. J Emerg Med. In Press, 2012.
6. Dziewit JA, Wei H. Supraglottic Jet Ventilation Assists Intubation in a Marfan’s Syndrome
Patient with a Difficult Airway. J Clin Anesth. 2011;23:407–409.
7. Dziewit JA, Wei H. Supraglottic Jet Ventilation Assists Intubation in a Patient with Difficult
Airway Due to Unrecognizable Supraglottic Structures. J Anesth Clin Res. 2011;2:141. doi:
10.4172/2155-6148.1000141.
ADDITIONAL READING
• Boyce JR, Peters GE, Carroll WR, et al. Preemptive vessel dilator cricothyrotomy aids in the
management of upper airway obstruction. Can J Anesth. 2005;52:765–769.
• Caplan RA, Benumof JL, Berry FA, et al. Practice guidelines for management of the difficult
airway. An updated report by the American Society of Anesthesiologists Task Force on
Management of the Difficult Airway. Anesthesiology. 2003;98:1269–1277.
• Pneumothorax
• Cricothyroidotomy
• Bronchoscopy
CLINICAL PEARLS
• Jet ventilation has unique features that differentiate it from CMV. It provides an open
airway system, has respiratory rates between 12 and 1,000 breaths/minute and greater dead
space ventilation (Vd in adults is usually 150 mL; however, can still provide efficient
oxygenation and ventilation with unclear mechanisms). Additionally, jet ventilation has low
PIP, auto-PEEPing is a desired feature (results from high frequencies), inhalational
anesthetics cannot be used, and is poorly humidified.
• Perioperative utilization includes situations where a “still” surgical field is desired, there is a
shared surgical site, and difficult airway management.
• Unfortunately, there is a poor ability to monitor FiO2, PetCO2, Paw, and tidal volume.
JUGULAR VENOUS OXYGEN SATURATION (SJO2)
Keren Ziv, MD
BASICS
DESCRIPTION
• Jugular venous oxygen saturation (SjO2) is a measurement used to indirectly assess global
cerebral oxygen extraction by measuring the balance of oxygen consumption and delivery in
the brain. It is the most widely used method of continuous cerebral oxygenation monitoring.
• It involves percutaneous catheter insertion into the jugular bulb that then measures SjO2 via
fiberoptic reflectance oximetry or by manual blood draws analyzed via co-oximetry.
• Studies have demonstrated that early SjO2 catheter insertion may improve patient outcome.
• The brain is an exceedingly, metabolically active organ and accounts for ∼20% of the
resting total body O2 consumption. Most of the oxygen consumption is used for excitation
and conduction of the neuronal signals in the brain, and a smaller amount is used for
synthesis and metabolism of neurotransmitters as well as cellular homeostasis.
• Cerebral metabolic oxygen consumption (CMRO2) is normally 3–3.5 mL of O2 per 100 g of
brain tissue per minute (3.5 mL/100 g/min).
• SjO2 provides an assessment of the balance between oxygen delivery and consumption in the
brain, to allow an estimate of the CMRO2.
– Normal values range from 50% to 75% (equating to an approximate 25–50% oxygen
extraction).
– Saturation of jugular venous blood is dependent on the cerebral blood flow (CBF), arterial
saturation, and CMRO2.
• The calculation of SjO2 utilizes the Fick equation: CMRO2 = CBF × (CaO2–CjO2), where
CaO2 is arterial oxygen content and CjO2 is jugular (venous) oxygen content; it represents
the arteriovenous oxygen difference.
– CMRO2 ∼ [CBF × 1.34 × Hb(SaO2–SjO2)]. Oxygen has a blood solubility of 0.003; the
dissolved contribution is negligible and hence deleted from the equation.
– Assuming that Hb and SaO2 are constant, SjO2 ∼ CBF/CMRO2. Thus, SjO2 is
predominantly dependent on the SaO2, CMRO2, and CBF.
• During SjO2 monitoring, a spectrophotometric catheter using three light wavelengths is used
to measure both the hemoglobin value and oxygen saturation.
ANATOMY
• The majority of the blood from the brain drains into the internal jugular (IJ) veins therefore
making it a practical site to assess for cerebral venous oxygen saturation.
– The left IJ predominately drains subcortical areas while the right IJ predominately drains
the cortical areas. Studies have suggested that:
– Oxygen saturations are similar in both IJ veins, particularly with diffuse cerebral injury.
– Focal disease may produce a larger saturation difference between the sides.
– Catheter placement is typically on the side of greatest flow; some advise placement on the
side of the injury (controversial).
• The catheter can be inserted into the IJ vein between the two heads of the
sternocleidomastoid muscle (distally) or at the level of the cricoid ring (proximally) and is
directed cephaladly toward the jugular bulb. On radiography, the tip should be at about the
C1–C2 vertebrae and as close to the skull base as possible, to minimize facial vein
contamination.
• Decreased SjO2 suggests ischemia and can result from increased oxygen extraction (demand)
or decreased CBF (supply).
– Increased demand
Intracranial hypertension
Seizures
Pyrexia
– Decreased supply
Systemic hypoxia
Hypotension or vasospasm leading to decreased CBF
Intracranial hypertension with decreased CPP
• Increased SjO2 can result from decreased brain oxygen extraction (demand), increased CBF
(supply), or impaired oxygen extraction.
– Decreased demand (CMRO2)
Increased cell death suggesting worsening brain damage
– Increased supply
Hyperemia
– Impaired oxygen extraction
Shunting (arteriovenous malformations); oxygenated blood does not perfuse ischemic
areas (bypasses).
Failed oxygen extraction.
– Measurement errors: Contamination from extracranial drainage; can range from 0% to
6.6% (mean 2.7%). Sampling a rate >1–2 mL/minute can result in sampling or
contamination by the facial vein.
• Severe brain injury
– CBF and CMRO2 are altered during the first few days and SjO2 provides a measure of
objective insight into worsening brain injury.
– Following injury, patients are at increased risk of secondary cerebral insults caused by
hypoxia and ischemia, leading to further brain damage.
– SjO2 unfortunately provides information on a global scale and may therefore be inaccurate
in situations dealing with local ischemia. It may be incorrectly assumed that SjO2 is
normal in a heterogeneous brain because areas of local ischemia may be compensated for
by areas of luxury perfusion.
• Potential complications of insertion
– Carotid artery puncture (1–4%)
– Thrombosis
– Hematoma
– Infection
• Cerebrovenous oxygen saturation, in combination with hemodynamic and intracranial data,
can aid in the detection and treatment of cerebral ischemia following stroke, trauma,
cardiac arrest, or cardiopulmonary bypass.
• Although individual SjO2 values may prove to be less than accurate, using SjO2 trends is a
useful tool in the perioperative period to help guide both the anesthetic and intensive care
unit management.
• While the normal range of SjO2 is considered to be 50–75%, it is not clear whether this is
true for patients with TBI. Studies, however, have demonstrated that a single episode of
SjO2 <50% is associated with a twofold increase in mortality. Therefore, current
recommendations dictate maintaining the SjO2 between 55% and 75% in order to extend
the margin of error.
• SjO2 may be altered by several coincident factors such as hemoglobin concentration,
temperature, oxygenation, and carbon dioxide levels. Other modalities of measuring oxygen
utilization such as near-infrared spectroscopy are often monitored in addition to SjO2.
• Choosing side to monitor. One technique is to test intracranial compliance. This may be
done by compressing each jugular vein, one at a time, and observing the rise in ICP. The
side with the greatest increase in ICP drains more blood and suggests a larger vascular
territory of the brain. When there is no difference, the right side is often chosen as it is more
commonly the dominant anatomical site.
• Cannulation technique. Placement should be performed in the horizontal or Trendelenburg
position, while avoiding ICP >20 mm Hg.
EQUATIONS
• CMRO2 = CBF × (CaO2–CjO2); where CMRO2 is the cerebral metabolic oxygen
consumption, CBF is cerebral blood flow, CaO2 is the arterial oxygen content, CjO2 is the
jugular venous oxygen content.
• SjO2 = SaO2 – (CMRO2/[CO × Hb × 1.39]); where SaO2 is arterial blood oxygen
saturation, CMRO2 is the cerebral metabolic oxygen consumption, CO is cardiac output, Hb
is hemoglobin, and 1.39 represents the amount of oxygen that one gram of hemoglobin can
carry.
REFERENCES
1. hite H, Baker A. Continuous jugular venous oximetry in the neurointensive care unit – A
brief review. Can J Anesth. 2002;49(6):623–629.
2. ohlwink UK, Figaji AA. Methods of monitoring brain oxygenation. Childs Nerv Syst.
2010;26:453–464.
3. Gopinath SP, Valdaka AB, Uzura M, et al. Comparison of jugular venous oxygen saturation
and brain tissue PO2 as monitors of cerebral ischemia after head injury. Crit Care Med.
1999;27(11):2337–2345.
4. Macmillan CSA, Andrews PJD. Cerebrovenous oxygen saturation monitoring: Practical
considerations and clinical relevance. Intensive Care Med. 2000;26:1028–1036.
ADDITIONAL READING
• Steiner IA, Andrews PJD. Monitoring the injured brain: ICP and CBF. Br J Anaesth.
2006;97:26–38.
• Pulse oximetry
• Cerebral metabolic oxygen consumption (CMRO2)
CLINICAL PEARLS
• SjO2 monitoring indirectly assesses the brain’s ability to extract and metabolize oxygen; it
relies on the Fick principle of oxygen consumption (supply versus demand). At this time,
there are no direct methods to measure the adequacy of the oxygen supply at the cellular
level.
• May be inaccurate in measuring focal ischemia.
• Assumptions are dependent on the CMRO2 and CBF being coupled.
• Research regarding use in children with TBI is limited.
JUNCTIONAL RHYTHM
BASICS
DESCRIPTION
• Junctional heart rhythms and premature junctional (escape) beats originate from the area
around the atrioventricular (AV) node. They occur when the AV node takes over as the
primary pacemaker site in the heart because either the
– Sinoatrial (SA) node has failed, or the
– AV node is firing faster and overtakes the SA node
• Junctional rhythms classification
– Junctional rhythm: Rate is 40–60 beats per minute (bpm).
– Junctional accelerated rhythm: Rate is 60–100 bpm.
– Junctional tachycardia: Rate is >100 bpm.
• Junctional rhythms are an example of a supraventricular rhythm in which the QRS complex
morphology is usually narrow (<0.12 seconds) and regular. There are no P waves seen
before the QRS complexes; instead, they occur either simultaneously with the QRS
complexes or are retrograde.
EPIDEMIOLOGY
Prevalence
Common in patients with sick sinus syndrome or in patients who have significant bradycardia
that allows the AV nodal region to determine the heart rate
Prevalence
• Episodes of AV nodal reentrant tachycardia may occur at any age. However, commonly
presents for the first time in childhood or adolescence.
• Common during sleep in children and in athletic adults.
Morbidity
• Junctional ectopic tachycardia (JET) often presents in the first 24–48 hours after surgery for
congenital heart defects (1).
• A congenital form exists with normal cardiac anatomy, and a positive family history is
present in up to 50% patients with congenital form of junctional tachycardia.
Mortality
• No evidence exists to suggest an increased mortality for incidental junctional rhythm.
• The permanent form of JET is rare and constitutes <1% of pediatric arrhythmias. It
commonly leads to cardiomegaly and congestive heart failure in up to 60% of patients, with
an associated mortality rate of 35%.
• Demographics
– Younger population and/or athletic individuals during periods of increased vagal tone on
the SA node.
• Coexisting disease
– Ischemia of the AV node, especially with acute inferior infarction involving the posterior
descen-ding artery, the origin of the AV nodal artery branch
– Sick sinus syndrome (including drug-induced)
– Chronic obstructive pulmonary disease (COPD)
– Less common: Congenital form, systemic amyloido-sis, diphtheria, acute rheumatic fever,
Lyme disease
• Surgery or procedure
– Valve surgery
– Direct current cardioversion
– Cardiac catheterization
– Maneuvers that enhance vagal tone: Laparoscopy, peritoneal retraction, eye surgery, etc.
• Medications
– Inhaled anesthetics; most commonly with enflurane
– Drugs that induce sinus bradycardia: Beta-blockers, calcium channel blocker, and most
antiarrhythmics
– Digoxin toxicity
– Isoproterenol infusion
• Metabolic
– Hyperkalemia
• Increased adrenergic tone
• Junctional rhythms (and escape beats) are the result of
– SA node that has failed due to ischemia, intrinsic disease, vagal tone, changes in
autonomic tone, or medications that suppress the SA node.
– AV nodal firing at a faster rate than the SA node; subverts hierarchy and overtakes a
“normal” sinus node. Less commonly, it is observed in digitalis toxicity, following cardiac
surgery (particularly valve replacement), during acute myocardial infarction, or during
isoproterenol infusion (2).
• Junctional rhythms can result in a decreased or absent atrial contribution or “kick” during
ventricular diastole. This can result in decreased preload and hence, stroke volume (Frank–
Starling curve); ultimately leads to a decrease in cardiac output (stroke volume times heart
rate). This discor-dant contraction can also result in atrial contraction against a closed
tricuspid valve, resulting in increased right atrial and central venous pressures.
• Congenital form. There are no preventative measu-res or perioperative factors that have
been identified to target prevention at the time of surgical repair.
• Symptomatic cases may benefit from a consultation with a cardiologist to better define the
etiology and approach to prevention.
Intraoperatively
• EKG findings
– Rate: Typically 40–60 bpm; accelerated rhythms reach 60–100 bpm, while junctional
tachycardia can be as high as 100 bpm.
– P wave (atrial depolarization). Is either missing or inverted. When present, it can be seen
before, during (hidden), or after the QRS complex and is most noticeable in leads I and II,
and aVL.
– P–R interval. When the P wave occurs before the QRS complex, the interval will be <0.12
seconds.
– QRS wave. Typically a normal waveform is seen; may appear abnormal when the P wave
falls within the QRS complex.
– Escape beats. Premature beat, with above-described P and QRS waveforms. No pause is
seen prior to the next beat.
• Physical exam
– Regular pulse
– Prominent jugular venous pulsations
– Cannon “a” waves may be seen on central venous pressure waveforms due to the right
atrium contracting against a closed tricuspid valve.
• Labs
– Electrolytes
– Digoxin level (if appropriate)
Awake or Outpatient Setting
• Symptoms are typically nonspecific and include palpitations, fatigue, poor exercise
tolerance, dyspnea, and presyncope.
• A two-dimensional echocardiograph in patients with suspected structural heart disease
• A stress echocardiograph or nuclear imaging test in patients with symptoms consistent with
coronary ischemia
• An implantable loop recorder may help diagnose junctional rhythm in patients with very
infrequent symptoms.
• In specific cases an electrophysiologic study (EPS) or invasive electrophysiologic evaluation.
• AV block
• AV dissociation
• Atrioventricular nodal reentry tachycardia (AVNRT)
• Digitalis toxicity
• Sinus node dysfunction
• Low atrial ectopic foci can cause inverted P waves.
TREATMENT
• Intraoperative treatment is dependent on the underlying cause and if the rhythm is causing
hemodynamic instability (3). The junctional rhythm serves as an escape mechanism to
maintain the heart rate during periods of bradycardia or asystole and should not be
suppressed.
– Underlying cause. Ischemia and metabolic derangements should be identified and treated
accordingly. Treatment of digitalis intoxication may include correcting potassium levels
and/or administering atropine, digoxin immune Fab (Digibind).
– Stable patients. Pharmacologic therapy is not typically needed when junctional rhythms
result from increased vagal tone.
– Unstable patients.
Decrease the dose of inhalational anesthetics.
Administer anticholinergic drugs such as glycopyrrolate or atropine to speed up the SA
node and re-establish hierarchy.
Vasopressor support as needed
JET is generally treated medically; amiodarone may be the best antiarrhythmic
medication.
• Postoperative JET
– Initial approach: Discontinue vagolytic agents and reduce the doses of inotropic agents.
– Serum calcium and potassium should be normalized.
– IV amiodarone is the first-line agent in patients with JET from all causes. Beta-blockers,
with or without procainamide may be also considered; however beta-blockers may depress
myocardial contractility, and procainamide may accelerate JET
– When JET is not eliminated
– In rare, resistant, life-threatening cases, transcatheter radiofrequency ablation or
modification of the His bundle may be necessary.
– Postoperative JET is limited
– Core temperature cooling has value in the infant and small child; cooling blankets can be
utilized to obtain a temperature of ~34–35°C.
• Congenital and adult JET warrant aggressive management, especially in the young, with
amiodarone or sotalol.
FOLLOW-UP
• Symptomatic cases may benefit from a consultation with a cardiologist and/or an

electrophysiologist to better define the etiology and approach to prevention.
• Sick sinus rhythm, high-grade, or complete AV block. Patients may be considered for a
permanent pacemaker implantation.
• Radiofrequency catheter ablation also can be used to treat JET if there is no response to
pharmacological therapy.
• A treatment option for JET is an AV junction ablation with permanent pacemaker
implantation.
REFERENCES
1. Haas NA, Plumpton K, Justo R, et al. Postoperative junctional ectopic tachycardia (JET). Z
Kardiol 2004;93(5):371–380.
2. Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emerg
Med Clin North Am. 2006;24(1):1–9.
3. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. European Society of Cardiology
Committee, NASPE-Heart Rhythm Society. ACC/AHA/ESC guidelines for the management
of patients with supraventricular arrhythmias–executive summary: A report of the
American college of cardiology/American heart association task force on practice
guidelines and the European society of cardiology committee for practice guidelines
(writing committee to develop guidelines for the management of patients with
supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm
Society. J Am Coll Cardiol. 2003;42(8):1493–1531.
ADDITIONAL READING
• Libby P, Bonow RO, Mann DL, et al. Specific arrhythmias: Diagnosis and treatment. In:
Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 8th edition.
Philadelphia, PA: WB Saunders, 2007:640–645.
• Josephson ME. Clinical Cardiac Electrophysiology. 4th edition. Baltimore, MD: Williams &
Wilkins, 2008.
• Intraoperative myocardial ischemia
• Phosphate
CODES
ICD9
• 427.0 Paroxysmal supraventricular tachycardia
• 427.89
ICD10
• I47.1 Supraventricular tachycardia
• I49.8 Other specified cardiac arrhythmias
CLINICAL PEARLS
• No pharmacologic therapy is needed for asymptomatic, otherwise healthy individuals with
junctional rhythms that result from increased vagal tone.
• Emergency care includes evaluation of the 12-lead EKG findings, airway protection and
oxygenation, and BP support, depending on the cause of the rhythm.
• In patients with complete AV block, high-grade AV block, or symptomatic sick sinus
syndrome (i.e., sinus node dysfunction), a permanent pacemaker may be needed. The
junctional rhythm serves as an escape mechanism to maintain the heart rate during periods
of bradycardia or asystole and should not be suppressed.
FIGURE 1. Junctional rhythm. Rate of 40–60 bpm
FIGURE 2. Accelerated junctional rhythm. Rate of 60–100 bpm
FIGURE 3. Junctional tachycardia. Rate >100 bpm

KASAI PROCEDURE (HEPATOPORTOENTEROSTOMY)
BASICS
DESCRIPTION
General
• The Kasai procedure is a therapeutic/palliative procedure for biliary atresia (BA). BA is
characterized by extrahepatic biliary duct fibrosis with some extension into the liver. The
obliteration of the extrahepatic bile ducts prevents bile from draining, leading to liver
cirrhosis and ultimately liver failure.
– Fetal form: 10–20% of cases, born jaundiced, ABSENCE of bile ducts
– Perinatal form: 80–90% of cases, healthy neonate, develops symptoms
• Not a treatment for Alagille syndrome (intrahepatic biliary fibrosis)
• Mostly done via an open technique, but some centers are gaining experience with robotic
and laparoscopic techniques.
• The liver is mobilized, the porta hepatis is exposed, and the fibrous tissue is excised widely.
• A roux-en-y is created with the intestine (typically jejunum) and sutured widely to the porta
hepatis.
Position
• Supine
• Prep from the nipples to the pubic bone
Incision
Right subcostal incision
Approximate Time
3 hours
EBL Expected
Typically 10–20 mL/kg, primarily during dissection of the porta hepatis
Hospital Stay
2–3 weeks
Intraoperative cholangiography may be done to verify occlusion.
EPIDEMIOLOGY
Prevalence
5–10/100,000 newborns have BA.
Prevalence
BA is increased in:
• Non-Caucasian races
• Maternal multiparity
• Female sex of baby
Morbidity
• >70% will need a liver transplantation following the Kasai.
• It is commonly believed that survival of the native liver is related to the age of the patient at
the time of the Kasai with most studies showing best results for those infants under 60 days
of age (this is controversial, as some studies show no difference).
Mortality
• Varies widely depending on the surgeon and study
• 5-year survival after Kasai ranges from 20% to 70%.
• Decreased mortality with open procedure versus laparoscopic
• Hemorrhage can occur at any point due to the proximity of portal vessels. Blood products
should be readily available.
• Intravascular volume is critical. Excess will cause liver edema.
• Liver disease may result in anemia, coagulopathy, decreased total body proteins, vitamin
deficiencies, and prolonged drug life.
SYMPTOMS
• Lack of appetite
• Pruritus
• Stigmata of liver disease
History
Patients often present with acholic stools, jaundice, and direct bilirubinemia. The diagnosis is
usually made in the first 3–4 months of life.
Signs/Physical Exam
• Jaundice
• +/– Hepatomegaly
• Poor weight gain
• Ascites
• Pale stools
MEDICATIONS
• Preoperative vitamin K 1–2 mg/day
• Postoperative steroids, antibiotics, and fat-soluble vitamins
Labs/Studies
• CBC
• Chemistry panels
• Coagulation studies (PT, PTT, INR): Elevated PT can be corrected with vitamin K
administration.
• Liver function tests: Increased conjugated hyperbilirubinemia
Liver failure
TREATMENT
Premedications
Anxiolysis is not necessary in this age group.
• Consent for blood transfusion
• Consent for arterial line and central line, if needed
• Consent for epidural (if no coagulopathy)
INTRAOPERATIVE CARE
• General anesthesia with endotracheal tube
• Epidural placed for postoperative pain management. In small infants a caudal catheter is
utilized and threaded up to T7–T8. Patient should be assessed for coagulopathy.
Monitors
• Standard ASA Monitors
• Arterial line for continuous blood pressure monitoring and lab draws
• 2 large-bore IVs for rapid resuscitation
• Central line may be necessary if unable to obtain adequate peripheral access or at the
surgeon’s request.
• In the absence of increased intra-abdominal pressure (from ascites), an inhalation induction
is acceptable.
• An IV induction is preferred in cases where an IV has been placed for preoperative hydration
or tests.
Maintenance
• Because of the age of the patient, it is easiest to place a caudal epidural in the lateral
position once the patient is anesthetized.
– The catheter is threaded cephalad to the low thoracic level (typically T8–T9 corresponds
with the incision).
– Epidural placement can be confirmed with the injection of radio-opaque dye through the
catheter under fluoroscopy.
– Epidural solution varies by institution. Bupivacaine 0.25% + opioid (fentanyl) is very
common.
• Maintenance is typically with volatile agents, oxygen, and air. Avoid nitrous oxide as it can
cause bowel distention. Muscle relaxation should be appropriately administered to provide
optimal surgical exposure. Consider organ-independent NMBD if severe liver disease.
• Normothermia should be maintained; the neonate resorts to non-shivering thermogenesis to
maintain heat.
• Maintain euvolemia. Hypovolemia will cause decreased cerebral flow from hypotension, but
increased intravascular volume increases portal pressures and can result in liver swelling.
• Blood products should be ready to administer in the event of portal injury (typically 1 unit
of packed red blood cells). If the patient is significantly coagulopathic from liver failure,
fresh frozen plasma may also be available.
• Incision is usually small, and most of the surgical repair is done after the liver has been
externalized from the abdomen. This can result in torquing of portal vessels with resultant
hypotension.
• Since most of the operation is done outside of the abdomen, there is usually minimal impact
on ventilation.
• Extubation should be considered if the patient is awake, strong, able to protect their airway,
and hemodynamically stable.
• If an epidural is in place, it should be adequately dosed.
FOLLOW-UP
BED ACUITY
Neonatal or pediatric ICU
ANALGESIA
Pain can be controlled via epidural +/– IV opioid. If IV opioids are used, the epidural
solution should be opioid-free.
COMPLICATIONS
• Cholangitis
• Bile leak (10–15%)
• Malabsorption syndrome
• Portal hypertension and subsequent esophageal varices
• Liver failure
• Bowel obstruction (10%)
• Bleeding
• Infection/sepsis (5–10%)
REFERENCES
1. u LN, Chen HL, Chang CJ, et al. Prophylactic oral antibiotics in prevention of recurrent
cholangitis after the Kasai portoenterostomy. J Pediatr Surg. 2003;38:590–593.
2. Ure BM, Kuebler JF, Schukfeh N, et al. Survival with the native liver after laparoscopic
versus conventional Kasai portoenterostomy in infants with biliary atresia: A prospective
trial. Ann Surg. 2011;253(4):826–830.
3. Leonhardt J, Kuebler JF, Leute PJ, et al. Biliary atresia: Lessons learned from the voluntary
German registry. Eur J Pediatr Surg. 2011;21(2):82–87.
ADDITIONAL READING
• Puri P, Hollwarth M. . New York: Springer, 2009.
CLINICAL PEARLS
• The Kasai procedure is palliative in most cases. >70% of cases will require a liver
transplant.
• There is a potential for massive blood loss (relative to the neonate’s blood volume).
• Maintain euvolemia.
• Epidurals work well for pain control postoperatively.
• The biggest postoperative concern is to prevent cholangitis with prophylactic postoperative
antibiotic treatment. If cholangitis is suspected, steroids are added.
KIDNEY TRANSPLANTATION
BASICS
DESCRIPTION
General
• Performed in patients with end-stage renal disease (ESRD) to eliminate or preempt dialysis,
prolong longevity, and improve the quality of the recipient’s life.
• ESRD can be due to a variety of causes, including diabetes, hypertension,
glomerulonephritis, polycystic kidney disease, chronic pyelonephritis, and systemic lupus
erythematosus.
• Procedure: A “3-way” Foley catheter is sterilely inserted with the additional lumen allowing
infusion of fluid before the ureteral anastomosis (and for possible continuous bladder
irrigation in the event of clot retention). The extraperitoneal space is dissected to expose the
iliac vessels and bladder. The external iliac vein is clamped, and the donor renal vein is
anastomosed to it (renal vein-to-iliac-vein anastomosis). The external iliac artery is
clamped, and the donor renal artery is anastomosed to it (renal artery-to-iliac-artery
anastomosis). The vessel clamps are then removed. A ureteroneocystostomy is then
performed (the donor ureter is anastomosed to the recipient’s bladder); the bladder is
distended with antibiotic irrigation to aid with visualization and the detrusor muscle of the
bladder is dissected away from the mucosa.
• Advances in immunosuppression and organ preservation techniques, as well as acceptance
of brain death, development of an organ donor network, and establishment of
reimbursement mechanisms have all led to the development of renal transplantation as a
relatively common procedure.
• A limited donor pool has been extended with living donation. Living donors may be related,
unrelated “Good Samaritans,” paired or even chain donations.
Position
Supine
Incision
Lower abdominal to transplant the kidney to the iliac fossa
Approximate Time
3 hours; if combined with a pancreatic transplant (in diabetics) time may double
EBL Expected
Usually <200 mL
Hospital Stay
3–7 days
An organized multidisciplinary transplant team that is integrated with the national organ
transplant organization
EPIDEMIOLOGY
Prevalence
• 17,413 transplants performed in the US in 2008 (1)
– 11,382 deceased donors (1)
– 5,968 living donors (1)
Prevalence
• 547,982 ESRD in the US in 2008 (1)
– 382,343 managed by dialysis (1)
– 165,639 managed by a kidney transplant (1)
Morbidity
• Cardiovascular and infectious morbidity seem to predominate among those with ESRD.
Infection is related to both dialysis access and other independent sources.
• Problems with vascular access are an additional common reason for hospital admission.
Mortality
88,620 deaths in patients with ESRD in the US during 2008 (1)
• Taking the often “dry” renal failure patient to an adequately volume loaded state is the goal
in renal transplantation. Recipients, however, often have cardiovascular conditions that can
put them at risk for CHF.
• Once adequate volume loading has been assured, adequate perfusion of the new kidney may
need to be supplemented by means of an inotrope such as dopamine.
• Low bicarbonate, high potassium, and low hematocrit are expected in these patients;
excessive deviations might need to be treated with dialysis or transfusion preoperatively.
SYMPTOMS
Any recent changes should be elicited especially with regard to chest pain, dyspnea, or
exercise tolerance.
History
• Typically patients presenting for renal transplantation will come with an extensive
preoperative evaluation. For deceased donor transplants, the goal is to have patients in
optimal condition for transplant to occur with limited warning. Despite this, the anesthesia
preoperative evaluation may serve as the last chance to ensure that important changes in
the patient’s condition have not occurred. Hence, the preoperative visit may concentrate on:
– The usual dialysis schedule and the most recent dialysis
– History of chest pain, dyspnea, cardiac history and evaluations, exercise tolerance
– In the diabetic patient, the duration of treatment and usual glucose levels
– Bleeding tendencies
Signs/Physical Exam
A careful cardiovascular exam, especially paying attention to volume status and apparent
changes in the exam
MEDICATIONS
Typically ESRD patients are on a plethora of drugs: Beta-blockers, calcium channel blockers,
diuretics, angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, statins,
protein pump inhibitors, laxatives, iron/erythropoietin, vitamins/electrolyte supplements,
and insulin (in diabetics)
Labs/Studies
• Electrolytes, especially potassium level and evidence of acidosis
• Preoperative glucose
• Hemoglobin and hematocrit
• Review any preoperative cardiac workup, including stress tests and EKG.
• Diabetes
• Hypertension
• Cardiovascular disease
– About 50% of transplanted patients die of cardiovascular disease or stroke.
– The usual risk factors for atherosclerotic cardiovascular disease (smoking, hypertension,
abnormal cholesterol and lipid levels, diabetes, male gender, advanced age) are often
found in renal failure patients as well.
– Renal failure can create challenges for the patients with cardiovascular disease; anemia,
volume overload, and labile blood pressures add additional risk for these patients.
– For patients with prior transplants, immunosuppressants, graft rejection, and dysfunction
can further add to the cardiac risk and management challenges (2).
• A variety of bleeding abnormalities
• Hepatitis C
• Anemia
TREATMENT
Premedications
As determined by the patient’s coexisting disease and general condition
Consent for planned or possible invasive monitors, a review of the risks in light of
comorbidities, and the possibility of postoperative intubation and ICU admission (though
perhaps not especially common) might be appropriate.
Routine antibiotics for urological procedures. Infectious disease precautions are even more
crucial in light of perioperative immunosuppression.
INTRAOPERATIVE CARE
• Most under general anesthesia
• Can be done under spinal or epidural anesthesia, and some centers have even reported
combined general and regional to improve postoperative pain control and improved
respiratory function. Concerns about uremic coagulopathy and remaining heparin from
dialysis or potential intraoperative administration have dampened enthusiasm for regional.
Monitors
• Central venous monitoring is useful for monitoring volume loading throughout the
perioperative period. Difficult IV access, frequent blood draws, and the potential for
dopamine administration might also influence the placement of a central line. Planned
thymoglobulin administration (with the risk of vessel sclerosis) also encourages the
placement of central lines in some centers although others have successfully administered
this drug via a high-flow vessel using a dilute solution.
• Arterial line placement and other invasive monitoring are dependent upon the medical
condition of the patient. Some centers attempt to minimize arterial line use as the radial
artery may be used for dialysis access.
• A “3-way” urinary catheter is placed not only to monitor urine output following reperfusion,
but is also often clamped with irrigation infused into the bladder during attachment of the
ureter to facilitate this portion of the procedure. Complete emptying of the irrigant from the
foley following ureteral anastomosis allows a more accurate assessment of urine output
from the newly transplanted kidney.
• Succinylcholine will increase potassium levels 0.5–1 mEq/L (to the same extent as those
without renal disease). It can be used if the potassium is not already elevated.
• Consider a rapid sequence induction based upon NPO status and diabetic gastroparesis.
• As the patient is usually postdialysis, and therefore volume depleted, propofol should be
used with caution and etomidate might be considered. Propofol, however, is often well
tolerated.
Maintenance
• Muscle relaxant: Cisatracurium offers a theoretical advantage of Hoffman elimination (not
dependent on renal metabolism). Rocuronium, vecuronium, and mivacurium may all be
prolonged in renal failure. While a longer acting agent is probably not advisable, these
moderate duration relaxants have been used with careful monitoring.
• Opioids: Meperidine and morphine in high doses pose concerns with accumulation of renally
excreted active metabolites. The metabolite of meperidine, normeperidine, can cause
seizures. Fentanyl, alfentanil, sufentanil, and remifentanil drug effects are minimally
affected by renal failure.
• Volatile agent: Some practitioners avoid sevoflurane due to the potential for renal toxicity.
Others are not convinced that this is an issue given the paucity of convincing human data,
even in patients with renal dysfunction.
• Immunosuppression and hemodynamic management vary by institution; it is best to
establish preoperative consensus among the teams involved. Immunosuppression may begin
with tacrolimus (often given orally in the preoperative period) followed by steroids and
either basiliximab or thymoglobulin. Thymoglobulin must be given slowly (typically over 6
hours), with a 0.22 μm filter and into a high-flow vessel (to reduce vessel sclerosis).
• Heparin infusion may be needed if there is concern with the anastomosis.
• Lasix and mannitol may be used to induce diuresis.
• If CVP is used to manage fluid administration, the plan is to reach the “ideal” level by the
time of reperfusion.
• Dopamine might be added (perhaps at 2–10 mcg/kg/min) to achieve an adequate blood
pressure for renal perfusion.
• Periodic checks of electrolytes (and in diabetics, glucose) are advisable.
Most patients are extubated at the end of surgery. Volume overload or other complications
may preclude immediate extubation.
FOLLOW-UP
BED ACUITY
ICU typically not needed unless underlying disease or intervening complication requires this
level of monitoring
ANALGESIA
• Mild-to-moderate pain usually managed with parenteral narcotics, often with a PCA or via
epidural analgesia.
• Ketorolac and other NSAIDs should probably be avoided due to potential nephrotoxic side
effects.
COMPLICATIONS
• Cardiovascular complications: CHF, MI, CVA
• Delayed graft function, graft failure, rejection, vascular thromboses
• Infections
PROGNOSIS
5-year survival after renal transplantation is 70% versus only 30% in a comparable dialysis
group. Serious comorbidities may be reduced or resolve completely after transplantation.
REFERENCES
1. S Renal Data System. , National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases, Bethesda, MD, 2010.
2. Kiberd BA. Cardiovascular disease in kidney transplant recipients. Adv Stud Med.
2007;7:169–178.
ADDITIONAL READING
• Jankovic Z, Sri-Chandana C. Anaesthesia for renal transplantation: Recent developments and
recommendations. Curr Anaesth Crit Care. 2008;19:247–253.
• Lemmens HJM. Kidney transplantation: Recent developments and recommendations for
anesthetic management. Anesth Clin N Am. 2004;22:651–662.
• End-stage renal disease
• Uremia
CODES
ICD9
• V42.0 Kidney replaced by transplant
• 585.6 End stage renal disease
ICD10
• N18.6 End stage renal disease
• Z94.0 Kidney transplant status
CLINICAL PEARLS
• The typical concerns with fluid restriction in renal failure are dramatically altered due to the
desire to provide an adequate perfusion to the new kidney. Hence volume loading (and if
necessary an inotrope, such as dopamine, at relatively low doses and after adequate volume
has been assured) has been the typical management of renal transplants. This is done with
caution and the hope that the new kidney begins to produce urine. Volume overloading,
especially in the setting of delayed kidney function, is a definite possibility that fortunately
occurs in a small number of cases. If this scenario is suspected, keeping the patient
intubated, consideration of more invasive monitoring, and dialysis in the postoperative
period may be necessary.
LACTATION AND ANESTHESIA
BASICS
DESCRIPTION
• Every health care organization, based on numerous studies, has found breastfeeding to
significantly benefit both the mother and the infant.
• Anaesthetists are likely to encounter breastfeeding mothers in their practice, and concerns
about the transfer of medications (including local anesthetics, benzodiazepines, opioids, and
volatile agents) into breast milk will arise.
• There is very limited data regarding the transfer of medications into human milk. Current
practice and recommendations are mostly empiric and “common sense.”
• The interruption of breastfeeding for long periods is difficult for the infant, uncomfortable
for the mother, and may interrupt bonding.
• During informed consent, the various modalities, risk of the therapies, effect on the
newborn, and possible breastfeeding effects must be discussed.
EPIDEMIOLOGY
Incidence
• The incidence of surgery during pregnancy ranges from 0.3% to 2.2%. In the US, up to
75,000 pregnant women undergo surgery.
• There is limited data regarding the incidence of lactating women undergoing surgery.
Morbidity/Mortality
Neonatal abstinence syndrome may be seen in neonates who have been exposed to
intrauterine opioids; more applicable to chronic substance abuse. However this cannot be
extrapolated to transfer of opioids from breast milk.
• The transfer of drugs into milk is determined by the equilibrium forces between the
maternal plasma and milk compartment. They include:
– Concentration
– Half-life of drug
– Lipophilicity
– Molecular weight
• Anesthetic medications: The good majority of drugs used perioperatively have short half-
lives with rapid redistribution.
– Anesthetic agents are rapidly cleared from the maternal plasma within minutes secondary
to redistribution to deep tissue compartments, thus minimizing the degree of exposure.
– Medications with longer durations of action and active metabolites may have a higher risk
to the infant. However, short-term use of these medications is unlikely to produce harmful
effects.
– Essentially, it is assumed that if the mother is awake and alert, the medications have left
the plasma/milk compartment and have entered the muscle and fat tissue compartments,
from which it will be released slowly.
• Timing of pumping or breastfeeding in relation to the peaks and troughs of medication has
effects on the dose of medication transferred to the milk. Additionally, the amount of milk
ingested by the infant affects the amount of drug transfer.
• Reduced milk production can occur with aggressive fluid resuscitation. When the plasma
oncotic pressure is decreased, breast engorgement can result.
• The early return to breastfeeding is advantageous for both mother and infant.
• Consider continuing breastfeeding without any interruptions in the following instances:
– Early breastfeeding, when the colostrum volume is small (reduces the amount of drug
transfer)
– Single doses of medications
– Short procedures
– Drugs with a short duration of action
– Drugs without long-acting active metabolites
– Most instances
• Consider holding or interrupting breastfeeding in the following instances:
– Premature and younger infants; can be more susceptible to small doses of medications.
– Infants who are prone to apnea and hypotension; may require interruption of
breastfeeding for 12–24 hours.
TREATMENT
• Normal term or older infants can resume breastfeeding as soon as the mother is awake,
stable, and alert.
• A single pumping and discarding of milk after surgery will eliminate any drug retained in
milk fat. However, this is seldom necessary and not recommended.
• Induction drugs, including propofol, midazolam, etomidate, and thiopental, enter the milk
compartment only minimally due to their brief distribution phases. The transport to milk is
low to nil.
• Anesthetic gases have brief plasma distribution phases, and milk levels are likely nil.
However, there are no reports in the literature.
• Ketamine use in breastfeeding mothers has not been reported in the literature. Secondary to
its side effects of hallucination and dissociative anesthesia, ketamine may not be considered
an ideal anesthetic agent in the breastfeeding mother.
• Remifentanil may be appropriate for short procedures due to its short duration of action.
However, there is no published data to document its effects on fetal sedation.
• Diazepam has a long duration of action and consequently transfers into breast milk. The
active metabolites have been reported to cause drowsiness in infants.
• Midazolam, with a rapid onset of action and metabolic elimination, is preferred for the rapid
induction of anesthesia. The amount of midazolam transferred to an infant via milk is
minimal.
• Optimal maternal pain control is necessary for initiation and continuation of breastfeeding.
For postpartum pain management, non-opioids are preferred.
– Acetaminophen at appropriate doses is effective and safe.
– Ibuprofen has low-to-nil transfer and is a moderately effective analgesic.
– Ketorolac has extremely low transfer into breast milk and is a potent analgesic in mothers
without contraindications to it. In the peripartum period, it is frequently used.
– Prolonged naproxen use has been associated with GI disturbances in the infant despite low
transfer into milk.
• Mothers should be encouraged to control pain with the lowest effective dose. High-dose
opioid analgesia may affect the infant’s suckling vigor and alertness.
– Morphine, in low-to-moderate doses, appears to be reasonably safe in most studies.
However, there are variations in the effects of morphine, and some infants are more
susceptible to morphine-related sedation than others.
– Hydromorphone has been shown to transfer to breast milk.
– Hydrocodone and codeine have been safely used in millions of breastfeeding mothers.
However, there is no data regarding its transfer through milk. Higher doses may lead to
infant sedation.
– Fentanyl levels in breast milk have been studied and have been found to be low.
– Sufentanil transfer should be similar to fentanyl, even though it has not been published.
– Meperidine has a greater incidence and duration of neonatal depression, cyanosis, and
bradycardia and should be used minimally. Small doses may be used 1 hour before
possible delivery time. When PCA is chosen, morphine and fentanyl are preferred over
meperidine.
• Local anesthetics:
– Bupivacaine enters breast milk in very low doses and in small doses is considered safe.
– Parenteral lidocaine infusion for the treatment of arrhythmias was studied in a lactating
mother and found to be exceedingly low.
– Surgical cases that require large amounts of infiltrated drug, such as plastic surgery,
consider pumping and discarding milk for 12 hours before resuming breastfeeding.
• Regional anesthesia is preferred over general anesthesia for maternal safety in the
peripartum period due to the reduced amount of medications that are globally
administered. The same concept may be extrapolated to the breastfeeding mother, and
should be considered and discussed.
– Minimize local anesthetic dose
– Minimize motor blockade
– Opioids are commonly added to local anesthetics in both epidurals and spinals for its
synergistic effect of producing powerful and longer duration of pain control. Also it
reduces the concentration of local anesthetic needed for optimal pain relief, thus reducing
motor blockade, hypotension, and overdose reactions. However, there are reports of
neonatal sedation and poor suckling following fentanyl epidural anesthesia.
– Vasoconstrictors such as epinephrine are used to improve quality of regional block by
allowing greater penetration of local anesthetic and reduced diffusion from the epidural
space. Epinephrine may enter breast milk but is rapidly destroyed in the infant’s GI tract
prior to absorption.
• Atropine use is controversial. Infants are sensitive to anticholinergic agents. Atropine is
passed into the milk and may interrupt milk production and produce antimuscarinic effects
in infants. There is no data regarding the transfer of glycopyrrolate into milk. However,
glycopyrrolate, with its poor lipophilicity and oral bioavailability, is preferred over
atropine.
FOLLOW-UP
If the mother continues to have difficulty breastfeeding postoperatively, refer to a lactation

consultant.
REFERENCES
1. Montgomery A, Hale TW, Academy of Breastfeeding Medicine Protocol Committee. ABM
clinical protocol #15: Analgesia and anesthesia for the breastfeeding mother. Breastfeed
Med. 2006;1(4):271–277.
2. American Academy of Pediatrics Committee on Drugs. Transfer of drugs and other
chemicals into human milk. Pediatrics. 2001;108(3):776–789.
3. Hale TW. Anesthetic medications in breastfeeding mothers. J Hum Lact. 1999;15(3):185–
194.
ADDITIONAL READING
• Spigset O. Anaesthetic agents and excretion in breast milk. Acta Anaesthesiol Scand.
1994;38(2):94–103.
• Zeisler JA, Garder TD, De Mesquita SA. Lidocaine excretion in breast milk. Drug Intell Clin
Pharm. 1986;20:691–693.
• Substance abuse during pregnancy
CLINICAL PEARLS
• The type of anesthetic depends on the type of surgery and must be tailored to the needs of
the individual mother and infant.
• The effect of anesthesia on the postpartum mother and infant depends on multiple factors
including age of infant, stage of lactation (early or late), and ability of infant to tolerate
small quantities of anesthetic medications.
• Discontinuing breastfeeding for long periods of time results in suffering for both the nursing
infant and mother.
• Current opinion is that breastfeeding can be resumed as soon as the mother feels physically
and mentally capable to do so and that there is no time interval needed before restarting
breastfeeding.
• Limited data and evidence is available and guidelines are lacking.
LAMINAR AIR FLOW
Theodore J. Cios, MD, MPH
Khaled Sedeek, MD
BASICS
DESCRIPTION
• Laminar airflow, also sometimes referred to as streamlined flow, occurs when adjacent
layers of a fluid (air, water) slide steadily past each other without disruption. Laminar flow:
– Has a pattern that is parallel to the long axis of the tube
– Occurs at a lower velocity than the critical velocity
– Is dependent upon viscosity (1,2)
– Obeys the Hagen–Poiseuille equation
– Is more likely to occur at low speeds, small diameters, low densities, and high viscosities
• Turbulent flow occurs when flow rates exceed the critical velocity. Turbulent flow:
– Has a continuously changing flow pattern (magnitude and direction) and is not linear. It is
characterized by irregular fluctuations or mixing of the fluid or gas. The mechanical
energy dissipates as heat.
– Is dependent upon density (1,2)
– Inertial forces overcome viscous forces, and there is not enough viscosity to dissipate
motion.
– Does not follow the Hagen–Poiseuille equation
– Is more likely to occur at high speeds, large diameters, high densities, and low viscosities
• The Hagen–Poiseuille equation describes the changes in pressure of a non-compressible fluid
or gas flowing in a cylindrical tube (1). Changes in pressure are directly related to the fluid
viscosity, length of the tube, and flow; it is indirectly related to the radius to the 4th power.
ΔP = (8 nLQ) / r4, where ΔP is the pressure gradient, n is the viscosity of the fluid, L is the
length of the tube, Q is the flow, and r is the radius.
– Viscosity: Can be thought of as the internal/ inherent resistance of a fluid or gas to being
deformed. The greater the viscosity, the more energy that is required to move that fluid
(e.g., water vs. lava).
– Flow through a cylindrical tube: The material in the center of the tube has the greatest
velocity, whereas the material adjacent to the walls is stationary due to friction.
– Radius: Inversely related to the change in pressure to the 4th power; that is, a small
change in the radius of a tube will produce a disproportionate change in pressure.
• The Reynolds number quantifies the amount of inertial and viscous forces for specific fluid
flow conditions (1).
– It is directly related to velocity, density, and diameter; it is inversely related to viscosity.
Reynolds number = (vpd)/n, where v is linear velocity, p is the density of the fluid, d is
the diameter of the tube, and n is the viscosity of the fluid.
– Increases in fluid viscosity will indirectly decrease the Reynolds value; it is more difficult
for viscous lava to move fast enough to attain turbulence.
– Turbulent flow results when a critical Reynolds number is reached. Numbers >2,000
make turbulent flow likely (1).
• Asthma: In bronchoconstriction, narrowing the diameter/radius of the bronchiole by smooth
muscle contraction creates a sizeable change in the pressure (radius is raised to the 4th
power). This creates a transition point in the airflow pattern and can potentially cause
turbulence.
• Tracheal stenosis: Similar to bronchoconstriction, a decrease in radius creates a transition
point in airflow pattern; the increased pressure can result in turbulence.
• Atherosclerosis: Deposits can cause abrupt changes in the vessel diameter (decreased radius)
that can result in turbulent flow. Additionally, if there is a compensatory increase in vessel
diameter distal to the lesion, turbulent flow is more likely to result.
• Anemia/polycythemia: In anemic patients, blood is less viscous and has a greater propensity
to undergo turbulent flow (inertial forces are greater than viscous forces). The opposite is
true for patients with polycythemia and other conditions with higher blood viscosity.
• Anesthetic circuit
– Corrugated anesthetic circuit tubing causes turbulent flow to occur at a lower velocity
than if tubes were smooth (2,3). Corrugated tubing is designed to allow bending of the
hose while preventing twisting and interruption of gas flow. It is less likely to kink and
obstruct airflow, especially when making turns or attempting to overcome potentially
acute angles. It maintains its diameter during bending (increased Reynold’s number); thus
the tubing continues to function well when coiled or bent.
– Connector pieces of anesthetic circuits have sharp angles and also increase the likelihood
of turbulent flow (2,3).
– Endotracheal tube: Flow is laminar, and a small change in diameter will have a profound
impact since these 2 parameters are inversely related to the 4th power. Kinking or the
presence of secretions will also lead to greater changes in pressure and the development of
turbulence.
– Applying the Reynolds number equation, the density of a gas has a more significant effect
at high flow while viscosity is more significant at low flow.
– Vessels: Elastic vessels decrease the tension against the walls and decrease turbulent flow
by accommodating changes in flow velocity and changes in diameter that may otherwise
alter the Reynolds number. However, large diameters with high velocity tend towards
turbulent flow.
– At sharp angles/transition points such as arterial bifurcations (carotid, iliac, etc.),
previously laminar flow is likely to become turbulent for a period due to changes in the
frictional forces encountered.
• Respiratory system
– Tracheal stenosis: Results in acute constriction of flow by altering the diameter of the
tube, thereby creating transition points proximal and distal to the obstruction at which
turbulent flow can occur. May be potentially auscultated over the anterior larynx.
– During a resting breathing state (low velocity) airway flow becomes laminar at the level of
the bronchioles. However, with exertion (increased velocity), laminar flow may be limited
to even smaller airways.
• Therapeutic modalities
– Helium: Has a lower density than oxygen; thus using high concentrations in a mixture of
fresh gas decreases the total density and resistance to flow, with a resultant decrease in
the Reynold’s number and potentially turbulence (4). Heliox, a mixture of oxygen and
helium, can be useful in certain clinical scenarios such as upper airway obstruction
secondary to foreign body, vocal cord dysfunction, respiratory distress, post-extubation
stridor, and similar causes (5).
– Xenon: An inert gas with a greater density than oxygen can increase turbulence at lower
flow rates, when administered as part of a gas mixture. Xenon inhalation can cause a
significant increase in peak airway pressure during mechanical ventilation and may limit
its use as an anesthetic agent (6,7).
– Altitude: At high altitudes, there is lower atmospheric pressure and lower gas density, but
little change in viscosity. Consequently, the gas flow through a rotameter will be greater
than expected at high flows (turbulence, and more affected by density) but not affected at
low flows (laminar, and more influenced by viscosity).
EQUATIONS
• Hagen–Poiseuille equation: ΔP = 8 nLQ/r4, where Q = flow, ΔP = pressure gradient, r =
radius, L = length of the tube, n = viscosity of the fluid
• Reynolds number = vpd/n, where v = linear velocity, p = density of the fluid, d =
diameter of the tube, n = viscosity of the fluid
GRAPHS/FIGURES
REFERENCES
1. Young HD, Freedman RA. University physics, 10th ed. Addison-Wesley, 2000.
2. min E. Physics in anesthetic practice, 1st ed., 2003.
3. arbrook GD, Davis PD, Kenny GN. Basic physics and measurement in anaesthesia, 5th ed.
Elsevier, 2003.
4. atz IM, Martin AR, Muller PA, et al. The ventilation distribution of helium–oxygen mixtures
and the role of inertial losses in the presence of heterogeneous airway obstructions. J
Biomech. 2011;44(6):1137–1143.
5. Mihaescu M, Gutmark E, Murugappan S, et al. Modeling flow in a compromised pediatric
airway breathing air and heliox. Laryngoscope. 2008;118(12):2205–2211.
6. Rueckoldt H, Vangerow B, Marx G, et al. Xenon inhalation increases airway pressure in
ventilated patients. Acta Anaesthesiol Scand. 1999;43:1060–1064.
7. Abramo A, Di Salvo C, Foltran F, et al. Xenon anesthesia improves respiratory gas
exchanges in morbidly obese patients. J Obesity. 2010;2010. pii: 421593. Epub 2010
March 2.
• Asthma
• Turbulent flow
• Tracheal stenosis
CLINICAL PEARLS
• Heliox is usually 21% oxygen and 79% helium but concentrations of 30% and 70%,
respectively, can be used (5).
• Using heliox in subglottic pediatric obstruction with in vitro models has been shown to
decrease airway resistance by up to 40% (5).
• Xenon significantly increases airway pressure and may be of limited use in clinical practice
(6,7).
LAPAROSCOPY
Colin Bauer, MD
BASICS
DESCRIPTION
• Laparoscopy describes minimally invasive surgical procedures within the chest, abdomen,
pelvis, and/or neck. Carbon dioxide (CO2) insufflation expands cavities (e.g.,
pneumoperitoneum [PPN]) to facilitate surgical visualization and intervention.
Visualization of joints (arthroscopy) and the bladder (cystoscopy) can be performed with
fluid insufflation.
• Patient position varies depending on surgery. Common positions include lateral decubitus
(nephrectomy), supine (appendectomy), Trendelenburg (prostatectomy), and/or reverse
Trendelenburg (gastric bypass).
• Generally requires 2–5 incisions for the insertion of multiple ports/trocars; however, some
procedures may be performed through a single incision (e.g., appendectomy).
• Surgical time varies depending on the patient’s prior surgical history and the specific
procedure being performed; simple procedures such as cholecystectomy and appendectomy
are generally <1 hour.
• Greater than 2 million laparoscopic procedures are performed annually.
• Insufflation is generally accomplished using a gas, although liquid is used for a small subset
of procedures (arthroscopy, cystoscopy).
– CO2 is the most commonly used gas for insufflation because it is colorless (enhances
visualization), inexpensive, non-combustible, and highly soluble in blood (decreases risk
of a venous air embolism).
– Nitrous oxide and oxygen are combustible and are associated with an increased risk of OR
fires.
– Air and helium have decreased blood solubility and are more likely to cause gas emboli.
• Physiologic effect of a pneumoperitoneum:
– Cardiac: Decreased preload, increased afterload (secondary to norepinephrine), and
decreased cardiac output. Initiation of PPN may be associated with a vagal response
and/or asystole; atropine or glycopyrrolate should be immediately available.
– Respiratory: Decreased functional residual capacity (FRC), decreased lung compliance,
decreased PaO2, and increased peak inspiratory pressures caused by insufflation-induced
cephalad migration of the diaphragm and abdominal contents
• Trendelenburg or reverse Trendelenburg position is used to improve visualization by using
gravity to displace the bowel and other organs from the surgical site.
• Physiologic effects of Trendelenburg position:
– Cardiac: Increased venous return and cardiac output. Mitigates some of the adverse
cardiac effects of a PPN.
– Respiratory: Decreased FRC, lung compliance, and PaO2, and increased peak inspiratory
pressures caused by gravity-induced cephalad displacement of diaphragm and abdominal
contents
• Physiologic effects of reverse Trendelenburg position:
– Cardiac: Decreased venous return (caused by venous pooling in lower extremities) and
decreased cardiac output
– Respiratory: Increased FRC and pulmonary compliance, and decreased peak inspiratory
pressures by facilitating caudal displacement of diaphragm and abdominal contents.
Mitigates some of the adverse respiratory effects of a PPN.
• Mortality related to laparoscopy is rare, estimated at 1 in 10,000.
• Morbidity associated with laparoscopic procedures usually involves complications related to
formation of PPN, physiologic effects of hypercarbia, and/or trocar placement (inadvertent
insufflation of a cavity or space other than peritoneum occurs in ~2% of laparoscopic
surgeries).
• Vagal reflex or asystole with institution of the pneumoperitoneum
• CO2 venous embolus: Insertion of a Veress needle or trocar directly into a blood vessel may
lead to a CO2 embolus (associated with a 28% mortality). Manifestations range from
subclinical to hypoxemia, profound hypotension, dysrhythmias, and even cardiac arrest.
• Referred shoulder pain from diaphragmatic irritation (C3–5 innervation)
• Hypercarbia: CO2 insufflation can lead to hypercarbia if minute ventilation does not
increase proportionately. The ensuing respiratory acidosis can lead to:
– Cardiac contractility
– Arrhythmias
– Pulmonary vasoconstriction
– Hyperkalemia
– Increased intracranial pressures
• Perforation: Placement of Veress needle or trocars can lead to inadvertent organ or blood
vessel perforation.
– Vascular injury is the most lethal complication (up to 15% mortality); insertion of a Veress
needle or trocar into a major blood vessel can cause life-threatening bleeding and is an
indication for conversion to an open procedure.
• Pneumothorax/pneumomediastinum:
– Risk factors include insufflation pressures >15 mm Hg, surgery duration >200 minutes,
and congenital or acquired defects in the diaphragm or pleura.
– Signs include hypercarbia, increased airway pressure, and hemodynamic instability
(tension pneumothorax).
– Treatment involves release of the PPN; placement of a chest tube may be necessary in the
event of hemodynamic instability.
• Subcutaneous emphysema
– Risk factors include malposition of Veress needle in subcutaneous tissue, insufflation
pressures >15 mm Hg, and/or surgery duration >200 minutes.
– Manifestations include crepitus, increased EtCO2, and respiratory acidosis.
• Advantages of laparoscopy:
– Improved cosmesis
– Shorter recovery time
– Decreased pain
– Decreased blood loss
– Decreased pulmonary complications
– Lower incidence of wound infections
– Faster recovery of bowel function
– Minimizes stress, inflammatory, and metabolic response
• Relative contraindications to laparoscopy:
– Intracranial hypertension
– Hypovolemia
– Severe cardiac disease (coronary, valvular, cardiomyopathy)
– Severe pulmonary disease (chronic obstructive pulmonary disease, restrictive diseases)
– Coagulopathy
• Length of hospital stay varies; simple procedures may be performed as outpatient surgeries.
GRAPHS/FIGURES
See Table
REFERENCES
1. Gerges FJ, Kanazi GE, Jabbour-khoury SI. Anesthesia for laparoscopy: A review. J Clin
Anesth. 2006;18:67–78.
2. Henny CP, Hofland J. Laparoscopic surgery: Pitfalls due to anesthesia, positioning, and
pneumoperitoneum. Surg Endosc. 2005;19:1163–1171.
3. Saggar VR, Singhal A, Singh K, et al. Factors influencing development of subcutaneous
carbon dioxide emphysema in laparoscopic totally extraperitoneal inguinal hernia repair. J
Laparoendosc Adv Surg Tech. 2008;18(2):213–216.
4. Permpongkosol S, Link RE, Su LM, et al. Complications of 2,775 urological laparoscopic
procedures: 1993 to 2005. J Urol. 2007;177:580–585.
5. Fuller J, Scott W, Ashar B, et al. Laparoscopic trocar injuries: A report from a U.S. Food
and Drug Administration (FDA) Center for Devices and Radiological Health (CDRH)
Systematic Technology Assessment of Medical Products (STAMP) Committee. November 7,
2003. Available at: http://www.fda.gov/medicaldevices/safety/alertsand
notices/ucm197339.htm
ADDITIONAL READING
• Kuczkowski KM. Nonobstetric surgery in the parturient: Anesthetic considerations. J Clin
Anesth. 2006;18:5–7.
• Manchanda G, Bhalotra AR, Bhadoria P, et al. Capnothorax during laparoscopic
cholecystectomy. Indian J Anaesth. 2007;51:231–233.
• Takahata O, Kuniswa T, Nagashima M, et al. Effect of age on pulmonary gas exchange
during laparoscopy in the Trendelenburg lithotomy position. Acta Anaesthesiol Scand.
2007;51:687–692.
• Cystoscopy
• Appendectomy
• Cholecystectomy
• Video-assisted thoracoscopic surgery (VATS)
CLINICAL PEARLS
• Complications of laparoscopy include pneumothorax/pneumomediastinum, hypercarbia,
hypotension, subcutaneous emphysema, and/or injury to bowel/ureter/blood vessels or
other organs.
• Pregnancy considerations: Laparoscopy is the most common surgical procedure performed
during the first trimester. General anesthesia for laparoscopy can be safely performed
during pregnancy but fetal monitoring should be considered.
• Geriatric considerations: EtCO2 is a less reliable estimate of PaCO2 in the elderly. The
baseline increase in alveolar dead space seen in the geriatric patient is exacerbated by
laparoscopy and the Trendelenburg position.
• Pediatric considerations: Consider using a cuffed endotracheal tube. Increased intra-
abdominal pressure with a PPN may necessitate increased peak airway pressures.
LARYNGOSCOPY POSITIONING
Davide Cattano, MD, PhD
BASICS
DESCRIPTION
There are a number of alternative head and neck positioning techniques that can be
performed to improve visualization of the vocal cords during direct laryngoscopy. They
include the:
• Sniffing position
• Neutral “in-line” position
• Ramped position
• Beach chair position
• “Sniffing” position is generally thought to be the best position for a patient in preparation
for intubation and airway management. Ivan Magill, who first proposed the position and its
definition, described it as somebody “sniffing the morning air” or “drinking a pint of beer.”
– Main advantages: Optimizes airway patency and facilitates mask ventilation. Provides
good exposure of the glottis in most adult subjects and facilitates intubation of the
trachea.
– Studies have shown conflicting evidence of its efficacy compared to other combinations of
extension and flexion of the upper and lower cervical spine and atlanto-occipital joint.
Results and conclusions appear to be dependent on the type of population investigated,
the endpoints of the studies (easiness of visualization as opposed to easiness of
intubation), the experience of the providers, and the type of blades utilized.
– Although no univocal conclusion has been reached so far, the sniffing position is most
likely a very reasonable “starting point” in preparation for laryngoscopy in the majority of
adult patients. Additionally, it may occasionally require adjustments to improve glottis
visualization, depending on an individual patient’s variability.
• Neutral “in-line” position is the term used to define the cervical spine and head alignment in
the natural position assumed while supine. There is no head elevation, cervical spine
flexion, or extension.
– Main advantages: Provides the best axes alignment for children and infants. Avoids further
injury or potential injury in patients with a traumatized cervical spine or at risk for such
conditions, respectively.
– Disadvantages: Glottis exposure with conventional direct laryngoscopy can be suboptimal
in most adults.
• “Ramped” position may be achieved by placing blankets or other specifically manufactured
devices underneath the upper body and head of the patient.
– Main advantages: Facilitated ventilation and visualization of the glottis. Fat tissue at the
level of the neck and chest is favorably displaced by gravity, and can aid with
maneuvering the laryngoscope blade and handle.
• Beach chair position describes the elevation of the OR bed to 45°.
– Main advantages: Offers optimal airway patency in conditions in which there is a risk of
airway collapse and obstruction with the patient in the supine position.
– Some anaesthetists advocate that even a 25° “back-up” position of the OR bed offers
significant improvement of the laryngeal view compared to the classical supine position,
and consider this a valuable alternative to the “ramped position.”
ANATOMY
• Sniffing position: Following the observations of Magill, Bannister and Macbeth first studied
the angles of the oral, pharyngeal, and laryngeal axes with the head in different positions.
Their aim was to identify the best possible alignment of the 3 axes for the purpose of
exposing the glottis and facilitating endotracheal tube insertion with direct laryngoscopy.
– In the studies by Bannister and Macbeth, the key components to optimal alignment were
identified as: Flexion of the lower cervical spine, extension of the upper cervical spine,
and extension of the atlanto-occipital joint (same as “sniffing position” of Magill).
– The external landmarks used were: The position of the chin, the angle of the mandible
with respect to the OR table, and the position of the ears anterior to (or at level with) the
sternum. These positions were noted and correlated with optimal exposure of the glottis
(Figure 1). Although in reality the perfect alignment of these axes does not seem to be
achieved, as shown in recent MRI studies, this still seems to be the position that offers the
best approximation to the illustrated “ideal alignment.”
FIGURE 1. “Sniffing position (1).”
• Neutral position: There is no elevation of the head compared to the rest of the body, and the
cervical spine rests in its natural position without being flexed or extended. In this position
the oral, pharyngeal, and laryngeal axes are not aligned.
FIGURE 2. Neutral “in-line” position. There are 3 distinct axes (1).
• Ramped position: The presence of a “wedge” underneath the upper body of the patient
creates a horizontal alignment between the external auditory meatus and the sternal notch.
The aim is to achieve in obese patients the same “best alignment” of the 3 axes (oral,
pharyngeal, and laryngeal) that is reached with the sniffing position in nonobese patients.
FIGURE 3. Ramped position (1).
• Beach chair position: The patient’s head is in line with the anesthesia provider’s xiphoid
process. In this position airway patency is maintained better than in the supine position and
access to the airway by the anesthesia provider is still relatively easy. The provider may be
on a step and at an angle of the backrest to facilitate direct laryngoscopy and manual bag-
mask ventilation.
FIGURE 4. Beach chair position (1).
• The presence of medical conditions that alter the patient’s anatomy and/or the body habitus
may significantly influence the choice of the appropriate position to secure the airway.
– Obese patients may benefit from a “ramped,” “beach chair,” or other “back-up” position to
optimize glottis exposure.
– Known or suspected cervical spine injury patients are at risk of spinal cord lesions if
positioned in the “sniffing position.” Neutral position with “in-line” manual stabilization
techniques and/or awake fiberoptic technique is recommended for these patients.
– In rheumatoid arthritis patients, anterior atlantoaxial subluxation and displacement or
fracture of the odontoid process may occur in the “sniffing position.” Extreme caution is
recommended with any movement of the cervical spine during intubation.
– Scoliosis and previous cervical spine surgery may alter neck mobility and prevent optimal
positioning for laryngoscopy.
– Conditions affecting the ability of the patient to maintain airway patency, such as the
presence of extrinsic or intrinsic obstruction of the upper airway, may require the use of
alternative techniques for intubation (e.g., fiberoptic-assisted intubation in the sitting or
beach chair position with the patient spontaneously breathing).
• In infants and small children, the prominence of the occiput in relation to the body results in
slight neck flexion when the child is supine, and, according to some experts, head elevation
is not required to obtain optimal positioning for direct laryngoscopy.
• Moderate head flexion may facilitate nasotracheal intubation in infants and young children.
• Overall there is substantial lack of agreement among experts on the best position for direct
laryngoscopy in young children.
• Down syndrome and other congenital syndromes associated with craniofacial anomalies
require special attention in planning for laryngoscopy and intubation.
• The choice of one specific position over another may have a critical impact on intubation
success rate and/or maintenance of adequate oxygenation while managing the airway. It is
critical to identify patients who may require airway management in the ramped, beach
chair, or “back-up” position (high risk of airway obstruction in the supine position) and
patients who require “in-line” stabilization in the neutral position (unstable cervical spine).
It is also important to be able to recognize anatomical anomalies/changes that may require
adjustments of the head and neck position in order to obtain better access to the airway for
intubation and/or ventilation. While no predefined formula exists to help in any given
condition, attention to this matter and careful consideration of alternative positioning is an
important component of a successful strategy for airway management.
• Non-pathological modifications of the body habitus must not be disregarded when planning
for direct laryngoscopy positioning. Certain hairdos may affect the possibility to
appropriately extend the superior cervical spine and the atlanto-occipital joint (e.g., large
mass of thick hair pulled up at the back of the head or hair that is worked into firm braids).
REFERENCES
1. Illustration by Cavallone L, MD.
2. Greenland KB, Eley V, Edwards MJ, et al. The origins of the sniffing position and the Three
Axes Alignment Theory for direct laryngoscopy. Anaesth Intensive Care. 2008;36(Suppl
1):23–27.
3. Lee BJ, Kang JM, Kim DO. Laryngeal exposure during laryngoscopy is better in the 25°
back-up position than in the supine position. Br J Anaesth. 2007;99(4):581–586.
4. Rao SL, Kunselman AR, Schuler HG, et al. Laryngoscopy and tracheal intubation in the
head-elevated position in obese patients: A randomized, controlled, equivalence trial.
Anesth Analg. 2008;107(6):1912–1918.
5. Fox WT, Harris S, Kennedy NJ. Prevalence of difficult intubation in a bariatric population,
using the beach chair position. Anaesthesia. 2008;63(12):1339–1342.
6. Vialet R, Nau A. Effect of head posture on pediatric oropharyngeal structures: Implications
for airway management in infants and children. Curr Opin Anaesthesiol. 2009;22(3):396–
399.
• Esophageal intubation
CLINICAL PEARLS
• Correctly positioning a patient on the OR bed prior to induction of general anesthesia and in
preparation for laryngoscopy is a fundamental part of preoperative planning and one of the
determinants of success at managing the airway.
• It is critical to utilize the appropriate position for each patient and for each intubating
device.
• For example, video-laryngoscopes that have a side tube channel to guide ETT insertion
through the glottis appear to have increased success with an “in-line” (neutral) neck
position compared to a “sniffing position.” Additionally, it has been suggested that these
devices may present a higher rate of success and less cervical movement during intubation
in conditions that require in-line manual stabilization compared to a Macintosh blade.
• Optimal pre-oxygenation also depends on patient positioning. Pre-oxygenation in the head-
up position seems more efficacious than pre-oxygenation in the supine position since it
improves the functional residual capacity.
• While the “sniffing” analogy has been used for almost a century, other analogies, such as
“win with the chin” with reference to the best position for winning a foot race (Brindley
2010), have been proposed and considered effective in teaching basic positioning for
laryngoscopy to novices.
LARYNGOSPASM
Pascal O. Owusu-Agyemang, MD
BASICS
DESCRIPTION
• Laryngospasm is a protective reflex closure of the glottis as a result of abnormal stimulus (1)
[B].
• Perioperatively this can result in airway obstruction with resultant desaturation.
EPIDEMIOLOGY
Incidence
• The overall incidence of laryngospasm is 0.87% (2)[C].
• The incidence ranges from 1.74% in children aged 9 years old to 2.82% in infants (2)[C].
Prevalence
• Increased in children
• More frequent during emergence from anesthesia
• Tonsillectomies and adenoidectomies have the highest incidence of post-extubation
laryngospasm.
Morbidity
• Oxygen desaturation
• Anoxic brain injury
• Bradycardia
• Pulmonary aspiration
• Cardiac arrest
Mortality
Although laryngospasm has been quoted as a preceding cause of airway obstruction and
ultimately death, the exact incidence of mortality is unknown.
• Insufficient depth of anesthesia
• Young age
• Airway irritation (blood/secretions, regurgitation)
• Airway manipulation
• Upper respiratory tract infections
• Smokers
• Passive smoke exposure
• Type of surgery (e.g., tonsillectomy and adenoidectomy)
• Afferent fibers of the superior laryngeal nerve control laryngeal muscle contractions which
protect the airway during swallowing.
• Laryngospasm occurs when there is loss of inhibition of the laryngeal closure reflex as a
result of abnormal excitation (3)[A]. This commonly occurs during induction and upon
emergence from anesthesia. The patient is particularly vulnerable during the second stage of
anesthesia. The presence of saliva, mucus secretions, and airway devices (endotracheal tube,
trumpets) can elicit abnormal excitation and can lead to laryngospasm.
• It is important to note that laryngospasm is mediated by skeletal muscle while
bronchospasm is smooth muscle mediated.
• Laryngospasm is characterized by the prolonged interruption of respiration due to a ball
valve mechanism of the vocal cords, false cords, and supraglottic tissue.
• Topical lidocaine can blunt the airway response to irritation and instrumentation.
• If mask induction is performed, sevoflurane or halothane should be used as these 2 agents
are the least irritating to the airway.
• Desflurane is very irritating to the unprotected airway and should be avoided during mask
inductions.
• If IV line insertion is performed after a mask induction, it should be done after deep
anesthesia has been achieved.
• The use of an adequate dose of muscle relaxants will minimize the chances of laryngospasm
during intubation. An appropriate amount of time should be allowed for full onset.
• Suctioning of the oropharynx before emergence (stage 2) from anesthesia
• Antisialagogues (to reduce secretions) may be considered.
• Avoid painful stimulation during emergence.
DIAGNOSIS
• Laryngospasm can be characterized as partial or complete.
• Partial laryngospasm is generally associated with an audible inspiratory or expiratory sound
of airway obstruction.
• As the obstruction becomes worse, tracheal tug and paradoxical respiratory movements of
the chest and abdomen will develop.
• Should laryngospasm progress from partial to complete, the audible signs cease, leaving
only visible signs of airway obstruction.
• Oxyhemoglobin desaturation, cyanosis, bradycardia, and subsequently cardiac arrest may
follow if the symptoms are not treated promptly.
• Supraglottic obstruction: This is usually relieved by performing a jaw thrust, chin lift, and
insertion of an oropharyngeal airway (2)[C].
• Bronchospasm: This is characterized by wheezing on auscultation and diminished breath
sounds (2)[C].
TREATMENT
• Partial laryngospasm
– CPAP with 100% oxygen and a tight-fitting mask can help facilitate ventilation and/or
deepen the level of anesthesia
• Complete laryngospasm
– CPAP will not break complete laryngospasm because forced inflation of the pharynx
distends the piriform fossa on either side of the larynx and presses the aryepiglottic folds
more firmly against each other. Oxygen will fill the stomach instead of the lungs.
– In the absence of an IV line, perform continuous positive airway pressure (CPAP) with
100% oxygen, optimize airway with a jaw thrust and chin lift, and deepen anesthesia with
an inhalational agent (preferably sevoflurane or halothane). If these measures fail,
administer succinylcholine 4 mg/kg intramuscularly.
– In addition to IV propofol, airway optimization should be performed. This should be done
by performing a jaw thrust and chin lift maneuver. This will stretch the geniohyoid
muscle to partially open the larynx and allow for ventilation and further deepening of
anesthesia with inhalational agents.
– If the above measures fail a muscle relaxant may be given to relax the vocal cords.
Succinylcholine 0.1 mg/kg allows for quick onset and recovery.
– Emergence even after treatment with succinylcholine. It is therefore important to
eliminate contributing noxious stimuli before attempting another emergence.
– In the presence of an IV line, complete laryngospasm should be treated by deepening
anesthesia with propofol (0.25–0.8 mg/kg) (1)[B].
• Succinylcholine administration in children may be associated with severe bradycardia and
cardiac arrest; thus, it is highly recommended to give atropine (0.02 mg/kg) with
succinylcholine.
• Gentle chest compression with 100% oxygen in children. 3 theories for efficacy:
– Vocal cord spasm prevents entrance of air into the lung, but not its exit; thus, chest
compression “pushes” air in the lung directly on the vocal cords to relieve the spasm. It
functions to deliver positive pressure, but from the “opposite” direction of CPAP.
– Second, chest compression stimulates fast, shallow breathing with or without increases in
minute ventilation. This results in an increased respiratory drive.
– Third, the Hering–Breuer deflation reflex mediated via the vagus nerve is activated by
stimulation of stretch receptors or stimulation of proprioceptors activated by lung
deflation. Thus, vocal cord relaxation may result from vagal nerve impulses.
– Benefits over CPAP include not distending the stomach or splinting of the diaphragm (4)
[A].
• Magnesium: Doses of 15 mg/kg over 20 minutes appeared to significantly decrease the
incidence of laryngospasm in pediatric patients (5).
FOLLOW-UP
• Patients without immediate, apparent complications should be observed for 2–3 hours and
then discharged.
• Negative pressure pulmonary edema can occur after laryngospasm. This is the result of
decreased intrathoracic pressure generated by an attempted inspiration against a closed
glottis. This creates a mean negative transpulmonary pressure, leading to transudation of
fluid from the pulmonary capillaries into the interstitial space.
– The clinical signs are oxygen desaturation, pink frothy sputum in the airway, or signs of
alveolar infiltration on CXR.
– Treatment is directed at supplementation of oxygen and diuretics. Occasionally, patients
may require reintubation to facilitate adequate oxygenation.
• Patients who develop cardiopulmonary complications including negative pressure
pulmonary edema should be admitted for further care.
CLOSED CLAIMS DATA
• A review of the malpractice database from 1973 to 2000 revealed that airway obstruction
including laryngospasm (n = 8) was the most common respiratory event.
• Another review of the Pediatric Perioperative Cardiac Arrest Registry from 1998 to 2004
determined that causes accounted for 27% of all cardiac arrest episodes and that airway
obstruction from laryngospasm was the most common cause (6%).
REFERENCES
1. Al-alami AA, Zestos MM, Baraka AS. Pediatric laryngospasm: Prevention and treatment.
Curr Opin Anaesthesiol. 2009;22(3):388–395.
2. Alalami AA, Ayoub CM, Baraka AS. Laryngospasm: Review of different prevention and
treatment modalities. Paediatr Anaesth. 2008;18(4):281–288.
3. Burgoyne LL, Anghelescu DL. Intervention steps for treating laryngospasm in pediatric
patients. Paediatr Anaesth. 2008;18(4):297–302.
4. Al-Metwalli RR, Mowafi HA, Ismail SA. Gentle chest compression relieves extubation
laryngospasm in children. J Anesth. 2010;24:854–857.
5. Gulhas N, Durmus M, Demirbilek S, et al. The use of magnesium to prevent laryngospasm
after tonsillectomy and adenoidectomy: A preliminary study. Paediatr Anaesth.
2003;13(1):43–47.
ADDITIONAL READING
• Olsson GL, Hallen B. Laryngospasm during anaesthesia: A computer-aided incidence study in
136,929 patients. Acta Anaesthesiol Scand. 1984;28(5):567–575.
CODES
ICD9
478.75 Laryngeal spasm
ICD10
J38.5 Laryngeal spasm
CLINICAL PEARLS
• Laryngospasm results in obstruction of the larynx and may lead to desaturation, post-
obstructive pulmonary edema, bradycardia, and cardiac arrest.
• The incidence is highest in children and during emergence from anesthesia.
• For partial laryngospasm, the initial treatment typically consists of CPAP and 100% oxygen,
combined with a jaw thrust maneuver. If unsuccessful, propofol and muscle relaxants may
be required to relax the vocal cords.
LATEX ALLERGY
BASICS
DESCRIPTION
• Allergy to latex manifests as a variety of clinical symptoms and is often categorized into
Type IV and Type I hypersensitivity reactions.
• Type IV hypersensitivity is a cell-mediated or delayed type reaction. It is often localized to
the area of contact and occurs 48–72 hours after exposure. Often referred to as allergic
contact dermatitis, T-cell-mediated allergy, or chemical allergy.
• Type I hypersensitivity is IgE-mediated and results in an immediate response. It is systemic
and ranges from contact urticaria to occupational rhinoconjunctivitis, asthma, or
anaphylaxis.
• Latex is the second most common cause of anaphylaxis in the operating room. Under
general anesthesia it presents as cardiovascular compromise, airway swelling and
obstruction, flushing, and edema.
EPIDEMIOLOGY
Incidence
• Sensitivity to latex has been increasing in prominence since the introduction of Universal
Precautions.
• Life-threatening reactions in the US occur in approximately 1 in 30,000–50,000 people
undergoing general anesthesia.
Prevalence
• General population in the US (sensitization or allergy): 1–2%
• Healthcare workers: 3–14%
• Rubber industry workers: 10%
• Spina bifida and congenital urogenital anomalies: 24–60%
Morbidity/Mortality
Anaphylactic reactions under anesthesia have a mortality of 3.4%.
• Anaphylactoid reaction
• Repeated exposure to latex over time (repeated bladder catheterizations, spinal bifida
patients, multiple surgeries, especially laparotomies)
• Occupational exposure to latex (healthcare workers, latex factory workers)
• Urticaria
• Asthma
• Rhinitis
• Spina bifida patients
• Atopic patients
• Female preponderance
• Cross-reactivity with allergies to a variety of fruits (bananas, avocadoes, mangoes,
watermelons) and chestnuts
• Raw latex is the milky sap from the rubber tree (Hevea brasiliensis), to which ammonia is
added as the main preservative.
• Type I hypersensitivity is an IgE-mediated reaction to natural rubber latex antigen. It can
manifest as mild to life-threatening symptoms that include contact urticaria, occupational
rhinoconjunctivitis, asthma, or anaphylaxis.
– Latex sensitization occurs when exposure (airborne, parenteral, mucosal routes) to latex
antigen induces CD4+ and T cells to produce IL-4, IL-5, IL-6, IL-10, granulocyte-
macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor (TNF). These
cytokines and mediators result in the production of IgE antibody specific to latex antigen.
– Upon re-exposure (airborne, parenteral, mucosal routes) to latex antigen, there is a cross-
linkage of IgE molecules by latex on the surface of mast cells. This results in mast cell
degranulation and the release of mediators such as histamine, tryptase, slow-reacting
substance-A (SRS-A), prostaglandin, and leukotrienes.
– These mediators increase mucous secretion, capillary permeability, bronchial smooth
muscle tone (H1 receptor activation bradykinin), as well as decrease arterial tone (H2
receptor activation). Manifests as bronchospasm, V/Q mismatch, hypoxemia, and
hypotension.
– Activation of Hageman factor can start a cascade of disseminated intravascular
coagulation.
– Transudation of fluid into the extravascular space can lead to a clinical hypovolemia
which may result in myocardial ischemia.
• Type IV hypersensitivity is a contact dermatitis reaction to chemicals used to process rubber
by Langerhans and T cells. The patient presents within 48–72 hours of exposure with
erythema, vesicles, scaling, hyperpigmentation, and lichenification of the contacted areas.
• Irritant contact dermatitis is not a latex allergy; it is, however, the most common reaction
associated with latex, and is not life-threatening. It results from various alkaline chemicals
added during rubber production. The dermatitis appears within minutes to hours as a
localized abrasion with pruritus, erythema, cracking, dryness, and chapping of the skin.
• Prevention of exposure to latex in known latex-sensitized patients is the keystone to
preventing a potentially life-threatening allergic reaction. A latex-safe protocol in each
institution should be in place and should consist of identification of patients at risk,
establishment of a latex-free environment, and close coordination between all staff involved
in the management of these patients.
• Absolute avoidance of any latex-containing products is essential throughout the
perioperative period and during the hospital stay. Anesthetic equipments that may contain
latex include gloves, some syringe plungers, Foley catheters, medication vials with rubber
stoppers, disposable anesthesia bags, bandages (adhesives), tourniquets, some endotracheal
tubes, bellows, IV ports, blood pressure cuffs, some face masks. All manufacturer packaging
should indicate the presence of latex in any medical grade product.
• Preoperative prophylaxis with corticosteroids and antihistamines is controversial. At best, it
may attenuate a reaction but will not prevent true anaphylaxis.
• Latex-sensitive patients should be scheduled as first cases because the quantity of latex
aeroallergens is likely to be the lowest early in the morning. Airborne latex antigen can be
suspended in the air for up to 5 hours after a case.
• A latex-free cart should be used that contains non-latex alternatives, and all latex gloves and
products should be removed from the operating room. The room should also be labeled as
latex-free.
• A resuscitation cart should be placed adjacent to the operating room.
• The American Academy of Allergy and Immunology recommends that clinical testing should
be offered to high-risk patients in a latex-free environment.
DIAGNOSIS
• Signs and symptoms depend on the type, route, and amount of latex exposure as well as the
individual’s sensitivity.
– Awake patients may manifest swelling of contact areas, hives/welts, sneezing, runny nose,
ocular redness and tears, sore throat, GI cramping, wheezing, shortness of breath, and
chest tightness. Respiratory manifestations include bilateral rales, stridor, and cyanosis.
– Anesthetized patients may have a more dubious presentation. Dermatologic symptoms
(hives, welts, flushing, swelling) may not be immediately recognized under drapes and
warming devices. Hypotension is the first presenting sign in approximately 1/3rd of
patients in anaphylactic shock. Additionally, respiratory manifestations such as bilateral
rales, may not be immediately recognized.
• Monitors
– Noninvasive blood pressure monitoring: Look for worsening hypotension over a few
minutes, although some patients will present with a more precipitous decline in blood
pressure.
– EKG: Tachycardia, dysrhythmias, ST changes; pulseless electrical activity may be the first
manifestation in anaphylactic shock.
– Airway pressure monitors: High peak and plateau inspiratory pressures may be seen in the
mechanically ventilated patient. If the bronchospasm is severe, the patient may also have
auto-PEEP which will further contribute to hypotension. Decreased pulmonary compliance
may not be immediately recognized with LMAs.
– End-tidal carbon dioxide: May be increased with upsloping of capnograph tracing. It
should be noted that complete airway obstruction may occur with a supraglottic device,
mask GA, or supplemental oxygen modality (nasal canula, face mask) for a sedation case;
this will result in the extinguishment of the capnograph tracing.
– Pulmonary artery catheter (PAC) or pulse contour cardiac output monitoring (PiCCO): If
present, a low systemic vascular resistance will be present.
• Serum tryptase levels should be sent at the time of the event, at 1 hour, and 6–24 hours
after the episode.
• Serologic testing: Carries no risk of anaphylaxis and is the test of choice if the history
reveals a high probability of allergic reaction.
– Radioallergent absorbent testing (RAST) is capable of measuring the level of drug-specific
IgE antibody in the serum. It is highly specific (80–87%), but has a low sensitivity (50–
60%); false-negatives occur 25% of the time.
• Skin testing: Carries the risk of inducing systemic anaphylaxis and should only be performed
by physicians with training and resources to respond to an emergency situation.
– Skin prick testing uses an antigen solution at a variety of dilutions. It has been found to be
very sensitive and specific.
– Intradermal testing uses an antigen solution.
– Patch testing may be useful in establishing the diagnosis of contact dermatitis (Type IV
allergic reaction).
• Anaphylaxis due to other antigens (neuromuscular blocking agents, antibiotics, protamine,
blood transfusions):
• Asthma
• Angioedema
• Septic shock
• Carcinoid syndrome
TREATMENT
• Management of anaphylaxis due to latex does not differ from any other type of anaphylactic
reaction.
• Discontinue the exposure to latex.
• Communicate the emergency situation with the operating room team.
• Administer 100% oxygen; maintain a clear airway with a low threshold for intubation.
• Administration of epinephrine 10–100 μg IV
• Inhaled bronchodilators may be necessary.
• IV crystalloid fluid as clinically indicated
• Diphenhydramine 50–75 mg IV
• Hydrocortisone up to 200 mg IV or methylprednisolone 1–2 mg/kg
• Consideration of sodium bicarbonate if severe acidosis persists
• Consider central line placement for monitoring and therapy if not already in place.
FOLLOW-UP
• After an episode of anaphylaxis, the patient should be closely monitored in an ICU setting
since symptoms can recur in up to 20% of patients.
• If the patient experienced their first allergic reaction, then they should be referred to an
allergist or dermatologist for further testing. They should also be fully informed of the
situation and wear a Medic-Alert bracelet indicating their allergy.
• If no episode of anaphylaxis occurred in a latex-sensitive patient, they can likely be
discharged to the ward with continued latex precautions.
REFERENCES
1. Hepner DL, Castells MC. Latex allergy: An update. Anesth Analg. 2003;96:1219–1229.
2. Kam PC, Thompson JF. Latex allergy: An emerging health hazard for operating theatre
staff. Anaesthesia. 1997;84(3):570–575.
3. Farley CA, Jones HM. Latex allergy. Contin Educ Anaesth Crit Care Pain. 2002;2(1):20–23.
4. Ryder SA. Anaphylaxis. Contin Educ Anaesth Crit Care Pain. 2004;4(4):111–113.
ADDITIONAL READING
• American latex allergy association
• Anaphylaxis
• Asthma
• ETCO2
CODES
ICD9
V15.07 Allergy to latex
ICD10
Z91.040 Latex allergy status
CLINICAL PEARLS
• Latex allergies have increased since the introduction of Universal Precautions in the
healthcare setting.
• Known latex allergies allow the operating room team to make preparations to avoid a
potentially life-threatening reaction. In addition to absolute avoidance of latex-containing
products, patients should be scheduled as first cases since aeroallergens can be suspended in
the air for up to 5 hours.
• Unknown allergies pose the greatest threat since signs and symptoms are not specific to
latex anaphylaxis and may also be delayed. Dermatologic signs may not be immediately
obvious under surgical drapes and cardiovascular collapse (hypotension, PEA) may be the
first presenting symptom. Furthermore, inadequate circulation may delay dermatologic
manifestations.
• Latex antigens are found in several products in the operating room and should be well
known to the anaesthetist. Additionally, the anaesthetist is responsible for clearing out
items specific to their care (disposable anesthesia bag, tourniquets, syringe plungers,
medication vials with rubber stoppers, and some face masks, ETTs, etc.).
LEFT BUNDLE BRANCH BLOCK
Davinder Singh, MD
Jennifer Scovotti, MA
BASICS
DESCRIPTION
• A left bundle branch block (LBBB) occurs when transmission of a cardiac electrical impulse
is delayed across the main left bundle branch or both the anterior and posterior fascicles.
• The left bundle branch originates at the crest of the muscular ventricular septum and
descends inferiorly along the left ventricular septal surface. It branches into 3 major
fascicles:
– Anterior
– Posterior
– Central (proceeds to the midseptal region)
EPIDEMIOLOGY
Incidence
• LBB affects 1% of the general population.
• Occurs in up to 30% of patients with heart failure.
• May occur in 20% of patients after aortic valve replacement.
Prevalence
Increases with age:
• Age 50 years, affects 0.4% of people
• Age 75 years, affects 2.3%
• Age 80 years, affects 5.7%
Morbidity
• Outcome is excellent in younger subjects while older patients (mean = 62 years old) have
shown an increased risk for coronary disease and heart failure (20–30% incidence of each).
• Patients also have an increased risk (1% per year) for progression to AV block.
Mortality
• Independent predictor of mortality in patients with known or suspected coronary artery
disease
• The cumulative cardiovascular disease mortality rate is 3–4 times greater than the general
population.
LBBB can result from:
• Left ventricular hypertrophy
• Cardiomyopathy
• Hypertension
• Ventricular septal defect repair
• Septal myectomy
• Aortic valve surgery
• Neuromuscular and sclerodegenerative diseases
• Benign condition
PATHOPHYSIOLOGY
Impaired transmission of the left bundle’s electrical impulse is associated with:
• Asynchronous left ventricular activation that reduces the efficiency of left ventricular
contraction
• Sequential activation of the left and right ventricles (rather than simultaneous); this can lead
to wall motion abnormalities.
• Shortened duration of diastolic flow that can disturb coronary perfusion
• Concern for complete heart block if the procedure involves intracardiac manipulation (e.g.,
right heart catheterization, PA catheter placement). There is a 2–5% chance of complete
heart block with PA catheter placement.
• A retrospective study has shown that asymptomatic LBBB patients undergoing noncardiac
surgery do not have a higher incidence of cardiac complications, but did suggest that they
may have more difficulty tolerating increased stress from noncardiac complications such as
sepsis.
• In patients who have heart failure from dilated cardiomyopathy and bundle branch block,
resynchronization pacing has become an important component to therapy.
SYMPTOMS
• Often clinically silent
• Some patients experience exercise intolerance, presyncope, and syncope.
History
• Patients with isolated LBBB are usually asymptomatic; however, history of syncope is
concerning for occult coronary artery disease, impaired ventricular function, or higher level
conduction disturbance and should be thoroughly investigated.
• Assess for concurrent cardiac disease
Signs/Physical Exam
Auscultatory findings include an absent or diminished first heart sound and reversed splitting
of the second heart sound (S2 is split in expiration and single in inspiration).
TREATMENT HISTORY
Resynchronization therapy may be performed in patients with dilated cardiomyopathy, a
history of syncopal episodes, or for other underlying cardiac disease.
MEDICATIONS
• No medications are routinely used for treatment.
• Class I (including lidocaine) and III antiarrhythmic agents (including amiodarone and
sotalol) can delay conduction in the His-Purkinje system and should be avoided.
Labs/Studies
• LBBB can be seen on an EKG tracing, and the electrical patterns show where the block is
located.
• EKG criteria includes:
– QRS duration ≥120 ms
– Broad notched R wave in leads I, aVL, V5, V6
– P and T waves usually opposite in direction to QRS
• SVT may be mistaken for ventricular tachycardia in patients with LBBB because of the wide
QRS.
LBBB is often a marker for 1 of 4 underlying conditions:
• Hypertensive heart disease
• Aortic valve disease
• Cardiomyopathy
• New onset of LBBB during anesthesia (most often during hypertensive or tachycardic
episodes) has been shown to be a sign of myocardial ischemia.
• Abnormal electrolytes; hypokalemia, hypomagnesemia, and hypocalcemia delay
repolarization and should be corrected.
CLASSIFICATIONS
• LBBB has been defined as homophasic (concordant: cLBBB) or heterophasic (discordant:
dLBBB) when associated with a positive or negative T wave in leads I and V5-V6,
respectively.
• In systolic heart failure, dLBBB is associated with a worse clinical, neurohormonal, and
prognostic profile.
• There are also partial blocks of the left bundle branch: “Left anterior fascicular block”
(LAFB) and a “left posterior fascicular block” (LPFB).
TREATMENT
Premedications
Consider preoperative sedation when appropriate. Limiting anxiety and sympathetic outflow
is crucial as tachycardia can induce LBBB.
None
INTRAOPERATIVE CARE
• Whether general or regional is chosen, operative management should focus on prevention of
excessive sympathetic activity and avoidance of factors that cause tachycardia.
• There is no evidence that general or regional anesthesia is safer than the other.
• Ketamine should be used cautiously due to its ability to cause tachycardia.
Monitors
• LBBB prevents diagnosis of ischemia with EKG because ST and T wave changes are already
present, and therefore more invasive monitoring may be required depending on operative
risk factors.
• Temporary pacing should be available, and pacing pads should be placed for any cardiac
procedure.
• Sympathetic outflow caused by laryngoscopy, intubation, suctioning, and cold inspired gases
should be attenuated by short-acting opioids and/or esmolol.
• Lidocaine, despite being used without complications, is a class Ib antiarrhythmic agent and
can theoretically worsen conduction and left ventricular dyssynchrony.
Maintenance
• Avoid factors that increase sympathetic activity and maintain normocarbia, normothermia,
normoglycemia, normovolemia, and normoxia.
• Patients should also be kept adequately anesthetized to prevent sympathetic outflow from
innocuous stimuli.
Consider a “deep” extubation while the patient remains in a surgical plane of anesthesia to
decrease sympathetic outflow.
POSTOPERATIVE CARE
BED ACUITY
LBBB patients may have less ability to tolerate stressful states and warrant close clinical and
laboratory monitoring.
Maintain a low threshold for a myocardial ischemia workup given the unreliability of an EKG.
COMPLICATIONS
• Complete heart block
• Failure to detect cardiac ischemia
• Sudden cardiac death
GRAPHS/FIGURES
FIGURE 1. Left bundle branch block (LBBB). On the left, a homophasic LBBB is shown and named for its accompanying
positive T wave (also known as concordant LBBB). On the right, a heterophasic LBBB is shown and named for its
accompanying negative T wave (also known as discordant LBBB).
REFERENCES
1. Hesse B, Diaz LA, Snader CE, et al. Complete bundle branch block as an independent
predictor of all-cause mortality: Report of 7,073 patients referred for nuclear exercise
testing. Am J Med. 2001;110(4):253–259.
2. Rotman M, Triebwasser JH. A clinical and follow-up study of right and left bundle branch
block. Circulation. 1975;51(3):477–484.
3. Imanishi R, Seto S, Ichimaru S, et al. Prognostic significance of incident complete left
bundle branch block observed over a 40-year period. Am J Cardiol. 2006;98(5):644–648.
4. Dorman T, Breslow MJ, Pronovost PJ, et al. Bundle-branch block as a risk factor in
noncardiac surgery. Arch Intern Med. 2000;160(8): 1149–1152.
5. Schneider JF, Thomas HE Jr, Sorlie P, et al. Comparative features of newly acquired left
and right bundle branch block in the general population: The Framingham study. Am J
Cardiol. 1981;47(4):931–940.
6. Keefe DL, Griffin JC, Harrison DC, et al. Atrioventricular conduction abnormalities in
patients undergoing isolated aortic or mitral valve replacement. Pacing Clin Electrophysiol.
1985;8(3 Pt 1):393–398.
ADDITIONAL READING
• Stoelting R, Hines R, Marschall K. Stoelting’s anesthesia and co-existing disease, 5th ed.
Philadelphia, PA: Churchill Livingstone, 2008:77–79.
• Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram. Part VI: Acute
ischemia/infarction. A scientific statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the
American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by
the International Society for Computerized Electrocardiology. J Am Coll Cardiol.
2009;53(11):1003–1011.
• Right bundle branch block
• 12-lead Electrocardiogram
CODES
ICD9
426.3 Other left bundle branch block
ICD10
I44.7 Left bundle-branch block, unspecified
CLINICAL PEARLS
• LBBB patients often have significant comorbidities; it is associated with cardiovascular
disease in older patients. Additionally, patients may not be able to handle cardiovascular
stress as well.
• LBBB prevents detection of ischemia by EKG.
• There is a concern for complete heart block if procedures involve intracardiac manipulation.
LEFT VENTRICULAR END DIASTOLIC PRESSURE (LVEDP)
Sumit Singh, MD
BASICS
DESCRIPTION
• Left ventricular end-diastolic pressure (LVEDP) is defined as the pressure in the ventricles at
the end of diastole. The measurement is used in clinical practice as a means to approximate
the left ventricular end-diastolic volume (LVEDV) or preload (LVEDP ∼ LVEDV).
• LVEDP can be ideally determined by left ventricular catheterization in the catheterization
laboratory. It is measured at the Z-point, the point on the left ventricular pressure trace
where the slope of the ventricular pressure upstroke changes (approximately 50 ms after the
EKG Q wave, and generally coincides with the R wave) (1).
FIGURE 1. The LVEDP is measured at the Z point. It is the point on the ventricular pressure upstroke where the slope
changes. It occurs approximately 50 ms after the Q wave and usually corresponds with the R wave.
• In most clinical situations, LVEDP is determined by Swan Ganz catheterization, by floating a

balloon-tipped catheter into the pulmonary artery. Although it does not enter the left
ventricle, when the balloon is inflated (wedged), it isolates the catheter tip and brings it in
continuity with the blood column in the left atrium and LV during end diastole.
– Measurements: The pulmonary artery wedge pressure (PAWP) is equal to the LVEDP,
given that there is no mitral valve pathology and the pulmonary artery catheter is in the
West zone 3 of the lung (where pulmonary artery pressure > pulmonary venous pressure
> pulmonary alveolar pressure).
– Waveforms: Left atrial tracings are similar to central venous pressure (CVP) tracing from
the right atrium, with “a”, “c”, and “v” waves.
• During an ideal ventricular diastole, the pressures in all cardiac chambers equilibrate: CVP
= RVEDP = PADP = PAWP = LAP = LVEDP; where CVP is central venous pressure,
RVEDP is right ventricular end diastolic pressure, PADP is pulmonary artery diastolic
pressure, PAWP is pulmonary artery wedge pressure, and LAP is left atrial pressure.
• Frank Starling principle states that the force of cardiac contraction is directly proportional to
end-diastolic muscle fiber length at any given level of intrinsic contractility or inotropy.
– Increasing the venous return of the left ventricle increases the volume and preload and
thereby LVEDP (increases stroke volume).
– Flat portion of diastolic filling: A significant increase in filling volume or preload results in
a small increase in filling pressure.
– Steep portion of diastolic filling: In comparison, there is a significant increase in filling
pressure with the same volume towards the end of diastole.
– Left-shifting describes abnormal decreases in compliance (e.g., sepsis, shock, myocardial
ischemia, or fibrotic chambers). Additionally, there is a paradoxical increase in filling
pressures with a decrease in filling volume.
FIGURE 2. The ventricular diastolic pressure-volume relationship forms a curvilinear line and the slope reflects wall
compliance. Compliance is dynamic and changes with chamber volume, thus affecting the ability of using the LVEDP to
approximate the LVEDV. Curve A represents normal compliance. Curve B represents a right shift or increased compliance,
as can occur with dilated cardiomyopathy, where a change in the volume (x) results in a smaller increase in pressure.
FIGURE 3. Frank Starling curve. Changes in venous return correlate to changes in LVEDP/LVEDV that affect the stroke
volume (SV). The inotropic state affects the stroke volume at a given preload (dashes–higher inotropy, dots–decreased
inotropy).
ANATOMY
• PAWP is taken at the pulmonary artery (distal tip of pulmonary artery catheter) with the
balloon inflated and occluding the branch of the pulmonary artery.
• The ability of proximal pressures (CVP, PAWP, etc.) to accurately reflect the LVEDP is
dependent on unobstructed continuity of blood flow during diastole. Any anatomical or
physiological condition that impairs this will result in inaccurate downstream pressure
estimation.
• Conditions in which PAWP underestimates LVEDP:
– Decreased left ventricular compliance (e.g., MI, LVH). The mean left atrial pressure (LAP)
is less than LVEDP, and there is an increased end-diastolic “a” wave.
– Aortic regurgitation (AR): The mitral valve closes before the end of diastole due to run-off
from the aorta (LAP < LVEDP).
– Pulmonary regurgitation: Bidirectional run-off of the pulmonary artery flow (PADP <
LVEDP).
– Decreased pulmonary vascular bed
• Conditions in which PAWP overestimates LVEDP:
– Positive end-expiratory pressure (PEEP): The pulmonary artery catheter may become
lodged in lung zone 1 or 2. Pulmonary venous pressure readings are actually lower than
airway pressure, leading to a falsely elevated PAWP.
– Pulmonary hypertension: Increases in the pulmonary vascular resistance will record a
higher PADP which does not reflect left ventricular pressures (PADP > mPAWP).
– Mitral stenosis: There is obstruction to the flow of blood through the mitral valve, which
results in a higher mean LAP and thereby overestimation of the LVEDP.
– Mitral regurgitation: A retrograde systolic “v” wave or regurgitant systolic flow raises the
mean atrial pressure.
• Increased compliance. In dilated cardiomyopathy, the left ventricle is very dilated without
any appreciable increase in ventricular wall thickness. This will result in increased
compliance and even though the LVEDV may be very high, the corresponding LVEDP
elevation might not be significant.
• Elevated LVEDP is an independent risk factor of mortality in cardiac surgery, independent of
left ventricular ejection fraction (2,3).
• Atrial kick: Normally provides 20% contribution to the LVEDV. In LVH, this may increase to
50% and the “a” wave may be prominent and provide a better estimate of LVEDP than
PAWP (4).
• Mitral valve: Both stenosis and regurgitation can overestimate the LVEDP.
• Perioperative presentation of cardiogenic versus hypovolemic shock can be differentiated by
using the LVEDP (CVP/PAWP) as a surrogate marker of preload. A low CVP, or PAWP, is
consistent with hypovolemia, and a high CVP/PAWP would indicate cardiogenic shock (e.g.,
MI, CHF). This can be clinically important in deciding when to give fluids versus other
interventions.
– The goal of all-fluid resuscitation is to increase preload and “recruit” stroke volume to
increase end-organ perfusion, as per the Starling mechanism.
– Markers of LVEDP (CVP/PAWP) can be trended over time with improvement or worsening
of cardiac output.
– Clinically, signs of increased cardiac output changes would relate to increased urine
output, decreased capillary refill time, improvement in mental status and blood pressure.
– Other more sophisticated monitors which can measure cardiac output changes with
preload changes are esophageal Doppler monitor, echocardiography, and systolic pressure
variations.
• Myocardial compliance: PAWP measurements are dependent on myocardial compliance.
Multiple studies on ICU patients have shown the failure of PAWP in acute illness to
correlate with LVEDV (5).
• Clinical use: CVP or PAWP alone is rarely used to guide therapy. In situations of shock, after
the patient has been given IV fluids to raise the CVP to around 12 mm Hg (adequate
preload), without improvement in blood pressure or cardiac output, other methods of
assessment such as bedside echocardiography may be used for cardiac assessment.
– The American Society of Anesthesiologist Practice Guidelines recommends PAC for high-
risk surgical patients only (6).
– Suggested clinical indications for monitoring LVEDV and LVEDP are severe sepsis and
trauma, high-risk cardiac surgery, pulmonary hypertension, abdominal compartment
syndrome, and therapy with PEEP.
REFERENCES
1. Braunwald E, Fishman AP, Cournand A. Time relationship of dynamic events in the cardiac
chambers, pulmonary artery and aorta in man. Circ Res. 1956;4:100–107.
2. Salem R, Denault AY, Couture P, et al. Left ventricular end-diastolic pressure is a predictor
of mortality in cardiac surgery independently of left ventricular ejection fraction. Br J
Anaesth. 2006;97:292–297.
3. Apostolakis EE, Baikoussis NG, Parissis H, et al. Left ventricular diastolic dysfunction of the
cardiac surgery patient: A point of view for the cardiac surgeon and cardio-
anesthesiologist. J Cardiothorac Surg. 2009;4:67.
4. Falicov RE, Resnekov L. Relationship of the pulmonary artery end-diastolic pressure to the
left ventricular end-diastolic and mean filling pressures in patients with and without left
ventricular dysfunction. Circulation. 1970;42:65–73.
5. Fontes ML, Bellows W, Ngo L, et al. Assessment of ventricular function in critically ill
patients: Limitations of pulmonary artery catheterization. Institutions of the McSPI
Research Group. J Cardiothorac Vasc Anesth. 1999;13:521–527.
6. American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization.
Practice guidelines for pulmonary artery catheterization: An updated report. Anesthesiology.
2003;99:988–1014.
ADDITIONAL READING
• Miller RD. Miller’s anesthesia, 7th ed. Philadelphia: Churchill Livingstone, 2009.
• Cardiac output
• Mitral stenosis
• Left ventricular hypertrophy
• Dilated cardiomyopathy
CLINICAL PEARLS
• LVEDP (pressure) is a surrogate measurement for LVEDV (volume).
• The assumption that the pulmonary artery catheter is in continuity with the left ventricle
during diastole is only valid when the catheter is in the West zone 3 of the lungs (e.g.,
where the pulmonary venous pressure is greater than the airway pressure).
• In using CVP and PAWP as a marker of LVEDP, it is important to be aware of the caveats of
interpreting the readings. Any situation which anatomically or physiologically interrupts the
continuity of blood in the heart during diastole will alter the CVP or PAWP readings.
Conditions, such as mitral stenosis or regurgitation, pulmonary regurgitation, and aortic
regurgitation, will all cause an overestimation or underestimation of the LVEDP by the CVP
and PAWP.
• The pressure volume curve in the heart is curvilinear and shifts to the right with increased
LV compliance or the left with decreased compliance.
LIVER FUNCTION TESTS
Jason Han Chua, MD
Anahat Dhillon, MD
BASICS
DESCRIPTION
• “Liver function tests” (LFTs) is the common vernacular for the standard biochemistry profile
provided by most laboratories. It typically includes:
– Aspartate aminotransferase (AST or SGOT)
– Alanine aminotransferase (ALT or SGPT)
– Alkaline phosphatase
– Bilirubin (total, unconjugated, conjugated)
– Albumin
• LFTs are more accurately described as tests of overall liver health (metabolic and synthetic
function) or inflammation (necrosis).
• True, specific tests of liver function (galactose clearance, aminopyrine clearance) are not
widely used.
• Aspartate transaminase (also known as serum glutamic oxaloacetic transaminase [SGOT]) is
an enzyme found in liver parenchymal cells, brain, heart, kidneys, muscle, and red blood
cells. It is responsible for transferring the aspartate amino group to ketoglutaric acid.
Elevated levels may indicate tissue damage or inflammation.
• Alanine aminotransferase (also known as serum glutamic pyruvic transaminase [SGPT]) is
an enzyme found primarily in liver parenchymal cells and, to a lesser extent, in the heart,
kidneys, and muscle. It is responsible for transferring the alanine amino group to
ketoglutaric acid. Values provide a measure of hepatic damage or inflammation and are
considered more specific than AST values.
• Alkaline phosphatase is an enzyme that catalyzes hydrolysis of phosphate esters at an
alkaline pH. More than 80% is found in the liver and bone; minor sites include the placenta,
intestine, and kidney. Measurements indicate inflammation, particularly in the biliary tract.
• Bilirubin is the byproduct of heme catabolism. When hemoglobin is released from red blood
cells (normal breakdown, damaged or old cells), the globin is turned into amino acids. In
reticuloendothelial cells, the heme is converted into unconjugated bilirubin which is water-
insoluble and binds to albumin. The liver conjugates it with glucuronic acid to form
conjugated bilirubin, which is water-soluble. Bilirubin values can, thus, provide a measure
of hepatic metabolic function.
• Albumin is synthesized by the liver and comprises 60% of plasma proteins. It has a serum
half-life of approximately 20 days. Measurements indicate hepatic synthetic function, but do
not necessarily reflect acute processes. Normal adult values: 3.4–5.4 g/dL.
• As many as 1/3rd of patients screened may have a nonspecific abnormality in LFTs.
Incidence of clinically significant disease is ∼1%.
• Differential diagnosis can be broken down into:
– Hepatocellular inflammation or dysfunction: Inflammation and necrosis of hepatocytes
result in the release of AST and ALT (e.g., hepatitis A). Normal levels of AST and ALT do
not fall within a Gaussian distribution. Instead, distribution is skewed rightward, meaning
levels up to 1.5 the upper limits of “normal” do not necessarily suggest liver disease.
Hepatic dysfunction results in decreased metabolic and/or synthetic function.
– Cholestatic disease: Includes intrahepatic and extrahepatic processes and is usually
accompanied by an elevation in bilirubin (direct or indirect) and/or alkaline phosphatase.
– Infiltrative disease such as amyloidosis can result in the release of AST and ALT as well as
decreased metabolic and synthetic function.
• Clinical history is important to help differentiate between causes:
– Family history is relevant since many genetic disorders can affect liver function (Gilbert’s
and Dubin Johnson, Wilson’s disease, etc.).
– Sexual and social history, travel, and work exposure can also point to causes such as viral
hepatitis.
– Systemic conditions affecting LFTs include cardiac disease, inflammatory bowel disease,
diabetes, arthritis, hypogonadism, and thyroid disease.
• Transaminases:
– Since AST is less specific for liver disease, an isolated elevation can suggest cardiac or
muscular disease.
– An elevated AST/ALT ratio >2 is more likely to be associated with alcoholic hepatitis.
When it is <1.0 it is more likely to be associated with viral hepatitis.
– In acute liver injury (choledocholithiasis, uncomplicated viral hepatitis, ischemic
hepatitis), transaminase elevation can be severe, but often resolves within days to weeks.
Normalization usually indicates improvement; however, rapid decreases may suggest
profound worsening and cell death.
– Non-alcoholic steatohepatitis, non-alcoholic fatty liver, obesity, and thyroid disease can
lead to elevated transaminases with or without significant disease.
– Pharmacologic causes include acetaminophen (potentiated with alcohol consumption),
NSAIDs, ACE inhibitors, nicotinic acid, and many antibiotics and antifungals.
• Alkaline phosphatase:
– Obstruction of bile ducts leads to increased bile duct epithelial production of alkaline
phosphatase (can occur with obstruction of small ducts without clinically significant
cholestasis).
– Cholestasis may be diffuse (intrahepatic cholestasis), extrahepatic (gallstones or tumors),
localized (cancer), or multifocal (granulomatous disease).
– Cholestasis can be differentiated from osteolytic disease either by fractionation for hepatic
alkaline phosphatase or by testing gamma glutamyl transferase levels (increase when
hepatic in origin).
– Other causes of elevation include hyperthyroidism, heart failure, and lymphoma.
– When elevated disproportionately to hyperbilirubinemia, may be due to granulomatous or
infiltrative liver disease (sarcoid, fungal infection, tuberculosis, lymphoma) or early
primary biliary sclerosis or primary sclerosing cholangitis.
– Pitfalls:
Must be performed while fasting
Parturients and children have baseline elevated levels (2–3 times normal).
May indicate excessive alcohol consumption
• Bilirubin:
– A greater than 80% fraction of unconjugated bilirubin suggests hemolysis or Gilbert’s
syndrome.
– A greater than 50% fraction of conjugated bilirubin suggests hepatocellular dysfunction or
cholestasis.
• Albumin:
– Can be decreased in severe systemic disease, liver disease >3 weeks duration, or in
rapidly progressive liver disease, where albumin is consumed rapidly
– Lower in parturients
– In the absence of other liver test abnormalities, low albumin is usually due to non-hepatic
causes such as proteinuria or malnutrition.
• Prothrombin time:
– Measures activity of vitamin K-dependent clotting factors which are synthesized in the
liver
– Cholestasis prevents absorption of vitamin K; hepatocellular disease prevents synthesis of
factors.
• Miscellaneous:
– IgM, ANA: Elevated in autoimmune disease
– Low serum copper, uric acid, and ceruloplasmin indicate Wilson’s disease.
– Transferrin saturation >60% suggests hemochromatosis.
• Preoperative LFTs can aid with diagnosing disease/hepatic insults and assessing severity.
• Associated disease:
– Infectious diseases (Hepatitis B, C): Care must be taken to minimize practitioner exposure.
– Hepatorenal syndrome: Renal failure associated with hepatic failure. May be reversible or
irreversible. Increased morbidity/mortality due to risk of fungemia, uremia, etc.
– Hepatopulmonary syndrome: Elevated pulmonary arterial pressure and increased
extracardiac shunting leading to hypoxemia
• Severity-dependent considerations:
– Encephalopathy: Increased risk in the presence of portocaval shunt
– Ascites, increased intra-abdominal pressure: Increased risk of aspiration and desaturation
– Coagulopathy: Transfusion may be indicated in procedures that may not otherwise require
blood; patients requiring transfusion are more prone to citrate toxicity.
– Vasoplegia, low SVR: Higher cardiac output required to maintain blood pressure
• Postoperative abnormal LFTs can occur in up to 25–75% of patients without liver disease,
and mild elevations are considered typical. Postoperative jaundice typically presents within
2 weeks following surgery and is unusual in patients without liver disease. It is commonly
the result of a combination of hypotension, hypoxemia, pigment overload, and sepsis.
EQUATIONS
Child-Pugh score:
• Class A = 0–1 point, good prognosis
• Class B = 2–4 points
• Class C = ≥5 points, limited life expectancy
Table 1 Relevant Child-Pugh Scores
REFERENCE
1. Faust TW, Reddy KR. Postoperative jaundice. Clin Liver Dis. 2004;8:151–166.
2. Kamath PS. Clinical approach to the patient with abnormal liver test results. Mayo Clin
Proc. 1996;71:1089–1096.
3. Kaplan MM. Laboratory tests. In: Schiff L, Schiff ER, eds. Diseases of the liver, 7th ed.
Philadelphia, PA: Lippincott, 1993:108–144.
4. Quinn PG, Johnston DE. Detection of chronic liver disease: Costs and benefits.
Gastroenterologist. 1997;5:58–77.
CLINICAL PEARLS
• Of the routine LFTs, only albumin, bilirubin, and PT are actual indicators of liver function.
• Patients with cirrhosis can have “normal LFTs.”
• Mildly elevated ALT can be due to normal age and gender variability or muscle injury.
LIVER RESECTION
BASICS
DESCRIPTION
General
• Liver resections are performed to remove diseased liver parenchyma: Tumors (primary and
secondary), cysts, and adenomas. It is not suitable for severely cirrhotic livers because of the
risk of postoperative hepatic failure.
• Outcome and, hence, the decision to resect, are dependent on the location, number, and
distribution of the mass, as well as the amount of liver that will remain. The liver has
significant reserve capacity that allows a large portion to be excised. Additionally, it has the
capability to regenerate; occasionally portal vein embolization may be performed to
facilitate this.
• Modalities prior to resection:
– Tumor shrinkage may be achieved with chemotherapy; it can either be systemic or
directed. Intra-arterial therapies can be utilized to decrease whole-body adverse effects. It
involves threading a catheter through the femoral artery in the groin to the feeding
vessels.
– Radiofrequency ablation (RFA): May be performed percutaneously with the aid of imaging
modalities or direct visualization during open procedures (or laparoscopic surgery). The
tip of a needle probe is heated utilizing alternating electric current to destroy tumors.
Alternatively, microwave ablation may be performed, particularly for tumors near large-
diameter vessels.
– Portal vein embolization: Blood vessels to the tumor are embolized, and nutrients and
flow are diverted to the other side with the goal of facilitating growth/regeneration.
Repeat imaging to assess hypertrophy is recommended 3–4 weeks after embolization.
• Following dissection, hepatic resection is either:
– Anatomic: Margins defined by segmental liver anatomy
– Non-anatomic: Margins defined by tumor
• Surgical maneuvers to decrease bleeding include portal triad clamping (Pringle’s maneuver)
and selective hepatic venous occlusion. Pringle’s maneuver is generally without
hemodynamic consequence to the patient. Hepatic tolerance of this maneuver is enhanced
by intermittent clamping for 15 minutes followed by unclamping for 5 minutes. Selective
hepatic venous occlusion (occlusion of the hepatic venous branches without caval
compromise) has been shown to be as effective as a low CVP (central venous pressure)
technique for reducing blood loss in patients who are unable to tolerate a CVP <5 mm Hg
(1).
• Laparoscopic resection may or may not be hand-assisted. Transection is accomplished via
repeated, layered application of endovascular staplers.
Position
Supine, bilateral upper extremities abducted to <90%
Incision
Bilateral subcostal incisions ± midline extension
Approximate Time
1.5–5 hours depending on the extent of resection
EBL Expected
100–1,500 mL, depending on extent of resection and use of cell saver
Hospital Stay
3–10 days
• Ultrasonic dissector
• Vascular stapler
• Tissue sealer
EPIDEMIOLOGY
Incidence
• 7,000 resections performed in 2004 (2)
• 18,920 new cases of hepatic/biliary cancer in US in 2004
Prevalence
Liver cancer is considered a “rare disease” by the National Institutes of Health (NIH); there
are <200,000 cases in the US.
Morbidity
23–56% depending on the extent of resection, and indication for surgery (3)
Mortality
2.6% among high-volume centers (3)
• Establish adequate venous access; large fluid shifts can occur in additional to massive
hemorrhage from hepatic vessels.
• Maximize patient warming measures.
• Help minimize blood loss by maintaining a low CVP (<5 mm Hg).
• Minimize transfusion with techniques such as preoperative autologous donation, cell saver,
or isovolemic hemodilution.
SYMPTOMS
• Usually asymptomatic. Often tumor is discovered as a result of metastatic workup or
preventive surveillance.
• May occasionally present with abdominal pain
History
• Resection candidates are usually screened for significant hepatic dysfunction.
• Liver cancer is commonly a metastatic disease from the colon.
Signs/Physical Exam
May have stigmata of cirrhosis and/or portal hypertension
MEDICATIONS
• Chemotherapy for primary tumor: Commonly utilized agents include 5-flurouracil,
oxaliplatin, and cetuximab.
• Antiviral medications for chronic viral hepatitis
Labs/Studies
• Standard labs are dictated by age and comorbidities.
• In chronic hepatic disease, use the INR, creatinine, and bilirubin values to calculate the
MELD score.
May have organ system dysfunction secondary to cirrhosis or portal hypertension
TREATMENT
Premedications
No absolute contraindications. Titrate carefully in the presence of known underlying hepatic
dysfunction, especially benzodiazepines.
• Epidural catheter placement for postoperative pain
• Potential need for invasive monitors such as arterial or central line
• Blood consent
• Biliary penetration/concentration requires Gram-negative coverage.
• Ceftriaxone, ampicillin/sulbactam, and piperacillin/tazobactam can provide broader Gram-
negative coverage.
INTRAOPERATIVE CARE
• Regional techniques for postoperative pain management are acceptable in patients with
normal preoperative coagulation parameters. Postoperative coagulopathy correlates with
the extent of resection and blood loss. INR peaks on POD #1, ranging from a mean of 1.3 in
left lateral segmentectomy to 1.6 in right hepatic lobectomy. Platelet count nadir is POD
#3, with a mean of 110–160 K in hepatic lobectomy (major resection). Thus, although
continuous epidural analgesia can be used for postoperative pain, the catheter will remain
in place for a few days (generally 2–5) until coagulation abnormalities have corrected
(ASRA recommendation: INR <1.5) (4,5).
Monitors
• Consider arterial line for larger procedures (e.g., hepatic lobectomy).
• Consider central line placement for larger procedures. There is literature to support the use
of peripheral venous pressures (PVP) in lieu of CVP for monitoring (6,7).
Consider a rapid sequence or modified rapid sequence induction in patients with portal
hypertension.
Maintenance
• Minimize and avoid agents that require hepatic metabolism to terminate their effects, if
possible.
• Consider cisatracurium if hepatic function is a concern.
• Isoflurane has an excellent track record; however, sevoflurane and desflurane are also
acceptable.
• Maintain a CVP <5 mm Hg until parenchymal division is complete, if possible. This can
minimize blood loss; the liver has multiple caval communications and elevated caval
pressures cause increased back-bleeding from the hepatic surface (8).
• Temperature: Implement warming measures early; hypothermia contributes to
coagulopathy.
Plan to extubate, unless there were large fluid shifts or blood loss during the surgery
POSTOPERATIVE CARE
BED ACUITY
• Varies according to extent of resection, degree of underlying disease
• Pulmonary issues: Upper abdominal surgery lasting 3–5 hours places patients at high risk for
postoperative pulmonary complications. The rate of complications also correlates with the
extent of resection and intraoperative blood transfusion.
ANALGESIA
• Patient-controlled analgesia
• Indwelling epidural catheters for postoperative analgesia are not contraindicated. However,
the INR may increase immediately postoperatively along with decreases in platelet count
(depending on the amount resected and underlying liver parenchymal disease).
COMPLICATIONS
• Bleeding
• Bile leak
• Hepatic failure: Primarily avoided by careful patient selection, preservation of adequate
remnant volume, and judicious use of Pringle’s maneuver. Postoperative causes include
sepsis, cholestasis, portal venous thrombosis, or remnant size/portal flow mismatch (9).
PROGNOSIS
Survival varies according to the extent of resection and underlying liver parenchymal disease.
REFERENCES
1. Smyrniotis V, Kostopanagiotou G, Theodoraki K, et al. The role of central venous pressure
and type of vascular control in blood loss during major liver resections. Am J Surg.
2004;187(3):398–402.
2. Dimick JB, Cowan JA Jr, Knol JA, et al. Hepatic resection in the United States. Arch Surg.
2003;138(2):185–191.
3. Virani S, Michaelson JS, Hutter MM, et al. Morbidity and mortality after liver resection:
Results of the patient safety in surgery study. J Am Coll Surg. 2007;10(3):1284–1292.
4. Schumann R, Zabala L, Angelis M, et al. Altered hematologic profiles following donor right
hepatectomy and implications for perioperative analgesic management. Liver Transpl.
2004;10(3):363–368.
5. Matot I, Scheinin O, Eid A, et al. Epidural anesthesia and analgesia in liver resection.
Anesth Analg. 2002;95:1179–1181.
6. Amar D, Melendez JA, Zhang H, et al. Correlation of peripheral venous pressure and
central venous pressure in surgical patients. J Cardiothorac Vasc Anesth. 2001;15(1):40–
43.
7. Stéphan F, Rezaiguia-Delclaux S. Usefulness of a central venous catheter during hepatic
surgery. Acta Anaesthesiol Scand. 2008;52(3):388–396.
8. Melendez JA, Arslan V, Fischer ME, et al. Perioperative outcomes of major hepatic
resections under low central venous pressure anesthesia: Blood loss, blood transfusion, and
the risk of postoperative renal dysfunction. J Am Coll Surg. 1998;187(6):620–625.
9. Garcea G, Maddern GJ. Liver failure after major hepatic resection. J Hepatobiliary Pancreat
Surg. 2009;16:145–155.
• Cirrhosis
• Hypothermia
CLINICAL PEARLS
• The extent of tolerable resection is inversely proportional to the degree of underlying
hepatic parenchymal disease.
• Maintain a low CVP <5 mm Hg, particularly during parenchymal division to reduce blood
loss.
• Complex coagulopathy is associated with large resections, with immediate increase in INR.
• Continuous epidural analgesia for postoperative pain management is not contraindicated. Be
aware that the epidural may need to be kept in place for several days postoperatively, and
that there is a risk of bleeding complications if it is displaced before coagulation function
has recovered.
LIVER TRANSPLANTATION
Cynthia Wang, MD
BASICS
DESCRIPTION
General
• Orthotopic or heterotopic liver transplantation is the definitive treatment of choice for end-
stage liver disease. The first successful liver transplant was performed by Dr. Thomas Starzl
in 1963.
• Following incision, the liver is dissected free, and major ligamentous connections are
skeletonized (common bile duct, hepatic artery and vein, portal vein). These structures are
then ligated, and the suprahepatic and infrahepatic vena cava are clamped followed by
removal of the diseased liver.
• The donor allograft is placed into the patient’s abdomen, and anastomoses are created
between the donor and recipient suprahepatic vena cava, infrahepatic vena cava, and portal
vein. The liver is then reperfused by unclamping the anastomoses.
• Following reperfusion of the organ, the hepatic artery anastomosis is completed, as well as
the bile duct, either to the patient’s native bile duct or to the small bowel (Roux-en-Y).
• In the piggyback technique, the donor hepatic vein is anastomosed end-to-side to the
recipient’s vena cava, preserving the recipient cava.
Position
Supine with bilateral upper extremities abducted <90°
Incision
Upper abdominal inverse T incision
Approximate Time
4–12 hours, depending on patient complexity and surgical difficulty
EBL Expected
• Can range from <500 mL to multiple times the patient’s total blood volume in extreme
cases. The average is 1,500–3,000 mL.
• Blood loss and transfusion requirements are generally higher in patients with higher MELD
scores.
Hospital Stay
1–3 weeks postoperatively; may be longer depending on patient complexity and surgical
difficulty
• Rapid infuser +/– cell saver
• For complex patients, consider veno-venous bypass (may need perfusionist) and
intraoperative dialysis (may need additional personnel).
EPIDEMIOLOGY
Incidence
• In 2008, there were 11,176 new registrants on the liver transplant waiting list (candidates
may register at multiple centers); there were 6,069 liver transplant recipients. In 2010,
there were 5,246 liver transplant recipients.
Morbidity
• Highly variable depending on patient complexity at the time of transplantation, coexisting
disease, and complications post-transplantation
• Increased with high MELD scores, morbid obesity, concomitant cardiopulmonary disease
and/or renal disease, postoperative rejection, and biliary complications
Mortality
• Patient survival rates:
– 3 months 94.3%
– 1 year 88.4%
– 5 years 73.8%
– 10 years 60.0%
• Patients presenting for liver transplantation must be evaluated thoroughly for multisystemic
ramifications of end-stage liver disease as well as concomitant disease unrelated to
underlying liver disease that may affect perioperative management.
• Anesthetic agents may have altered pharmacokinetics and pharmacodynamics (increased
volume of distribution, decreased clearance, and increased sensitivity).
• Veno-venous bypass (VVB) may be used in patients who may not hemodynamically tolerate
caval clamping. VVB involves cannulating the portal and femoral veins and returning the
circulation to the axillary or subclavian veins through a bypass circuit. This maintains
venous return to the heart and decompresses splanchnic venous congestion.
SYMPTOMS
• CV: Palpitations, episodes of lightheadedness or fainting due to overall decreased systemic
vascular resistance, decreased functional capacity
• Renal system: Polyuria, oliguria, or anuria
• GI system: Hematochezia, melena, hematemesis
• Hematologic system: Easy bleeding/bruising
• Skin/other: Jaundice, itching, weakness, fatigue, anorexia, weight loss
History
Etiology and course of disease
Signs/Physical Exam
• CNS: Altered mental status, asterixis
• CV: Decreased blood pressure, possible increased jugular venous pressure if fluid overload or
right heart insufficiency due to worsening pulmonary hypertension
• Pulmonary system: Hypoxia/hypoxemia, clubbing, decreased breath sounds due to effusion,
rales due to pulmonary edema
• GI system: Palpable liver edge, ascites, splenomegaly, GI bleeding due to esophageal varices
and hemorrhoids
• Skin/joints: Jaundice, icterus, fetor hepaticus
MEDICATIONS
• Furosemide, spironolactone, bumetanide, hydrochlorothiazide
• Lactulose, rifaximin
• Cholestyramine, colestipol
• Vitamin K
• Propranolol
• Midodrine, octreotide
• Interferon for viral hepatitis
• Corticosteroids for autoimmune hepatitis
• Penicillamine for Wilson disease
Labs/Studies
• CBC: Anemia, thrombocytopenia, leukopenia or elevated white blood cell count
• Chemistry panel: Hyponatremia, hypo- or hyperkalemia, hypocalcemia, hypomagnesemia,
hypoglycemia, acidosis, serum creatinine >1.5 mg/dL in hepatorenal syndrome (HRS)
• Coagulation panel: Increased PT/PTT/INR, hypofibrinogenemia
• Aminotransferases: Elevated, AST > ALT
• Alkaline phosphatase: Usually elevated
• Bilirubin: Increasingly elevated with progression of liver failure
• ECG, echocardiography, chemical or nuclear stress test to assess for areas of reversible
ischemia, possible cardiac catheterization to assess for CAD and more accurate
measurement of intracardiac and pulmonary pressures
• CXR to evaluate for edema or effusions
• Pulmonary function tests (if indicated)
• CT scan to evaluate for possible metastases in cases of hepatocellular carcinoma
• CNS: Hepatic encephalopathy, cerebral edema in patients with acute liver failure leading to
increased ICP
• Cardiovascular system: Hyperdynamic circulation; cirrhotic cardiomyopathy characterized
by systolic and diastolic dysfunction and electrophysiologic abnormalities; may have
coexisting CAD or valvular disease
• Pulmonary system: Hepatopulmonary syndrome (HPS), portopulmonary hypertension,
restrictive lung disease due to ascites, pleural effusions
• Renal system: HRS characterized the absence of primary renal disease, proteinuria,
hypovolemia, and/or evidence of ATN; renal tubular acidosis; tacrolimus/cyclosporine-
associated renal insufficiency
• GI system: Portal hypertension, ascites, delayed gastric emptying, portal hypertensive
gastropathy
• Hematologic system: Thrombocytopathia and predisposition to disseminated intravascular
coagulation (DIC), hyper- and hypofibrinolysis
TREATMENT
Premedications
Careful premedication at the discretion of the managing physician. May avoid premedication
if signs of encephalopathy, potentially difficult airway, or high risk of aspiration.
May have to be obtained from a designated health care proxy if the patient is
encephalopathic or incapacitated
• Need good penetration/concentration in bile
• Commonly, ceftriaxone, cefotaxime, ampicillin/sulbactam. Often avoid vancomycin due to
prevalence of vancomycin-resistant Enterococcus.
INTRAOPERATIVE CARE
General anesthesia; regional for postoperative analgesia is contraindicated
Monitors
• Direct arterial blood pressure monitor
• Central venous line and pressure monitoring
• Additional monitors depend on patient comorbidities and institutional practices and
provider (surgeon, anaesthetist) preference
– Pulmonary artery catheter with capability of measuring the CO/CI
– BIS monitor
– TEE
– Thromboelastogram (TEG)
• ICP monitor in patients with cerebral edema (i.e., acute liver failure patients); alternate
monitoring options when intracranial ICP monitoring is not available include transcranial
Doppler, cerebral oximetry, BIS, and EEG monitoring.
• Rapid sequence or modified rapid sequence induction to reduce the risk of aspiration
• Use of induction agents that optimize hemodynamic stability
• Gentle laryngoscopy in the coagulopathic patient
Maintenance
• Traditionally, isoflurane is used due to its ability to preserve splanchnic blood flow. In
patients with cerebral edema, may consider total IV anesthesia or only minimal doses of
volatile agents to decrease the degree of cerebral vasodilation.
• Long-acting narcotics; cisatracurium may be preferred due to its metabolism independent of
liver function if extubation in the OR is planned.
• Pre-anhepatic phase: Aggressive fluid resuscitation in preparation for caval clamping;
maintain hemodynamic stability; optimize coagulopathy to facilitate surgical exposure and
hepatectomy
• Anhepatic phase: Monitor acid–base status and electrolytes; attempt to maintain
normothermia in preparation for reperfusion
• Reperfusion: Quickly treat hypotension, acidosis, and dysrhythmias; correct hyperkalemia
and hypothermia
• Neohepatic phase: Maintain hemodynamic stability in order to ensure perfusion to the
newly grafted liver; correct coagulopathy; monitor for fibrinolysis and DIC; watch for
evidence of liver function/primary graft nonfunction
• Optional therapies: Antifibrinolytics, mannitol, furosemide, THAM, sodium bicarbonate,
insulin, methylene blue, dextrose
Most often, patients remain intubated and are extubated later in the ICU. In rare instances, if
the intraoperative course was very straightforward, extubation in the OR may be considered.
Return of neuromuscular function and adequate analgesia must be achieved prior to
extubation.
POSTOPERATIVE CARE
BED ACUITY
ICU
ANALGESIA
IV PCA
COMPLICATIONS
• Primary graft nonfunction: Within minutes to hours, often requires urgent re-transplantation
• Acute rejection: Occurs within days to weeks
• Chronic rejection: Occurs after 1 year
• Hepatic artery thrombosis (HAT)
• Bile duct stricture, biliary leak
• Bleeding, infection
PROGNOSIS
• Highly variable depending on comorbidities and perioperative hospital course
• Graft survival rates (cadaveric): 3 months 91.2%, 1 year 84.3%, 5 years 68.4%, 10 years
54.1%
• Outcomes slightly better for living donor recipients
REFERENCES
1. Steadman RH. Anesthesia for liver transplant surgery. Anesthesiol Clin N Am.
2004;22:687–711.
2. Ozier Y, Klinck JR. Anesthetic management of hepatic transplantation. Curr Opin
Anesthesiol. 2008;21:391–400.
3. Fabbroni D, Bellamy M. Anaesthesia for hepatic transplantation. Contin Educ Anaesth Crit
Care Pain. 2006;6(5):171–175.
4. Ramsay MAE. Anesthesia considerations in liver transplantation. Recent developments in
transplantation medicine: Liver transplantation. Available at:
http://www.centerspan.org/pubs/liver/ramsay1.htm
5. OPTN Annual Report. Available at: http://optn.transplant.hrsa.gov/data/annualReport.asp
6. Starzl TE, Marchioro TL, Vonkaulla KN, et al. Homotransplantation of the liver in humans.
Surg Gynecol Obstet. 1963;117:659–676.
7. Fonouni H, Mehrabi A, Soleimani M, et al. The need for venovnous bypass in liver
transplantation. HPB. 2008;10:196–203.
ADDITIONAL READING
• Carithers RL. Liver transplantation. Liver Transplant. 2000;6(1):122–135.
• Csete M, et al. Anesthesia for organ transplantation. In Barash PG, et al., ed. Clinical
anesthesia. Philadelphia: Lippincott Williams and Wilkins, 2006:1364–1367.
• Liver vasculature
CODES
ICD9
V42.7 Liver replaced by transplant
ICD10
Z94.4 Liver transplant status
CLINICAL PEARLS
• Liver transplantation surgery is associated with large fluid shifts, potentially massive blood
loss, and dramatic hemodynamic derangements that require adequate preparation and
vigilant monitoring.
• There may be some degree of institutional variability in surgical technique and monitoring
resources that require careful consideration in preparing for and managing liver transplant
procedures.
• Grafts are often reduced from the adult liver (commonly left lateral segment or left lobe),
and the raw surface of the graft is at risk of bleeding. Vascular access may be more
challenging, and veno-venous bypass is not an option for children under 35–40 kg because
of inadequate flow through small cannulae. Children have an increased risk of hepatic
artery thrombosis (HAT) due to the small caliber of vessels and fluid overload. Transfusions
must be carefully managed to avoid overtransfusion and overcorrection of coagulopathy due
to risk of HAT.
LIVER VASCULATURE
BASICS
DESCRIPTION
• The liver is the largest endocrine organ.
– It comprises approximately 2% of total body weight.
– It is located in the right upper quadrant of the abdominal cavity, directly under the
diaphragm.
– The gallbladder sits in the fossa against the inferior surface, to the right of the falciform
ligament.
• Blood supply
– The portal vein drains venous blood from the stomach, spleen, pancreas, and intestines. It
provides approximately 70% of the hepatic blood supply.
– The hepatic artery delivers arterial (oxygenated) blood; it provides approximately 30% of
the hepatic blood supply.
– The hepatic veins drain the liver and empty into the inferior vena cava.
• The liver receives a blood flow of approximately 1.5 Liters/minute and is responsible for
25% of the body’s metabolic activity.
• The dual blood supply from the portal vein and hepatic artery maintains oxygen supply by
reciprocal changes in flow in these vessels. Typically, the portal vein supplies 70–75% of the
blood supply, while the hepatic artery supplies 25–30% of the blood supply. However, the
oxygen supply from each of these sources is roughly 50%.
• The liver coordinates processing and distribution of nutrients from the portal circulation.
– Responsible for carbohydrate, protein, and vitamin metabolism
– Urea cycle eliminates waste nitrogen.
– Produces and secretes bile
– Synthesizes all procoagulants except Factor VIII and von Willebrand factor
– Clears activated coagulation factors and tPA
– Metabolizes and eliminates toxins
• Intrinsic regulation of blood flow:
– Autoregulation: Describes the body’s ability to maintain a constant blood flow over a
range of mean pressures. It is believed that the stretch from an increase in hepatic arterial
perfusion pressure results in a myogenic contraction. Studies have shown that in a fasting
liver, autoregulation is decreased (e.g., perioperatively). The portal circulation does not
appear to demonstrate autoregulation and flow is pressure-dependent.
– Metabolic control: Hepatic arterial blood flow increases during hypoxemia, hypercarbia,
acidosis, and decreased portal oxygen tension. Increased osmolarity (e.g., digestion) also
results in increased hepatic artery and portal venous blood flow.
– Hepatic arterial buffer response (HABR) describes the ability of the body to protect the
liver during low-flow states by increasing hepatic arterial flow when portal venous blood
flow is decreased. This results in a reciprocal relationship in order to maintain a stable
oxygen supply. It is hypothesized that the build-up of adenosine in low-flow states is
responsible for the vasodilation of the hepatic artery.
• Extrinsic regulation of blood flow:
– Neural control is via branches of the vagus and splanchnic nerves that enter the liver with
blood vessels and bile ducts. There is an intercommunicating plexus that forms from the
sympathetic and parasympathetic nerves and terminates on arterioles and venules.
Sympathetic stimulation can divert 80% or approximately 500 mL of hepatic blood
quickly, in response to hypercarbia, pain, or hypoxia; functions as a reservoir.
– Humoral factors
Epinephrine: The hepatic artery has both alpha- and beta-adrenergic receptors, and the
portal venous system possesses alpha-receptors.
Glucagon: A vasodilator of intestinal origin that causes splanchnic vasodilation, with
resultant increase in portal blood flow
Angiotensin II: Capable of profound vasoconstriction of the hepatic and portal systems,
with concurrent reduction in mesenteric outflow; this results in a substantial reduction
in total liver blood flow.
Vasopressin: Splanchnic vasoconstrictor that decreases venous inflow of blood to the
portal vasculature.
ANATOMY
• Functional anatomy divides the liver into 8 segments (Couinaud classification). Each
segment is supplied by its own branch of the portal vein, hepatic artery, and bile duct
(portal triad).
• Hepatic artery originates from the celiac axis. Studies have shown that there are anomalous
variations of the right or left hepatic artery in nearly 50% of dissections; additionally, when
present, they are often multiple.
• Portal vein is formed by confluence of the splenic vein and superior mesenteric vein.
• Portal hypertension can result from cirrhosis. Blood outflow from the portal bed is impaired,
resulting in increased pressure with the formation of collateral circulation to other areas of
the general circulation (spleen, arteries, stomach). Esophageal varices develop at a hepatic
venous pressure gradient (HVPG) of at least 10 mm Hg; variceal bleeding usually begins at
12 mm Hg. For prevention of variceal bleeding, portal hypertension is treated with non-
selective beta-blockade (usually propranolol) to a target resting HR in the 50s or 25% below
baseline. If beta-blockers are not tolerated, a long-acting nitrate may be used.
• Ascites: 85% is associated with cirrhosis, and 15% is non-hepatic, e.g., associated with
cardiac, renal, neoplastic, and tuberculous disease. Ascites associated with portal
hypertension is caused by consequent splanchnic vasodilation and increased splanchnic
lymph production.
• Thrombosis of the liver vasculature:
– Acute thrombosis is associated with pain, fever, and rapid development of ascites; varices
are not seen. Risk factors include intra-abdominal inflammatory processes, primary
prothrombotic disorders, malignancy, and splenectomy. Acute thrombosis following liver
transplantation is a devastating complication, requiring revascularization.
– Portal venous thrombosis is most often associated with underlying cirrhosis, especially
with concomitant malignancy.
– Hepatovenous thrombosis (Budd–Chiari) is often associated with underlying malignancy
and may cause massive blood loss during surgery.
• Ischemic injury: Can result from prolonged hypotension, cardiogenic or noncardiogenic
shock, hypoxemia, or surgical injury (hepatic artery ligation, post-transplant)
• Hepatic congestion can result from right or left congestive heart failure and may result in
hepatic fibrosis and cirrhosis.
• The extent of hepatic resection is described by segmental anatomy. For example:
– Left lateral segmentectomy = segments 2, 3
– Left hepatic lobectomy = segments 2–4
– Extended left hepatic lobectomy or left trisegmentectomy = segments 2–5
– Right hepatic lobectomy = segments 5–8
– Extended right hepatic lobectomy or right trisegmentectomy = segments 4–8
• Cross-clamping to control surgical bleeding:
– May involve selective clamping of inflow (portal triad) and/or outflow (hepatic veins)
– The Pringle’s maneuver describes cross-clamping of the porta hepatis to decrease surgical
bleeding; it is usually without significant hemodynamic consequence.
– An extreme measure to control surgical bleeding in hepatic resection, termed “total
hepatic vascular exclusion,” involves cross-clamp of the porta hepatis, infra-hepatic, and
supra-hepatic cava. This can reduce venous return by 60–70%.
• Transjugular intrahepatic portosystemic shunt (TIPS) is a percutaneous procedure that
involves the creation of a portal vein to the hepatic vein tract, under fluoroscopic guidance.
Primary indications include secondary prevention of variceal bleeding and refractory
ascites. It may also be potentially beneficial in refractory varices, acutely bleeding varices,
refractory hepatic hydrothorax, hepatorenal syndrome, failed anticoagulation in moderate
Budd–Chiari syndrome, and re-bleeding after medical management in portal hypertensive
gastropathy.
• Octreotide and early endoscopic variceal sclerotherapy can be performed for the treatment
of acute variceal bleeding. Shunt placement (either TIPS or surgical shunt) may be
warranted for recurrent bleeding despite pharmacologic and endoscopic therapy.
• Cholecystectomy requires isolation and detachment of the cystic artery.
REFERENCES
1. Abdel-Misih SRZ, Bloomston M. Liver anatomy. Surg Clin N Am. 2010;90:643–653.
2. Celinski SA, Gamblin TC. Hepatic resection nomenclature and techniques. Surg Clin N Am.
2010;90:737–748.
3. Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N
Engl J Med. 2010;362(9):823–832.
• Gastrointestinal blood flow
• Cirrhosis
• Transjugular intrahepatic portosystemic shunt (TIPS)
• Cell salvage
CLINICAL PEARLS
• Regardless of the procedure planned, extent of underlying hepatic disease guides anesthetic
management.
• The liver is a highly vascular organ. Any procedure on it has the potential for massive blood
loss. Assure adequate venous access.
• If the patient has Budd–Chiari syndrome, there is no such thing as too much venous access.
These patients have a high risk for massive, exsanguinating hemorrhage.
• If massive transfusion is anticipated (variously defined as acute replacement of >10 U
blood, >1 blood volume, or >1/2 blood volume per hour) discuss anticipated needs with
the Blood Bank, plan for a “keep ahead” supply of blood products and discuss potassium
minimization measures for RBCs.
LOCAL ANESTHETIC SYSTEMIC TOXICITY
Angela T. Hsu, MD
BASICS
DESCRIPTION
• Local anesthetic (LA) toxicity can range from mild symptoms to severe central nervous
system (CNS) and cardiovascular (CV) toxicity that can result in death.
• The severity of LA systemic toxicity is based on a variety of factors:
– Regional block technique
– Location
– Type of local anesthetic utilized
– Total dosage
– Timeliness of detection and appropriate treatment
– Individual patient risk factors
• In addition to LA toxicity, local anesthetics, can also result in other adverse reactions:
– Allergic reaction
– Methemoglobinemia
– Neurotoxicity (cauda equina syndrome, transient neurologic symptoms)
EPIDEMIOLOGY
Incidence
• Epidural injection: 1.2–11 per 10,000 blocks
• Caudal injection: 1.3–69 per 10,000 blocks
• Peripheral nerve blocks: 7.5–20 per 10,000 blocks
Morbidity
Severe cardiovascular and neurologic compromise
Mortality
According to the ASA Closed Claims review of peripheral nerve blocks from 1980 to 2000, 7
of 19 claims associated with death or brain damage were attributed to LA systemic toxicity.
• Risk factors for LA toxicity:
– Location of regional block: Areas with high vascularity favor uptake of local anesthetic
and result in higher blood levels. Intercostal > Caudal > Epidural > Brachial plexus >
Sciatic > Spinal.
– Type of local anesthetic:
More potent, longer-acting LAs tend to be more toxic.
The S(–) isomers (levobupivacaine and ropivacaine) seem to be less toxic than R(+)
isomers or racemic bupivacaine.
– Technique and dosage
Dose = volume × concentration
Unnecessarily high dosing can increase the risk of serious toxicity if intravascular uptake
occurs.
Studies on ultrasound-guided regional blockade have indicated that with proper
placement, smaller doses can provide adequate blockade.
• Individual patient risk factors:
– Patients at extremes of age (<4 months or >70 years)
– History of cardiac conduction defects or ischemic heart disease
– Cardiac, renal, and hepatic dysfunction are important predictors of local anesthetic plasma
levels after a specific dose rather than body weight or BMI.
• The mechanism of LA toxicity is highly controversial. Due to ethical concerns, no human
randomized controlled trials exist. Data on this topic relies on animal studies and case
reports.
• In general, the CNS is more sensitive to LA toxicity than the CV system. For most local
anesthetics, CV toxicity does not occur until 3 times the concentration necessary to produce
seizures. This CV/CNS ratio tends to be lower with bupivacaine.
• Hypoxia and hypercarbia can decrease the convulsive threshold and predispose to
myocardial toxicity.
• CNS toxicity: 2-phase pathophysiologic process:
– First, preferential blockade of the inhibitory CNS pathways leaves the excitatory pathways
unopposed. This can manifest as shivering/muscle tremors and proceed to tonic–clonic
seizures.
– With increasing plasma levels, both inhibitory and excitatory pathways are blocked.
Generalized CNS depression ensues with potential respiratory arrest.
• CV toxicity: One of the primary mechanisms of CV toxicity is thought to be from binding
and inhibition of Na+ channels by LAs. At higher concentrations, it is believed that cardiac
Ca2+ and K+ channels are also inhibited. LAs are also thought to antagonize beta-
adrenergic receptors. 2-phase pathophysiologic process:
– In the CNS excitatory phase, activation of the sympathetic nervous system results in
tachycardia and hypertension.
– With increasing plasma levels, bradycardia, hypotension, and ventricular arrhythmias
occur.
According to the 2010 American Society of Regional Anesthesia (ASRA) practice advisory:
• Use lowest effective dose of LA
• Incremental dosing: Pause 15–30 seconds between each 3–5 mL dosing.
• Aspirate for blood prior to each injection.
• Consider using a pharmacologic marker/test dose to identify inadvertent intravascular
injection:
– Epinephrine 15 μg produces a greater than 10 beat increase in heart rate or a greater than
15 mm Hg increase in systolic blood pressure.
– Note that beta-blockers, advanced age, labor, and general/neuraxial anesthesia may
inhibit this response.
– Fentanyl 100 μg produces sedation in laboring patients.
• Ultrasound guidance: Reportedly decreases the incidence of intravascular injection. Whether
it decreases actual incidence of LA systemic toxicity still remains to be answered.
DIAGNOSIS
• Classically in LA systemic toxicity, CNS symptoms are followed by CV symptoms. However,
in review of case reports, there is extreme variability in presentation.
• Particularly with potent local anesthetics, cardiac toxicity may occur simultaneously or
precede seizures. Sometimes CV toxicity is the only manifestation.
• CNS toxicity:
– Classic early symptoms: Circumoral numbness, metallic taste, lightheadedness,
visual/auditory disturbances, agitation/tremors
– Later symptoms: Seizure, coma, respiratory arrest
• CV toxicity:
– First, cardiac excitation: Tachycardia, hypertension, ventricular arrhythmias
– Later, CV depression: Bradycardia, hypotension, decreased contractility, asystole
Pain during uterine contraction may also produce increased heart rate.
TREATMENT
• Airway management is of utmost importance. Prevention of hypoxia and

hypercarbia/acidosis can halt progression of LA toxicity to seizures and/or CV collapse, as
well as aid in successful resuscitation.
• For seizures, the first-line therapy is benzodiazepines. Small doses of thiopental or propofol
may also be used, realizing this may worsen hypotension/CV depression. Avoid propofol
when there are signs of CV compromise. Future studies may support lipid infusion as the
initial treatment.
• If seizures persist, consider small doses of neuromuscular blockers to halt muscle
contractures, thus preventing further oxygen consumption and CO2 production. Seizures
(electrical function) may continue despite a lack of tonic–clonic muscle activity.
• For cardiac arrest, perform standard ACLS with the following modifications:
– Small doses of epinephrine (<1 μg/kg) if needed
– Avoid vasopressin
– Avoid calcium channel blockers and beta-blockers
– For ventricular arrhythmias, amiodarone is preferred. Avoid local anesthetics (i.e.,
lidocaine, procainamide).
• 20% Lipid emulsion therapy
– Consider starting the infusion immediately after airway management. Lipid emulsion can
be a significant aid in resuscitation, acting as a “lipid sink,” drawing lipophilic local
anesthetic from within cardiac tissues.
– Dosing
Bolus 1.5 mL/kg over 1 minute
Infusion of 0.25 mL/kg/min for at least 10 minutes after circulatory stability is achieved.
If the patient is still unstable, re-bolus and increase the infusion to 0.5 mL/kg/min.
Recommended upper limit: 10 mL/kg over 30 minutes
– Note: Propofol is not a substitute for lipid emulsion.
• Consider cardiopulmonary bypass (CPB) if inadequate responses to lipid emulsion and
vasopressor therapy.
FOLLOW-UP
• Delayed re-occurrence of LA systemic toxicity has been reported.

– Continue close monitoring of patients for 12 hours after severe episodes.
– Maintain oxygenation and ventilation.
– Once the patient is stabilized from the initial episode of LA systemic toxicity, consider
consultation with a cardiologist or intensivist.
– Recommend stay in a monitored setting/ICU setting to observe for signs of recurrent
cardiac or central nervous system toxicity.
• There are concerns of possible adverse effects following lipid therapy.
– Lipid emulsion for TPN is associated with pancreatitis; however, there have been no
reported cases associated with lipid infusion for LA toxicity.
– Further observation and studies are needed to fully elucidate the possible adverse effects
of lipid therapy for LA toxicity.
CLOSED CLAIMS DATA
LA systemic toxicity accounts for 1/3rd of claims for death or brain damage associated with
regional anesthesia.
REFERENCES
1. Butterworth JF. Local anesthetics: Mechanisms, toxicities, and controversies from a clinical
perspective. American Society of Anesthesiologists Annual Meeting, San Diego, CA, 2010.
2. Drasner K. Local anesthetic systemic toxicity: A historical perspective. Reg Anesth Pain
Med. 2010;35:160–164.
3. Groban L. Central nervous system and cardiac effects from long-acting amide local
anesthetic toxicity in the intact animal model. Reg Anesth Pain Med. 2003;28(1):3–11.
4. Lee LA, Posner KL, Cheney FW, et al. Complications associated with eye blocks and
peripheral nerve blocks: An American Society of Anesthesiologists Closed Claims Analysis.
Reg Anesth Pain Med. 2008;33(5):416–422.
5. Mulroy MF. Systemic toxicity and cardiotoxicity from local anesthetics: Incidence and
preventive measures. Reg Anesth Pain Med. 2002;27(6):556–561.
6. Neal JM, Bernards CM, Butterworth JF 4th, et al. ASRA practice advisory on local
anesthetic systemic toxicity. Reg Anesth Pain Med. 2010;35(2):152–161.
7. Weinberg GL, Ripper R, Murphy P, et al. Lipid infusion accelerates removal of bupivacaine
and recovery from bupivacaine toxicity in the isolated rat heart. Reg Anesth Pain Med.
2006;31:296–303.
• Epidural
• Caudal epidural
CODES
ICD9
968.9 Poisoning by other and unspecified local anesthetics
ICD10
T41.3X1A Poisoning by local anesthetics, accidental, init
CLINICAL PEARLS
• Be prepared to handle severe LA systemic toxicity by preparing a LA toxicity kit, including
lipid emulsion therapy and posting instructions on its use.
• When performing a regional or neuraxial anesthetic technique, use the smallest dose of local
anesthetic necessary.
• Use a pharmacologic marker/test dose to aid with identification of vascular injection.
• Inject 3–5 mL aliquots followed by aspiration to assess for blood. Pause for 15–30 seconds
prior to resuming injection to ask the patient if they are experiencing symptoms of toxicity
and observe for signs.
• Be vigilant. Monitor patient during and after the injection, noting that toxicity can present
>30 minutes after injection.
• Consider LA toxicity in any patient with altered mental status, neurologic symptoms, or CV
instability following a regional anesthetic.
• Note that >40% of cases do not follow the classic presentation of local anesthetic systemic
toxicity. Cardiovascular signs may be the only manifestation in severe cases.
LOWER EXTREMITY AMPUTATION
BASICS
DESCRIPTION
General
• Lower extremity (LE) amputation is one of the oldest known surgical procedures. It can be
classified as:
– Minor: Removal of a toe or part of the foot
– Major: Removal of part of the leg. It is further described as a below-the-knee amputation
(BKA) or an above-the-knee amputation (AKA).
• Indications for LE amputation include: End-stage peripheral vascular disease (PVD), trauma,
tumor, infection, congenital limb deficiency, and painful, non-functional limbs. In recent
years, as prosthesis technology has advanced, the indications for elective amputation have
expanded.
• Surgical technique is important for long-term functional outcome. Use of a pneumatic
tourniquet reduces blood loss and the need for transfusion (1)[B]. After incision, the muscle
compartments are isolated, and the main arteries, veins, and nerves are identified. Arteries
and veins are ligated separately, in order to avoid arteriovenous fistula formation. Nerves
are transected under tension as proximally as possible, and are then allowed to retract in
the soft tissues, in an attempt to avoid neuroma formation.
• The bone is cut and the bony edges are smoothed, to minimize postoperative soft-tissue
trauma and pain with application of a prosthesis. Several techniques (myoplasty or
myodesis) can be used to place muscle over the cut end of the bone. Enough skin should be
preserved to cover the muscle and achieve a symmetric, smooth, tension-free closure. At the
end of surgery, drains are placed to avoid formation of wound hematoma.
• A guillotine (or open) amputation is a quicker procedure, and is reserved for cases with
infection, contaminated trauma, or uncertain survival; it leave an open wound at the end of
the stump. Blood vessels are ligated and nerves are cut as described above, but the wound is
not closed. Instead, the stump is dressed with gauze and application of bandages. Later,
when the risk of infection is reduced, the amputation can be revised higher or grafted.
• Postoperative pain, depression, need for rehabilitation, and appropriate application of
prosthesis are important long-term considerations.
Position
Supine: A bump under the hip is often used to limit limb rotation.
Incision
Anterior and posterior, above the line of ischemic tissue demarcation
Approximate Time
1–2 hours
EBL Expected
• BKA: 200 mL
• AKA: >250 mL
Hospital Stay
Up to 7 days
• Saw or guillotine
• Pneumatic tourniquet
• Vascular and orthopedic instruments
EPIDEMIOLOGY
Incidence
In the US: 30,000–40,000 procedures per year (2)[B]
Prevalence
In the US in 2005, 1.6 million people lived with loss of a limb; this number is projected to
double by 2050 (2)[B].
Morbidity
Cardiac, respiratory (most patients are smokers), infection (most patients have diabetes), non-
healing wound, re-amputation, acute pain, phantom limb pain (PLP), and stump pain
Mortality
Very high given the comorbidities of the patient population. Median survival is 20–27 months
after AKA and 52 months after BKA (3)[B].
• Maintain hemodynamic stability: These patients are at high risk for coronary artery disease;
thus, hypotension and tachycardia should be avoided. Tourniquet pain can cause
tachycardia and hypertension, which can be treated with beta-blockers, opioids, or
increasing the anesthetic depth. Depending on preoperative hemoglobin and surgical blood
loss, transfusion of RBCs may be needed.
• Use of an epidural or regional block has the advantage of avoiding general anesthesia and
mechanical ventilation, and may decrease intraoperative and immediate postoperative pain.
It is not clear, however, if it decreases the incidence of PLP (4)[B].
SYMPTOMS
• Severe ischemic and/or neuropathic LE pain
• Symptoms of coronary artery disease or ischemic cardiomyopathy
History
Inquire about diabetes, smoking, hypertension, chronic obstructive pulmonary disease,
symptoms of coronary artery disease or congestive heart failure. Confirm the timing of
hemodialysis in patients with renal failure.
Signs/Physical Exam
MEDICATIONS
• Beta-blockers should be continued perioperatively.
• Antiplatelet agents: Generally should be discontinued for 7–14 days before surgery.
However, the risk of discontinuation (e.g., thrombosis to coronary or cerebral vasculature)
should be discussed with the surgeon and primary care physician. Additionally, it is not
always feasible when the amputation is urgent.
• Oral antihyperglycemics should be held on the morning of surgery to avoid hypoglycemia
while the patient is NPO. Blood glucose can be checked perioperatively, and insulin can be
administered to treat hyperglycemia.
• Antihypertensive medications should generally be continued throughout the perioperative
period. ACE inhibitors, however, have been associated with severe hypotension and should
perhaps be discontinued 24–48 hours before surgery.
Labs/Studies
• EKG (coronary artery disease)
• Hemoglobin: Values >10 g/dL are recommended to ensure adequate oxygen delivery for
wound healing.
• Blood glucose in diabetic patients: Hyperglycemia is associated with increased risk of
infection.
• Serum albumin: Values <3.5 g/dL indicate malnutrition and increased risk of impaired
wound healing.
• Respiratory (COPD related to smoking)
• Cardiovascular
• Renal, central and peripheral nervous system (history of stroke, diabetic neuropathy)
TREATMENT
Premedications
• Beta-blockers, insulin as appropriate
• Transfusion of FFP may be needed to correct coagulopathy (prolonged PT, INR). pRBCs
should be considered for anemia, in an attempt to increase oxygen tissue delivery and
improve wound healing.
BKA is an intermediate cardiac risk procedure, whereas AKA is a high cardiac risk procedure.
Reported perioperative mortality is 0.9–14% for BKA versus 2.8–35% for AKA, and median
survival is 52 months after BKA versus 20–27 months after AKA (3)[B].
• Cefazolin 1–2 g IV for skin organisms
• May need additional antibiotics in cases of infection, contamination, or gangrene
INTRAOPERATIVE CARE
• General anesthesia if the patient is on anticoagulants or antiplatelet medications
• Regional with/without general anesthesia
– Neuraxial (spinal or epidural) is an excellent choice (if no contraindications). Potential
benefits include improved perioperative analgesia, increased limb perfusion due to
sympatholysis, reduced blood loss, and reduced risk of deep venous thrombosis.
– Regional blocks (femoral and sciatic) could be considered in anticoagulated patients.
Monitors
Arterial line may be considered for tight blood pressure control, as well as glucose, and
hemoglobin monitoring.
Endotracheal intubation for general anesthesia should be considered in patients at risk for
aspiration, such as diabetes, pain, or trauma. Consider a rapid-sequence induction.
Maintenance
• Use of a pneumatic tourniquet during amputation significantly reduces blood loss and
transfusion requirements (1)[B], but can have significant hemodynamic effects.
• Tourniquet “up”
– Afterload: Systemic vascular resistance (SVR) is increased mechanically (from vascular
occlusion) and secondary to norepinephrine release in response to tourniquet pain.
– Preload: Increases due to “exsanguination” of the limb before the tourniquet is inflated
– Cardiac output (CO): Unchanged initially, but gradually increases above baseline.
• Tourniquet “down”
– Afterload: The mechanical afterload decreases, and acid metabolites (such as lactate) that
are released into the circulation on reperfusion cause vasodilation.
– Preload: Decreases, as blood is allowed to return to the remaining limb
– Cardiac output: Generally increases after amputation, but blood pressure decreases due to
reduced preload and afterload. Overall, hypotension is less pronounced compared to non-
amputation procedures because the load of return of metabolites entering the circulation
is reduced after removal of the ischemic limb.
POSTOPERATIVE CARE
BED ACUITY
• Recovery room and then regular floor
• ICU care may be considered if the patient was critically ill before surgery.
ANALGESIA
Acute postoperative and chronic PLP and stump pain are significant issues. The
pathophysiology of PLP is not fully understood, but cortical reorganization plays a major role.
Severe preamputation pain is associated with PLP development. Several analgesic
interventions, including preemptive analgesia, continuous nerve blocks, continuous epidural
analgesia, epidural or IV ketamine, and oral gabapentin have been evaluated for PLP
prevention, with inconclusive results. However, recent data suggest that optimized
perioperative analgesia reduces PLP incidence and intensity, regardless of the analgesic
modality used (4)[B]. Established phantom pain can be very difficult to treat.
COMPLICATIONS
• Cardiovascular (myocardial infarction, arrhythmias, congestive heart failure, stroke)
• Respiratory (pneumonia, respiratory failure)
• Ulcers, gangrene, non-healing wound
• Osteomyelitis
• Chronic pain, depression, and disability
PROGNOSIS
• Amputation for PVD: 15–30% of patients need contralateral amputation within 3 years.
• Amputation for trauma: Severe long-term disability regardless of amputation level (5)[B]
• Amputation for pediatric bone tumors: Survivors have significant long-term deficits in
education and employment (6)[B].
• The level of LE amputation is important because energy expenditure for walking increases,
and walking speed decreases with higher levels of amputation. In recent years there is a
trend for fewer AKAs and more BKAs.
REFERENCES
1. Choksy SA, Lee Chong P, Smith C, et al. A randomised controlled trial of the use of a
tourniquet to reduce blood loss during transtibial amputation for peripheral arterial
disease. Eur J Vasc Endovasc Surg. 2006;31:646–650.
2. Ziegler-Graham K, MacKenzie EJ, Ephraim PL, et al. Estimating the prevalence of limb loss
in the United States: 2005 to 2050. Arch Phys Med Rehabil. 2008;89:422–429.
3. Subramaniam B, Pomposelli F, Talmor D, et al. Perioperative and long-term morbidity and
mortality after above-knee and below-knee amputations in diabetics and nondiabetics.
Anesth Analg. 2005;100:1241–1247.
4. Karanikolas M, Aretha D, Tsolakis I, et al. Optimized perioperative analgesia reduces
chronic phantom limb pain intensity, prevalence, and frequency: A prospective,
randomized clinical trial. Anesthesiology. 2011;114:1144–1155.
5. MacKenzie EJ, Bosse MJ, Castillo RC, et al. Functional outcomes following trauma-related
lower-extremity amputation. J Bone Joint Surg Am. 2004;86-A(8):1636–1645.
6. Nagarajan R, Neglia JP, Clohisy DR, et al. Education, employment, insurance, and marital
status among 694 survivors of pediatric lower extremity bone tumors. Cancer.
2003;97:2254–2264.
ADDITIONAL READING
• Jaffe RA, Samuels SI. Anesthesiologist’s manual of surgical procedures, 4th ed. Philadelphia:
Lippincott Williams & Wilkins, 2009:1047–1051.
• Epidural
CODES
ICD9
897.4 Traumatic amputation of leg(s) (complete) (partial), unilateral, level not specified,
without mention of complication
ICD10
• S88.919A Complete traumatic amp of unsp lower leg, level unsp, init
• S88.929A Partial traumatic amp of unsp lower leg, level unsp, init
CLINICAL PEARLS
• Above-the-knee (AKA) or below-the-knee amputation (BKA) is a major procedure with a
high perioperative morbidity and mortality.
• Patients scheduled for AKA and BKA typically have numerous comorbidities including
diabetes, coronary artery disease, chronic obstructive pulmonary disease, renal
insufficiency, and peripheral neuropathy.
• Optimized perioperative analgesia may reduce phantom pain.
LOWER EXTREMITY BYPASS
BASICS
DESCRIPTION
General
• Most patients with peripheral vascular disease are managed medically. Endovascular
procedures with balloon angioplasty and stenting are less invasive procedures but are also
less durable and have technical limitations when the blockage is extensive.
• The goal of lower extremity bypass is to improve blood flow, reduce pain, improve
functional ability and quality of life, and prevent amputation. Common causes include:
– Arterial occlusive disease due to atherosclerosis; most common
– Thromboembolic, inflammatory, or traumatic events. Femoral and popliteal artery
aneurysms and pseudoaneurysms are often repaired to prevent thromboembolic events as
well as rare ruptures.
– Advential cysts, entrapment.
– As part of tumor resections
• The procedure entails creating an alternate conduit for blood flow to circumvent the area of
blockage and restore direct flow to the lower leg and foot. The conduit can include
harvested veins (saphenous or other vein from the arm or leg) or an artificial, prosthetic
graft.
• Acute occlusion is a surgical emergency and is treated with embolectomy, thrombolysis, or
bypass.
Position
• Usually supine
• Occasionally other positions may be required, such as prone for some popliteal aneurysms.
Incision
• Sufficient to expose the proximal and distal anastomosis
• Additional incisions (often long) for the vein harvest may be needed, though this may be
minimized with in situ grafts or endovascular harvests.
Approximate Time
Highly variable (1 hour to all day) depending on the extent of bypass and the anatomic
intricacies of the procedure
EBL Expected
• Usually minimal blood loss
• Revision procedures, infected grafts, or intraoperative difficulties can increase blood loss.
Hospital Stay
3–5 days in uncomplicated cases
In patients lacking suitable autologous veins (prior harvest or excision), synthetic graft (e.g.,
PTFE) or cryopreserved vessels may be needed. In an infected field, cryovessel is preferred
over PTFE.
EPIDEMIOLOGY
Incidence
Peripheral arterial disease (PAD) incidence increases with age.
Prevalence
• PAD estimates vary widely; American Heart Association (AHA) states about 8 million
Americans.
• PAD affects approximately 20% of adults over the age of 55 years.
Morbidity
• Per National Surgical Quality Improvement Program (NSQIP), in 2004, major 30-day
morbidity was 18.7%.
– Wound complications (∼75% of all complications): Dehiscence, wound and organ space
infection, sepsis, bleeding, and graft failure
– Systemic complications: Failure to wean, reintubation, pneumonia, renal failure,
pulmonary embolism, stroke, coma, cardiac arrest, and deep venous thrombosis
• Morbidity was also higher in those undergoing surgery for limb ischemia: 30.1% (1).
Mortality
• Operative mortality of approximately 1–3%
• Per NSQIP data, mortality was 2.7% in 2004; patients with critical limb ischemia had an
increased mortality of 3.6% (1).
• Although the surgery itself does not typically pose significant challenges for the anesthetist,
the comorbidities present significant risks and warrant careful evaluation and perioperative
management.
• The AHA guidelines rank infrainguinal bypass procedures as a high-risk procedure (on par
with open aortic procedures, and greater than intermediate-risk procedures such as carotid
endarterectomies and endovascular aortic repairs).
– Claudication makes clinical assessment more difficult (unable to assess exercise tolerance,
perform treadmill stress testing).
– Shared risk factors for coronary disease and peripheral vascular disease may also be more
prevalent in patients undergoing lower extremity bypasses. Hence having infrainguinal
vascular disease may be a “marker” for sicker patients.
SYMPTOMS
• Early–mild intermittent claudication: Pain or fatigue in the leg muscles with exercise and
relieved by rest
• Late–severe disabling claudication or rest pain: Pain may be worse when lying flat and
improved when the feet are dependent.
• Toe and foot sores that do not heal
• Acute occlusion is characterized by a sudden onset of the 5 “P”s: Pain, pallor, pulselessness,
paresthesias, and paralysis.
• Cardiovascular status
– Past cardiac disease and evaluations as well as symptoms of chest pain and dyspnea
– Evaluation of exercise tolerance should recognize that patients frequently have
asymptomatic cardiac disease due to claudication. They will frequently say their walking
is limited by leg pain and not chest pain. Exercise tolerance is thus often inconclusive as a
screen for cardiac reserve in these patients.
History
Focus on evidence of atherosclerotic vascular disease in the heart, brain, and kidneys.
Symptoms of cardiac disease may be masked since claudication may limit exertion.
Signs/Physical Exam
• Lower extremity pallor, cyanosis, dependent rubor, coolness, atrophy, and decreased hair or
nail growth may be noted with diminished or absent distal pulses in the evaluation by the
surgical consult.
– Evaluation by ankle brachial index (the ratio of the ankle to the arm pressure): A ratio
<0.9 or >1.3 is abnormal, and ≤0.4 indicates severe peripheral vascular disease.
– Further evaluation often leads to angiography along with attempts at angioplasty,
stenting, or other minimally invasive vascular procedures.
• Cardiac exam for evidence of heart failure
• Carotid bruits can be significant, though often a carotid duplex has already been performed.
• Pulmonary exam may indicate the adverse effects of smoking.
MEDICATIONS
• Due to concomitant disease
• Beta-blocker (and potentially a statin) may have been added to reduce cardiac risk.
Labs/Studies
• Electrolytes, BUN, creatinine, glucose
• EKG
• CXR
• Cardiac stress testing, echocardiogram, and/or cardiac catheterization data may have been
performed as part of a cardiac evaluation.
• Generalized vascular disease: Cardiac and cerebral
• Effects of smoking
• Diabetes
• Hypertension
• Dyslipidemia
• Renal failure
TREATMENT
Premedications
• Perioperative beta-blockade may be started (2)[B].
– However, studies with the most favorable outcomes initiated beta-blockade at least a week
before surgery (3)[B].
– A more recent study demonstrated reduced incidence of myocardial infarction, but
increased risk of stroke and a higher death rate (4)[B]. The dose of beta-blocker, however,
was criticized as being relatively high.
• Consent for possible blood transfusion, planned or possible invasive monitors
• Review of the risk of cardiac and cerebral vascular complications
Routine prophylactic antibiotics for skin organisms unless already on a specific antibiotic for
limb infection
INTRAOPERATIVE CARE
• General, epidural, spinal, and even nerve blocks have been successfully utilized.
• Epidurals have the possible advantage of avoiding airway instrumentation and the potential
stress of general anesthesia as well as improved graft patency. Reductions in cardiac and
pulmonary complications and graft thrombosis have been inconsistently seen in a variety of
studies.
• General anesthesia offers a secure airway, avoids the hemodynamic changes of a
sympathectomy, and may be better tolerated (and preferred by patients) in longer
procedures.
• Peripheral nerve blocks may offer an alternative to neuraxial techniques when
anticoagulants/antiplatelets therapy contraindicates neuraxial placement.
Monitors
• Arterial line monitoring is useful for blood pressure monitoring and frequent blood draws.
• A urinary catheter is frequently placed in expected lengthy procedures and to assist in
monitoring volume status.
• Consider central line monitoring per the patient’s underlying disease. Pulmonary artery
catheterization and/or transesophageal echocardiography may be indicated in more severe
cardiac disease.
A slow, controlled induction may produce fewer or more tightly controlled hemodynamic
swings.
Maintenance
Hemodynamic stability is critical to preserve perfusion through the cerebral, myocardial, and
renal vessels.
• Extubation at the end of the case is usually feasible.
• A hemodynamically smooth emergence and extubation may be beneficial in the setting of
cardiac disease.
POSTOPERATIVE CARE
BED ACUITY
ICU admission is dictated by the patient’s underlying disease and operative course, otherwise
a regular bed is appropriate.
ANALGESIA
Mild-to-moderate pain can be managed with opioids or, if present, epidural analgesia.
COMPLICATIONS
• Cardiovascular and cerebral vascular events
• Graft thrombosis; may be increased with prosthetic grafts
• Infection (including progression of a pre-existing limb infection); although successful
revascularization can facilitate improvement of an infection and closure of an ischemic
wound.
PROGNOSIS
For those with claudication, the risk for future cardiovascular events is higher than the risk of
limb ischemic events.
REFERENCES
1. LaMuraglia GM, Conrad MF, Chung MA, et al. Significant perioperative morbidity
accompanies infrainguinal bypass surgery: An NSQIP report. J Vasc Surg. 2009;50:299–
304.
2. Mangano DT, Layug EL, Wallace A, et al. Effect of atenolol on mortality and cardiovascular
morbidity after noncardiac surgery. Multicenter Study of Perioperative Ischemia Research
Group. N Engl J Med. 1996;335:1713–1720.
3. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality
and myocardial infarction in high-risk patients undergoing vascular surgery. Dutch
Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study
Group. N Engl J Med. 1999;341:1789–1794.
4. Devereaux PJ, Yang H, Yusuf S, et al. Effects of extended-release metoprolol succinate in
patients undergoing non-cardiac surgery (POISE trial): A randomised controlled trial.
Lancet. 2008;371:1839–1847.
ADDITIONAL READING
• Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 guidelines on perioperative
cardiovascular evaluation and care for noncardiac surgery: Executive summary. A report of
the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative
Cardiovascular Evaluation for Noncardiac Surgery). Circulation. 2007;116:1971–1996.
• Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the
management of patients with peripheral arterial disease (lower extremity, renal, mesenteric,
and abdominal aortic): Executive summary. A collaborative report from the American
Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular
Angiography and Interventions, Society for Vascular Medicine and Biology, Society of
Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing
Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial
Disease). Circulation. 2006;113(11):e463–e654.
• Cerebrovascular disease/TIA
CLINICAL PEARLS
• As endovascular options have begun to replace many lower extremity bypasses (due to
lower morbidity and mortality rates), the remaining operative procedures are often much
more challenging and complex.
LUSITROPY
BASICS
DESCRIPTION
• Lusitropy describes the ability of the myocardium to relax following contraction, and hence
the ventricle’s diastolic function.
• Maintaining cardiac output is a direct function of normal contraction (inotropy) and
relaxation (lusitropy) properties.
• Myocardial contraction: Electrical depolarization activates the voltage-gated sodium
channels and triggers a rapid release of calcium from the sarcoplasmic reticulum. The initial
burst of calcium release is inhibited by ryanodine (discontinues sarcoplasmic calcium
release into the intracellular space). Calcium is a principal controlling mechanism of actin–
myosin interaction.
• Calcium binds to troponin C which then allosterically modulates tropomyosin; this results in
uncovering of actin binding sites. When uncovered, myosin heads can bind and hydrolyze
ATP (converts the chemical energy in ATP into mechanical energy; ATP → ADP +
phosphate) to drive filament sliding; known as a cycle. Repeated cycles result in the
movement of myosin heads along actin filaments, resulting in contraction.
FIGURE 1. Tropomyosin chains cover actin binding sites. When calcium binds to troponin C, tropomyosin uncovers or
“exposes” the actin binding sites which allows myosin to bind.
• Myocardial relaxation, hence, results from the removal and sequestration of intracellular
calcium. A decrease in calcium concentration results in decreased binding to troponin C and
tropomyosin “re-covering” the actin binding sites, and myosin “unbinding.” Calcium
removal is performed by the:
– Sarcoplasmic reticulum calcium ATPase (SERCA): SERCA proteins are highly regulated by
phospholamban and sarcolipin; they are also sensitive to thyroid hormone action.
– Na+/Ca2+ ion exchanger
– Ca-ATPase (located in the sarcolemma)
• Positive lusitropy describes increased relaxation.
– Beta-agonists increase contractility/inotropy/chronotropy and are also important in
improving relaxation via improved calcium ion uptake. This allows for subsequent normal
filling and preload, and improved cardiac output.
– At a molecular level, beta-agonism decreases the amount of calcium available for binding
with troponin C by phosphorylating the phospholamban molecule. Normally, non-
phosphorylated phospholamban is a SERCA antagonist, and decreases intracellular
calcium removal.
FIGURE 2. Effects of left ventricular diastolic failur caused by decreased ventricular compliance (e.g., hypertrophy) on left
ventricular pressure-volume loop. Heart rate, inotropy and systemic vascular resistance are unchanged.
• Negative lusitropy describes decreased relaxation and involves:

– Increased intracellular calcium
– Impaired SERCA function: Seen with aging (also combined with interstitial fibrosis and
increased cross-linking of collagen that can cause stiffness).
– Increased affinity of troponin C to calcium
• Intracellular acidosis may inhibit calcium reuptake by the sarcoplasmic reticulum.
• Diastolic dysfunction, or negative lusitropy, results in impaired ventricular compliance.
– On a molecular level, it is related to an imbalance in the distribution of phospholamban
and SERCA. The increased levels of intracellular calcium result in impaired lusitropy.
– Increased left ventricular end-diastolic pressures (LVEDP) will decrease preload (LVEDV),
with resultant decreases in stroke volume and cardiac output
– Over time, left atrial and pulmonary arterial pressures can increase (this can result in
elevated right ventricular afterload)
– Coronary perfusion pressure (CPP) also decreases secondary to increased intraventricular
pressures during diastole (CPP = MAP – LVEDP, where MAP is mean arterial pressure).
• Diastolic dysfunction is an independent determinant of heart failure; poorer outcomes are
seen when it is present early in post-acute myocardial dysfunction. It is diagnosed in 3
steps:
– Clinical (heart failure)
– Normal ejection fraction
– Increased diastolic filling pressures
• Echocardiographic indices:
– Isovolumic relaxation time (normal 70 ms) is the time interval between aortic valve
closure and mitral valve opening. When prolonged, it indicates poor myocardial
relaxation.
– Transmitral inflow (E/A ratio): The “E” wave represents flow during the rapid filling
phase of ventricular diastole (after mitral valve opening); it represents the left atrial to left
ventricular gradient. The “A” wave represents flow during atrial contraction and is
approximately one-third to one-half the size of the E wave.
During impaired relaxation, the E wave decreases in size (decreased left atrial-left
ventricular gradient), the A wave increases in size (increased contribution), and the E/A
ratio is <1.
As impaired ventricular relaxation progresses, left atrial pressures increase in tandem
and can cause pseudonormalization of the E/A ratio (>1). The normal appearing E wave
reflects the increase in passive filling from the increased left atrial-left ventricular
gradient. The normal appearing A wave reflects the decreased contribution of the atrial
contraction.
– Deceleration time: Describes the time it takes for the E wave velocity to become zero
(normal is <220 milliseconds). In impaired relaxation, it exceeds 240 ms.
EQUATIONS
CPP = MAP – LVEDP, where CPP is coronary perfusion pressure, MAP is mean arterial
pressure, and LVEDP is left ventricular end diastolic pressure.
REFERENCE
1. Chemla D, Lecarpentier Y, Martin JL, et al. Relationship between inotropy and relaxation
in rat myocardium. Am J Physiol Heart Circ Physiol. 1986;250:H1008–H1016. [C]
2. Chen Y, Escoubert B, Prunier F, et al. Constitutive cardiac overexpression of
sarcoplasmic/endoplasmic reticulum Ca2+ ATPase delays myocardial failure after
myocardial infarction in rats at a cost of increased acute arrhythmias. Circulation.
2004;109:1898–1903. [A]
3. Coudray N, Beregi JP, Lercarpentier Y, et al. Effects of isoproterenol on myocardial
relaxation rate: Influence of the level of load. Am J Physiol Heart Circ Physiol.
1993;265:H1645–H1653.
4. Fein FS, Kornstein LB, Strobeck JE, et al. Altered myocardial mechanics in diabetic rats.
Circ Res. 1980;47:922–933.
5. Katz AM. Influence of altered inotropy and lusiotropy on ventricular pressure-volume
loops. J Am Coll Cardiol. 1988;11:438–445. [B]
6. Satoh N, Sato T, Shimada M, et al. Lusiotropic effect of MCC-135 is associated with
improvement of sarcoplasmic reticulum function in ventricular muscles of rats with
diabetic cardiomyopathy. J Pharmacol Exp Ther. 2001;298:1161–1166.
• Chronotropy
• cAMP
• Diastole
CLINICAL PEARLS
• Myocardial relaxation is influenced negatively by calcium overload.
• Diastolic dysfunction can independently cause heart failure or can be associated with
systolic heart failure. Emerging evidence has suggested that myocardial remodeling and
diastolic dysfunction are far more important in heart failure pathogenesis than systolic
dysfunction.
MAGNESIUM
BASICS
DESCRIPTION
• Magnesium (Mg2+) is a vital and abundant cation that plays a role in enzyme function, ATP
synthesis, potassium balance, bone stability, and neurotransmission. Consequently,
abnormalities can manifest as a variety of pathophysiologic scenarios.
• Hypomagnesemia commonly presents in the perioperative period with non-specific signs
and symptoms. Furthermore, it is associated with several pathologic processes
(hypokalemia, arrhythmias, mitral valve prolapse, migraines, anxiety and psychiatric
disorders, fibromyalgia, diabetes, hearing loss, osteoporosis, dysmenorrhea, asthma, and
allergies).
• Hypermagnesemia’s clinical presentation ranges from hyporeflexia to respiratory depression
to cardiac arrest. It often results from exogenous replacement for the treatment of
arrhythmias, hypokalemia, asthma, and preeclampsia, as well as hemolysis, or impaired
renal function.
• Mg2+ is the fourth most common cation in the body and the second most common
intracellular cation (following potassium) (1).
• Distribution: Similar to potassium, magnesium is unevenly distributed throughout the body.
It has been described as a physiologic calcium antagonist (regulates entry into the cell and
intracellular action). Intracellularly, it is bound to ATP and enzyme complexes (1).
– Bone (contains approximately 50% of total body stores). Functions to provide physical
structure or scaffolding and regulates calcium and phosphorus. By binding to vitamins B6,
D, and K, it regulates the absorption of calcium into bone. Thus, it is necessary for
mineralization. Bone also serves as a “storage” site that can be drawn upon during times
of low concentration.
– Muscle (contains approximately 25% of total body stores). Plays a role in relaxation by
blocking calcium influx.
– Nerve cells
– Nucleic acid synthesis
– Energy metabolism
– Red blood cells: Hemolysis may falsely elevate serum measurements.
• Extracellular or serum (contains approximately 0.3% of total body stores). Present in ionized
form, attached to anions, and bound to protein. Free Mg2+ is physiologically active. Similar
to potassium, serum levels do not necessarily reflect total body stores. Furthermore, plasma
levels are the major regulators of urinary Mg2+ excretion.
• Absorption is via dietary oral intake and gastrointestinal absorption (primarily in the ileum
and colon).
• Excretion: Renally cleared.
• Regulation: primarily renal. Serum magnesium is filtered at the glomerular level into the
renal tubule. Reabsorption occurs along the tubule to regulate serum levels. Its control is
complex and at this time, no single hormone has been implicated in this process. It is
known, however, that calcium and potassium levels affect reabsorption (2).
PATHOPHYSIOLOGY
• Hypomagnesemia (<1.4 mEq/L). Recently, the incidence of hypomagnesemia has increased,
and may be attributed to changes in modern diets. Studies have shown that up to 11% of
hospitalized patients and up to 65% of ICU patients may have Mg2+ deficiency.
• Causes of hypomagnesemia. In addition to reduced intake, levels can also be reduced by
gastrointestinal or renal loss.
– Gastrointestinal losses can result from small bowel disorders including acute and chronic
diarrhea, malabsorption, volume expansion (decreases passive transport), and gastric
bypass surgery.
– Renal losses can result from inhibition of sodium reabsorption or defects in Mg2+
reabsorption. Sodium reabsorption drives magnesium transport within the tubular
segments. Thus loop and thiazide diuretics may enhance the deficiency.
• Signs and symptoms of hypomagnesemia are non-specific and can be confused with signs
and symptoms of hypokalemia, hypocalcemia, and metabolic alkalosis. They can manifest
clinically as neuromuscular hyperexcitability, cardiac arrhythmias, and co-existing
electrolyte abnormalities (hypokalemia, hypocalcemia).
– Neuromuscular abnormalities: Excitability is manifest as tremor, twitching, tetany, and
positive Chvostek and Trousseau signs. In the CNS, Mg2+ normally blocks NMDA
receptors which function in excitation. Thus, it may result in generalized convulsions.
– Cardiac arrhythmias: Mg2+ is necessary for all reactions involving ATP, including the
Na+-K+-ATPase pump. Hypomagnesemia impairs function by impeding K+ efflux and
increasing the resting membrane potential (less negative). This decreases the excitation
threshold for an action potential. Additionally, the reduced intracellular K+ levels hinder
repolarization. This results in increased irritability (ventricular arrhythmias: Ectopy,
ventricular tachycardia and fibrillation, and Torsades de pointes) as well as conduction
disturbances. EKG manifestations include widening of the QRS complex along with
peaking of the T wave. Severe deficiency can flatten the T wave and may impair
myocardial contractility.
– Electrolyte derangements
Hypokalemia: As previously mentioned, Mg2+ is necessary for proper Na+-K+-ATPase
function and hypomagnesemia can result in reduced intracellular K+ levels.
Additionally, hypomagnesemia is associated with renal potassium wasting in the loop of
Henle (3).
Hypocalcemia: Mg2+ is necessary for the release of parathyroid hormone (PTH); thus, a
deficiency results in low PTH and calcium levels (3).
• Association with other disease processes (does not imply causation) include: Mitral valve
prolapse, fibromyalgia, diabetes, asthma, allergies, osteoporosis, and dysmenorrhea.
• Hypermagnesemia (>2.5 mEq/L) results from excessive exogenous intake/therapy,
hemolysis, or impaired renal excretion/function. Hemolysis may increase levels due to
increased intracellular stores.
• Signs and symptoms of hypermagnesemia include weakness, hypotension, respiratory
distress, arrhythmias, cardiac arrest, and coma.
– Neuromuscular: Hypermagnesemia inhibits pre-synaptic acetylcholine release in skeletal
muscles (manifests as weakness, hyporeflexia, and respiratory depression). In smooth
muscle, Mg2+ antagonizes calcium and results in urinary retention and ileus. In the CNS,
it can excessively block NMDA receptors which are involved in excitation.
– Cardiac: Vascular smooth muscle dilation causes hypotension (Mg2+ antagonizes
calcium). In the myocardium, it may hyperpolarize the cell membrane and cause sinus
bradycardia, SA and AV nodal blocks, and cardiac arrest.
• Hypomagnesemia can be present in patients presenting for surgery. Signs and symptoms are
often non-specific, or are overshadowed by hypokalemia or hypocalcemia. It may clinically
manifest as ventricular and neuromuscular excitability.
– Patients on certain medications (warfarin, birth control pills, lithium, laxative use), who
are diagnosed with asthma, allergies, MVP, migraines, congestive heart failure, acute
coronary events, psychiatric illness, or have had massive blood transfusions (citrate rich
blood products), may have hypomagnesemia. Serum levels should be assessed.
– Hypomagnesemia carries an increased risk for perioperative arrhythmias and resistance to
neuromuscular blockade.
– Treatment depends on the severity of clinical manifestations. In urgent and emergent
situations such as Torsades de pointes, magnesium 1–2 grams IV contains 8–15 mEq and
can be administered over 15 minutes followed by 1 g/h until serum levels have been
normalized (4).
• Hypermagnesemia can result from exogenous therapy, renal dysfunction, or hemolysis. It
has several perioperative effects that the anaesthetist must be able to identify and treat
appropriately.
– Sedative effects of anesthetic drugs and volatiles may be compounded.
– Hypotension (from reduced intracellular calcium levels in smooth muscle) can be
compounded by anesthetics that directly vasodilate or reduce sympathetic discharge.
– Muscle weakness (from inhibited release of synaptic neurotransmitters) may be
compounded by neuromuscular blocking drugs (NMBD). Furthermore, the calcium
antagonist effects of magnesium may potentiate NMBD.
– Respiratory depression from muscle weakness may be compounded by anesthetics such as
opioids, benzodiazepines, and volatiles.
– Local anesthetic effects may be potentiated.
• Preeclampsia: Magnesium is administered to parturients to reduce the incidence of
eclampsia. Seizures are believed to be due to the excessive release of the excitatory
neurotransmitter glutamate, which activates the NMDA receptor and leads to massive
neural activity. Mg2+ competitively antagonizes glutamate (5).
– Therapeutic levels are 5–7 mg/dL and are followed by physical exam (monitoring of deep
tendon reflexes) as well as laboratory testing. Deep tendon reflexes are reduced well
before either respiratory depression or cardiac arrest occurs. They are easy to perform,
non-invasive, and provide immediate information.
– Toxic serum concentration levels differ in preeclamptics:
Loss of patellar reflexes: 7–10 mEq/L
Respiratory depression: 10–13 mEq/L
Complete heart block: 15–25 mEq/L
Cardiac arrest >25 mEq/L
• Treatment of magnesium toxicity involves administering IV calcium gluconate. Calcium
antagonizes the actions of magnesium in neuromuscular and cardiac functions. Additionally,
in patients with normal renal function, IV diuretics may be used. In patients with abnormal
renal function or renal failure, hemodialysis may be utilized.
• Other therapeutic uses for magnesium include the management of patients with
subarachnoid hemorrhage or asthma.
• Plasma Mg2+ levels rise as renal function declines, because urinary excretion is its only
regulatory system.
REFERENCES
1. Fawcett WJ, Haxby EJ, Male DA. Magnesium: physiology and pharmacology. Br J Anaesth.
1999; 83(2):302–320.
2. Wagner CA. Disorders of renal magnesium handling explain renal magnesium transport. J
Nephrol. 2007;20(5):507–510.
3. Moe SM. Disorders involving calcium, phosphorus, and magnesium. Prim Care.
2008;35(2):215–237.
4. Yamamoto M, Yamagushi T. Causes and treatment of hypomagnesemia. Clin Calcium.
2007;17(8):1241–1248.
5. Lu JF, Nightingale CH. Magnesium sulfate in eclampsia and pre-eclampsia. Clin
Pharmacokinet. 2000;38:305–314.
ADDITIONAL READING
• Agus ZS. Hypomagnesemia. J Am Soc Nephrol. 1999; 10:1616–1622.
• Guillaume T, Krzesinski JM. Management of serum magnesium abnormalities. Rev Med
Liege. 2003; 58(7–8):465–467.
• Hypokalemia
• Preeclampsia
• Asthma
• Tachycardia
CLINICAL PEARLS
• Hypomagnesemia may increase the risk of arrhythmias and neuromuscular excitability
perioperatively.
• Hypermagnesemia may compound sedative, hypotensive, respiratory depressant, and
neuromuscular blocking effects of anesthetics. Local anesthetic effects may also be
compounded.
MALIGNANT HYPERTHERMIA
Edward Park, MD
Harvey K. Rosenbaum, MD
BASICS
DESCRIPTION
• Malignant hyperthermia (MH) is a pharmacogenetic disorder of the ryanodine receptor
(RYR1). It is characterized by triggering of acute skeletal muscle hypermetabolism with
increased oxygen consumption, as well as markedly increased production of carbon dioxide.
• Triggers include halogenated volatile anesthetics, succinylcholine, and possible heat
exposure or sustained strenuous exercise.
EPIDEMIOLOGY
Incidence
In 2009: 1:100,000 anesthetics.
Prevalence
Molecular genetic testing of certain populations suggests a prevalence of 1:3,000.
Morbidity/Mortality
Mortality is ~1%; it is increased when associated with significant medical co-morbidities,
advanced age, the development of DIC, and heavier and more muscular builds.
• Autosomal dominant pattern: Its heritability demonstrates incomplete penetrance and
variable phenotypic expression. Sporadic, de novo mutations, without known positive family
histories, are also known to occur.
• Children <15 years of age; male:female ratio of 2:1; Caucasian race.
• May be associated with congenital musculoskeletal defects such as clubfeet, idiopathic
scoliosis, etc.
• During normal skeletal muscle contraction, a propagated action potential reaches the L-type
voltage-gated calcium channels (dihydropyridine receptors or DHPRs) along the transverse
tubule system. DHPRs allow for intracellular calcium entry and cause a conformational
change in coupled intracellular calcium channels (RYR1s).
• RYR1s control the release of sequestered calcium from within the sarcoplasmic reticulum
(SR) into the cytoplasm of skeletal muscle cells to continue the process of excitation–
contraction coupling. This calcium binds to troponin complexes, allowing actin–myosin
cross-linking and sarcomeric contraction to occur.
• In MH, mutations in genes encoding for RYR1, DHPR, or other unidentified proteins lead to
disruption of the regulatory process that governs intracellular calcium movement from the
SR and, likely, entry from the extracellular space. This leads to the excessive and
unregulated release of calcium during excitation–contraction coupling.
• When triggered, MH leads to sustained contractions/inability to relax the skeletal
musculature, as the intracellular calcium remains outside of the SR. There is an increase in
aerobic and anaerobic metabolism, creating a combined respiratory and metabolic acidosis
as CO2 and lactate accumulate. Eventually, muscle tissue becomes hypoxic and
rhabdomyolysis develops, leading to myoglobinuria and hyperkalemia as metabolites are
released into the circulation.
• Patients with proven or suspected susceptibility to MH: Attain previous anesthetic records,
thoroughly review family history, and the presence of neuromuscular conditions. Additional
laboratory work, cardiodiagnostic evaluation, or radiographic imaging beyond what is
required for the work-up of the patient’s other underlying medical conditions is not
warranted.
• Avoidance of triggering agents: Strict avoidance of known triggers (succinylcholine, potent
halogenated volatile anesthetics); consider alternative techniques to general anesthesia
(conscious sedation, local infiltration, and regional anesthesia) if amenable to the surgical
procedure in question.
• Anesthesia machine: Remove (or temporarily disable) the vaporizers and all removable parts
that may have been previously exposed to halogenated volatile anesthetics (CO2 absorber,
etc.). Consider an initial 5 minute flush of the circuit at high flows with the circuit attached
during set-up. For the first 5 minutes of patient use, consider a fresh gas flow of 10
L/minute, with the filter attached, followed by an additional 5 minutes of flush at high
flows with the circuit attached; for the first 5 minutes of patient use, consider a fresh gas
flow of 10 L/min for the first 5 minutes of patient use, with the filter still attached, followed
by maintenance of flows at >2 L/min for the duration of the case.
• Prophylactic dantrolene: Controversial and probably unnecessary; may lead to clinically
significant muscle weakness and, in patients with clinical myopathy, respiratory
insufficiency. Scrupulous avoidance of halogenated volatile anesthetics and succinylcholine
make an MH episode very unlikely.
• Ambulatory setting: Ensure the availability of monitors and equipment necessary for the
rapid escalation of care, should an MH crisis occur. The on-site presence of sufficient
quantities of dantrolene (at least 10 mg/kg at a minimum adult dose or at least 36 vials of
20 mg doses) should also be confirmed.
• Discharge from PACU: Following an uneventful surgery and anesthetic, the patient can be
discharged home or to an appropriate hospital unit, after 2–4 hours of close postoperative
observation.
DIAGNOSIS
• Variable onset and presentation: Can range from a dramatic appearance shortly after
induction of anesthesia, to a delayed and smoldering presentation hours into a case, or
within the first hour after emergence from general anesthesia.
• Early clinical signs and symptoms represent increased metabolic demands. Unanticipated
hypercarbia is the most reliable early sign; tachycardia and blood pressure lability (typically
hypertension but hypotension can also occur); development of dysrhythmias; and masseter
muscle or generalized muscular rigidity.
• Later findings: Hyperthermia, sweating, skin mottling, hyperkalemia, myoglobinuria
(appearing as cola-colored urine), mixed acidosis, elevated creatine kinase (CK) levels, and
DIC. In fulminant cases, progression to malignant ventricular dysrhythmias and cardiac
arrest may occur in <30 minutes after onset of an episode.
• Masseter spasm: A potentially premonitory sign of an impending episode, and usually occurs
after the use of succinylcholine; referred to by the term “jaws of steel.” The clinician can
either cancel the case and consider referring the patient for workup of MH susceptibility or,
alternatively, continue with the procedure using a non-triggering anesthetic technique while
preparing to treat an episode of MH if it occurs.
• Acute processes that mimic the non-specific signs and symptoms of an MH crisis.
Hypercarbia may be seen with insufficient minute ventilation; CO2 insufflation with
laparoscopic surgical techniques; subcutaneous emphysema; anesthesia circuit rebreathing
from unacceptably low fresh gas flows, faulty inspiratory valves, or other equipment
malfunction; embolic phenomena (increased PaCO2 to ETCO2 gradient); and infusions of
Dextrose 25% as part of total parenteral nutrition. Hyperthermia can be seen with scoliosis
surgery, iatrogenic heating (warm fluids, heating blankets, etc.), and thyroid storm.
• Hyperdynamic hemodynamic perturbations: Insufficient depth of anesthesia, thyroid storm,
pheochromocytoma, tyramine crisis in a patient on an MAO inhibitor, neuroleptic
malignant syndrome (NMS), serotonin syndrome, cerebral ischemia and/or intracranial
hemorrhage, anticholinergic crisis, heat stroke, and recreational drug or other
sympathomimetic toxin ingestion (i.e., cocaine, methamphetamines, or Ecstasy).
Cardiovascular collapse can also be seen in an MH crisis, so septic shock and anaphylaxis
should also be considered.
• Muscular dystrophies, such as Duchenne or Becker muscular dystrophy, or some individuals
with heat- or exercise-induced rhabdomyolysis, may develop fatal hyperkalemia and
rhabdomyolysis after exposure to halogenated volatile anesthetics and succinylcholine.
TREATMENT
• MH is a life-threatening medical emergency, and an immediate call for additional trained

help should also be included in the first steps of treating a crisis. The surgeon should be
notified of the patient’s condition, and the procedure should be terminated or concluded as
expeditiously as possible while the patient is being resuscitated.
• Discontinue the administration of all known triggering agents, switch to non-triggering
anesthetic techniques, fluid resuscitation with cooled intravenous fluids, hyperventilate with
100% oxygen to 2 or 3 times normal minute ventilation, and administer dantrolene.
• Dantrolene binds to RYR1 and restores the balance between SR calcium release and uptake
as well as calcium entry from the extracellular fluid. Thus, it decreases myofibrillar
contraction (skeletal muscle relaxation) and “cools down" the hypermetabolic process. The
initial recommended dose is 2.5 mg/kg; improvement in the patient’s clinical condition can
begin in minutes. If not, additional boluses of 2.5 mg/kg can be administered until signs and
symptoms have receded. Defervescence typically trails resolution of hypercarbia. Doses in
excess of the manufacturer’s recommended total dose of 10 mg/kg may occasionally be
required in the treatment of fulminant MH.
• Monitors: Intravenous access with wide-bore cannulae should be obtained to aid in fluid
resuscitation, drug administration, and frequent laboratory blood draws. Consider an
arterial (blood gases) and central venous line, especially if the patient’s clinical condition
deteriorates. If not already in place, an indwelling urinary catheter is mandatory to evaluate
the brisk diuresis that occurs with fluid resuscitation and dantrolene therapy (as each vial
contains 3 g of mannitol) as well as the presence of myoglobinuria.
• Serial laboratory measurements: Serum electrolytes (especially potassium), renal and
hepatic function panels, coagulation tests, arterial and/or venous blood gases, and serum
myoglobin and CK levels.
• Temperature: Follow closely and if >38.5°C, implement cooling measures: Resuscitate with
chilled IV fluids and cool with ice packs, cool and dampened linens, and/or misted water
with warm air fanning to promote evaporative heat loss.
• Hyperkalemia: IV calcium and insulin with dextrose. Beta2-agonists may be considered after
dantrolene is started, though they may aggravate any pre-existing tachyarrhythmia and
should be used cautiously. Unstable cardiac rhythms may need to be cardioverted or treated
with appropriate antiarrhythmic agents (e.g., amiodarone). Exercise caution in the
treatment of wide QRS complex rhythms with lidocaine or procainamide, as this may be a
sign of hyperkalemia and treatment with class 1 antiarrhythmics may result in asystole.
• pH derangements (combined respiratory and metabolic acidosis): Hyperventilation along
with bicarbonate administration (concurrent therapy for hyperkalemia) when pH <7.2.
Emergent hemodialysis may be necessary for life-threatening hyperkalemia and/or acidosis.
• Postoperative care: Intensive care unit, where supportive measures may need to be
continued until the signs and symptoms have abated. Recrudescence can occur up to 24
hours after and requires dantrolene at doses of 1 mg/kg every 4–6 hours or via continuous
infusion at 0.25 mg/kg/hr. Recrudescence reflects recurrent hypermetabolism and skeletal
muscle injury. Signs can include increased ETCO2, paCO2, rapid spontaneous ventilation,
myoglobinuria, rigidity, tachycardia, or hyperthermia.
• Hospital discharge. There are no definitive laboratory values or criteria following an attack
of MH. Typically, the patients should be asymptomatic and clinically stable, and can
proceed towards an uneventful recovery at home within 2–3 days.
FOLLOW-UP
• After a suspected case of MH presentation, the patient and family members need to be
counseled regarding the potential future implications and ramifications of such a diagnosis.
As the physician most familiar with MH and the patient’s clinical course, the
anesthesiologist of record is the person most capable of beginning this process, and he/she
should write a letter for the patient’s personal medical records attesting to the events as
they have unfolded and how the diagnosis of MH was made.
• The Malignant Hyperthermia Association of the United States (MHAUS) is a nonprofit
organization that provides information on MH for patients, family members, and health care
personnel. It also offers medical assistance for elective and emergent questions and advice.
• In vitro contracture testing (IVCT) exposes biopsied muscle to caffeine and halothane and
tests for contracture. False-positive results can be as high as 15–20% under the North
American Malignant Hyperthermia Registry protocol; 6–7% with the European protocol.
False-negative results are believed to be very low. IVCT testing is limited by the cost of
maintaining the relatively few centers that can perform this form of complex testing, as well
as the invasive nature of the test.
• An alternative to IVCT is molecular screening for genetic mutations known to produce
susceptibility to MH. Although genes encoding for RYR1 proteins (located on chromosome
19) and DHPR proteins (located on chromosomes 1, 7, and 17) are most commonly
implicated, there exists considerable heterogeneity in the genetic loci and linkage sites
across known susceptible family lines. It must be emphasized that a negative mutation
screen does NOT exclude MH susceptibility. Incomplete penetrance and variable phenotypic
expression of MH raise the potential for a multi-genic predisposition towards MH
susceptibility, with possible epigenetic influences leading to a relatively common final
pathway.
REFERENCES
1. Allen GC, Larach MG, Kunselman AR. The sensitivity and specificity of the caffeine-
halothane contracture test: A report from the North American Malignant Hyperthermia
Registry. Anesthesiology. 1998;88(3):579–588.
2. Brandom BW. Ambulatory surgery and malignant hyperthermia. Curr Opin Anaesthesiol.
2009: 22(6):744–747.
3. Glahn KPE, Ellis FR, Halsall PJ, et al. Recognizing and managing a malignant hyperthermia
crisis: Guidelines from the European Malignant Hyperthermia Group. Br J Anaesth. 2010;
105(4):417–420.
4. Prather Strazis K, Fox AW. Malignant hyperthermia: A review of published cases. Anesth
Analg. 1993;77(2):297–304.
5. Wappler F. Anesthesia for patients with a history of malignant hyperthermia. Curr Opin
Anaesthesiol. 2010;23(3):417–422.
ADDITIONAL READING
• Malignant Hyperthermia Association of the United States (MHAUS): www.mhaus.org.
• The 24-hour telephone hotline of the MHAUS: (800) 644-9737 (MH-HYPER).
• Trismus
• Hyperthermia
CODES
ICD9
995.86 Malignant hyperthermia
ICD10
T88.3XXA Malignant hyperthermia due to anesthesia, initial encounter
CLINICAL PEARLS
• Diagnosis: Initially normal CK levels do NOT exclude MH. CK levels typically peak 8–12
hours following muscle injury and will slowly decline with successful treatment. If an MH
episode has been promptly diagnosed and treated, the rise in CK level may be unimpressive.
• Adverse drug reaction: Verapamil and/or diltiazem should NOT be used during treatment
with dantrolene; hyperkalemia, myocardial depression, and cardiac arrest may result.
• Monitoring: Hyperkalemia may also appear after hypermetabolism has been controlled. The
authors recommend checking serum potassium levels 1 and 2 hours after initiating
dantrolene therapy, and then every 8 hours for 24 hours, or as clinically indicated by ECG
signs or evidence of recrudescence.
MARIJUANA ABUSE
BASICS
DESCRIPTION
• Marijuana (MJ) is derived from Cannabis sativa, a member of the Cannabaceae plant family.
MJ is known by several different names, such as bhang, cannabis, ganja, grass, hash or
hashish, pot and weed.
– Chronic cannabis use is defined as almost daily use over a period of years.
– Cannabis dependence is defined by impaired control over MJ use and continuing use
despite harm.
• Marijuana contains over 60 compounds, of which several have psychoactive properties, but
delta-9 tetrahydrocannabinol (THC) is the primary component (1)[B].
• MJ can be smoked as a cigarette (joint), a cigar (blunt) or in a water pipe, but can also be
brewed as tea, mixed in food, or even (rarely) injected.
• Dronabinol (Marinol) and nabilone (Cesamet) are FDA-approved medications containing
cannabinoid-based synthetic compounds. Legitimate medical uses include:
– Analgesia, especially for neuropathic pain (2)[A].
– Antiemetic effects (patients receiving chemotherapy).
– Increased appetite (cancer or AIDS patients).
– Treatment of spasticity and glaucoma.
• The THC content of cannabis has increased markedly, from <2% in 1980 to 8.5% in 2006.
– THC acts on the CB1 and CB2 cannabinoid receptors.
– When smoked, THC is rapidly absorbed through the lungs into the circulation and carried
to the brain and other organs. The peak CNS effect occurs in 15 minutes, and can last for
2–4 hours (1)[B].
– When ingested orally, THC bioavailability is lower and onset is slower, but duration is
longer.
• Central nervous system:
– Acute effects include: Relaxation, euphoria, heightened or distorted perception of space or
time, nystagmus, tremor, impaired coordination, headaches and hyperemesis. Anxiety,
panic, dysphoria, hallucinations, or sedation can also occur.
– Chronic effects include: Lack of motivation, impaired memory and learning, and increased
risk of psychotic disorders.
– Withdrawal symptoms include irritability, impaired sleep, reduced appetite, and anxiety.
These symptoms subside after 1–2 weeks of abstinence.
• Airway:
– Acute effects include: Uvular edema or laryngospasm, leading to airway obstruction.
– Chronic effects include: Airway inflammation, and possibly increased risk of airway
cancer.
• Cardiac:
– Acute effects include: Coronary artery spasm resulting in myocardial ischemia, myocardial
infarction or ventricular arrhythmias (in MJ users with patent coronary circulation).
– Chronic effects include: Vasodilatation, tachycardia, increased myocardial oxygen
demand, increased risk of myocardial ischemia or infarction.
• Respiratory:
– Acute effects include: Bronchodilatation, increased carboxyhemoglobin levels (up to 5
times higher compared to tobacco smokers).
– Chronic effects include: Airway inflammation, as well as increased mucus secretion and
edema, thereby predisposing to increased bronchial irritability. Emphysema and
secondary pneumothorax have been reported in young chronic MJ users (3)[C]. There is
an increased risk of pulmonary infection due to impaired pulmonary defense and possible
MJ contamination by Aspergillus, Salmonella, or even fecal matter. Additionally, lung
cancer has been associated with chronic MJ use.
• Reproductive problems include reduced testosterone, reduced testicle size, impaired sperm
motility, lower libido, impotence, and menstrual abnormalities.
Chronic MJ use may cause fetal intrauterine growth retardation (IUGR) due to decreased
utero-placental perfusion.
• Children exposed to maternal MJ use during gestation manifest mild developmental
abnormalities and are at increased risk for non-lymphoblastic leukemia (10-fold).
• MJ use by children is a real concern, and should not be overlooked, especially in pediatric
patients over the age of 12.
• History:
– Obtain a detailed and complete history of substance abuse in every patient.
– Patients may attempt to hide their drug use from their family and their doctor, thus,
questioning about drugs should be conducted in private, as people may not be truthful
when questioned in the presence of friends or family. Unfortunately, marijuana use is very
common, especially among young patients, even pediatric patients.
– Possible red flags include an unexplained worsening of performance at work or school, as
well as problems with social functioning or relationships, and loss of interest in pleasant
activities. However, within the constraints of the perioperative period, such detailed
history may not always be elicited.
– Young patients with emphysema or spontaneous pneumothorax should be questioned
about MJ abuse (3)[C].
• Labs: Urine, blood, or hair drug testing can confirm or exclude MJ use. Due to high lipid
solubility, THC may remain in the body for up to 30 days, and can be detected in the urine
for several weeks or even months.
• Antidote: There is no clinically available specific antidote or antagonist for THC, and
therefore treatment of acute intoxication is symptomatic.
• Central nervous system: Acute MJ intoxication decreases the need for anesthetic drugs,
whereas chronic use may increase requirements for anesthetic medications, such as propofol
(4)[B].
• Airway: Consider using dexamethasone as prophylaxis against upper airway edema. Topical
use of local anesthetics suppresses laryngeal reflexes and may reduce the risk of
laryngospasm.
• Cardiac: Because MJ intoxication can increase the heart rate, drugs that cause tachycardia
(ketamine, pancuronium or rocuronium, atropine, ephedrine, and epinephrine) should be
avoided or used cautiously.
• Respiratory: Consider using a laryngeal mask airway (LMA) rather than intubation, to
reduce airway stimulation and trauma. Similar to asthma and reactive airway disease, limit
bronchospastic triggers: Ensure that the patient is deep prior to airway instrumentation,
consider introducing volatile anesthetics during bag mask ventilation, maintain an adequate
depth of anesthesia, avoid histamine releasing drugs, and consider a deep extubation, if
appropriate.
REFERENCES
1. Bryson EO, Frost EAM. The perioperative implications of tobacco, marijuana, and other
inhaled toxins. Int Anesthesiol Clin. 2011; 49:103–118.
2. Lynch ME, Campbell F. Cannabinoids for treatment of chronic non-cancer pain; a
systematic review of randomized trials. Br J Clin Pharmacol. 2011. doi: 10.1111/j.1365–
2125.2011.03970.x
3. Beshay M, Kaiser H, Niedhart D, et al. Emphysema and secondary pneumothorax in young
adults smoking cannabis. Eur J Cardiothorac Surg. 2007; 32:834–838.
4. Flisberg P, Paech MJ, Shah T, et al. Induction dose of propofol in patients using cannabis.
Eur J Anaesthesiol. 2009;26:192–195.
5. Arendt M, Munk-Jørgensen P, Sher L, et al. Mortality among individuals with cannabis,
cocaine, amphetamine, MDMA, and opioid use disorders: A nationwide follow-up study of
Danish substance users in treatment. Drug Alcohol Depen. 2011;114:134–139.
ADDITIONAL READING
• Hernandez M, Birnbach DJ, Van Zundert AA. Anesthetic management of the illicit-
substance-using patient. Curr Opin Anaesthesiol. 2005;18:315–324.
• Initiation of Marijuana Use: Trends, Patterns and Implications, published by SAMSHA, US
Department of Health and Human Services, accessed online on June 9, 2011 at:
http://oas.samhsa.gov/MJinitiation/chapter3.htm
• Hall W, Degenhardt L. Adverse health effects of non-medical cannabis use. Lancet.
2009;374(9698):1383–1391.
• Cocaine abuse
• Alcohol abuse
• Smoking
• Asthma
CODES
ICD9
• 304.30 Cannabis dependence, unspecified
• 305.20 Cannabis abuse, unspecified
ICD10
• F12.10 Cannabis abuse, uncomplicated
• F12.20 Cannabis dependence, uncomplicated
CLINICAL PEARLS
• The constraints of the perioperative period and nature of the patient–anaesthetist
relationship make diagnosis and counseling difficult, if not impossible. Ideally, management
should include education about the adverse effects of MJ, evaluation about the use of other
drugs and alcohol, and the treatment of coexisting psychiatric disorders. However, if use is
suspected or admitted, informed consent should discuss and describe the potential for
adverse effects and increased perioperative risk.
• The CNS, airway, pulmonary and cardiovascular effects of MJ are significant perioperative
concerns.
• Additionally, MJ is frequently combined with other substances of abuse such as alcohol,
benzodiazepines, amphetamines or cocaine, and is associated with significant psychiatric
and physical comorbidities.
• Epidemiology
– Incidence
According to data recently published by the US Department of Health and Human
Services, 2 million Americans a 12 and older used MJ for the first time in 1999.
Incidence of MJ use is higher, and the mean age of the first MJ use is lower in males,
compared to females.
There is a worrisome trend of starting MJ use at a younger age.
In 1999, the mean age for MJ initiation was 17.2 years for whites, 16.4 years for blacks
and Hispanics, 18.8 for Asians, and 15.8 years for those reporting more than one race.
– Prevalence:
MJ is the illicit substance most often used in the US and worldwide: Over 50% of people
in the US have used MJ at some point during their lifetime.
In the US, 15.7% of 8th graders, 32.3% of 10th graders, and 42.0% of 12th graders have
used MJ.
10–20% of 18–25 year-old patients use MJ.
In Australia, 9.8% of injured drivers sent to the hospital are THC-positive.
10% of people experimenting with MJ become daily users and 20–30%, weekly users.
Prevalence is higher among patients with psychiatric disease and/or chronic pain.
– Morbidity:
Compared to tobacco, marijuana smoking contains higher concentrations of airway
irritants and carcinogens.
Chronic MJ use increases the risk of throat and lung cancer, probably at a younger age
compared to tobacco abuse.
– Mortality:
The fatal human dose is estimated to be 15–70 grams.
Deaths related to cannabis overdose are unlikely, but cannabis is often detected along
with other substances in drug overdose deaths.
Compared to the general population, overall mortality is increased five-fold in MJ users,
likely due to road, industrial or other accidents, violent injuries and homicides (5)[B].
Cannabis body packing, in an attempt to smuggle large quantities of cannabis across
international borders, has been reported to cause fatal colonic perforation.
MASTECTOMY
Edna Ma, MD
BASICS
DESCRIPTION
General
• A mastectomy is a surgical procedure to partially or completely remove one or both breasts.
This operation is performed for either excision of a diagnosed cancerous tumor or
prophylactically (to prevent cancer when there is a genetic predisposition).
• A “lumpectomy” or “wide local excision” involves surgical excision of suspected tumor and
the margin of the surrounding normal breast tissue, while conserving as much normal breast
tissue as possible.
• For staging purposes, the surgery may involve an axillary lymph node exploration and
excision, called “sentinel lymph node biopsy” (1). The sentinel lymph node is the first
axillary lymph node that would demonstrate any metastatic disease, given the drainage of
lymph from the breast.
• Some patients elect for immediate reconstruction after the mastectomy (under the same
anesthetic), which could involve tissue grafting with either the latissimus dorsi flap or the
transverse rectus abdominis myocutaneous (TRAM) flap or insertion of a tissue expander.
Position
Supine with the arm prepped free for access to the axilla.
Incision
• Near the site of the overlying tumor
• May be periareolar if a nipple-sparing technique is used.
Approximate Time
Varies depending on the extent of disease and reconstruction: 1–5 hours.
EBL Expected
Ranges from <50 to several hundred milliliters, depending on the extent of reconstruction.
Hospital Stay
Lumpectomies may be discharged on the same day.
• If a sentinel lymph node biopsy is scheduled, a blue dye (by surgeon) or a small amount of
radioactively labeled tracer (by radiologist) is injected near the tumor in order to stain the
lymph vessels and nodes so that the sentinel lymph node is more easily visualized.
• A Geiger counter is utilized intraoperatively to locate the lymph node with the most active
uptake.
EPIDEMIOLOGY
Incidence
• Women: 124.2 per 100,000 per year. There is an overall decreasing rate, which is associated
with the discontinuation of hormone replacement therapy (2).
• Men: Accounts for 1% of all breast cancer.
Prevalence
Most frequently diagnosed cancer in women in the US (not including skin cancer).
Morbidity
Breast cancer rates decreased by about 2% between 1998 and 2007 (3). This decrease was
only among women aged 50 years and older.
Mortality
• Second-leading cause of cancer death among women in the US.
• Fortunately, the rate has been decreasing since 1990 at an overall rate of 2.3% per year
(3.3% for women aged 40 to 50 years). This decrease is largely attributed to the
combination of mammography screening with improved treatment.
• Approximately 1 in 35 women die from breast cancer in the US.
• Patients can present with anxiety over their diagnosis or potential diagnosis.
• Pain and postoperative nausea and vomiting are common issues in this patient population.
Multimodal, opiate-sparing regimens have been advocated and studied (including
paracetamol, dextromethorphan, celecoxib, gabapentin, dexamethasone, total intravenous
anesthesia, and intraoperative ondansetron).
SYMPTOMS
Varies widely from no symptoms to skin changes, fatigue, palpable mass, and rarely pain
from cancer that has metastasized to the bone.
History
Risk factors include age (>50 years old), family history (first degree relative), early
menarche, late menopause, late first pregnancy, and nulliparity, which are presumed to
prolong estrogen exposure to the breasts.
Signs/Physical Exam
• May include changes in the overlying skin (“peau d’orange”), nipple discharge, or palpable
mass identified by the patient or on routine examination.
• Lesions may also be identified by a screening mammography (2).
MEDICATIONS
• Chemotherapeutic agents: Doxorubicin, cyclophosphamide, paclitaxel, docetaxel,
cyclophosphamide.
• Hormone therapy: Tamoxifen (mixed estrogen agonist–antagonist) or letrozole (an
aromatase inhibitor to stop estrogen production).
• Anti-emetics for chemotherapy: Ondansetron or metoclopramide.
Labs/Studies
• Standard screening labs as dictated by the patient’s history (e.g., CBC, chemistries).
• Advanced stages or recent chemotherapy may be associated with pancytopenia.
• BRCA1 and BRCA2 are susceptibility genes associated with breast cancer. HER2/neu, a
proto-oncogene, is also expressed in breast cancer.
• In addition to regional lymph node involvement, metastatic disease may include the bone,
liver, and lungs.
• Assessment for organ damage from chemotherapeutic agents (doxorubicin, adriamycin).
TREATMENT
Premedications
• Anxiolytics should be considered and titrated to effect.
• Preoperative hydration to reduce postoperative nausea and vomiting (PONV) may be
appropriate.
• Patients often arrive earlier to have the radiology department either place a wire to localize
the tumor site or for lymphoscintigraphy involving injection of radionuclide. Under these
circumstances, ensure that consents for surgery are completed and signed prior to the
administration of anxiolytics.
• If deep sedation is performed for lumpectomies or biopsies, discuss appropriate sedation
goals.
• Biopsies and lumpectomies may not require prophylaxis. However, needle localization and
wire placement require prophylaxis.
• Broad spectrum, 3rd generation cephalosporin such as cefazolin can protect against skin
flora.
INTRAOPERATIVE CARE
• Deep sedation may be appropriate in lumpectomies or biopsies.
• General anesthesia with an LMA or ETT is appropriate for mastectomies.
• Reconstructive procedures often necessitate neuromuscular blockade to provide a still
surgical field; hence ETT is chosen.
• Cervical epidural anesthesia (CEA) as the sole technique has been discussed in the literature
as having the potential benefit of good analgesia and avoidance of PONV, as well as lower
overall cost. However, it is seldom practiced due to its reported complications (4).
• Thoracic epidural anesthesia (TEA) as a sole technique has also been discussed in the
literature for its potential benefit of improved postoperative pain relief and recovery as well
as lower cost than general anesthesia for modified radical mastectomies (5).
Monitors
• Avoidance of intravenous access and non-invasive blood pressure (NIBP) in the arm
ipsilateral to the surgical site, to minimize the risk of lymphedema or interference with the
surgical field.
• If an indwelling, tunneled catheter is present for chemotherapy, it may be accessed.
Consider aspirating heparin before flushing the port.
• Deep sedation: Titrate to a level appropriate for local anesthetic injection.
• GA: Intravenous induction; a mask induction may be performed if IV access is difficult or
limited.
Maintenance
• Balanced intravenous or volatile anesthetic. Total intravenous anesthesia with a propofol-
based technique may reduce PONV.
• Dexamethasone for PONV should be administered after induction to avoid rectal itching or
burning.
• If isosulfan blue dye is injected by the surgeon, a transient spurious decrease in the pulse
oximetry reading may result from systematic absorption.
Standard extubation criteria apply.
POSTOPERATIVE CARE
BED ACUITY
• For uncomplicated mastectomy, a floor bed is usually adequate.
• Free TRAM reconstructions require a higher level of care.
ANALGESIA
• PCA
• Indwelling catheter delivering local anesthetic in the wound (e.g., “On-Q PainBuster”
pump).
• Thoracic epidural.
• Intercostal nerve blocks.
COMPLICATIONS
• Positive margins requiring reincision.
• Infection.
• Hematoma or seroma.
• Lymphedema.
• Failed reconstruction.
• Postoperative nausea and vomiting.
PROGNOSIS
Prognosis is dependent on its stage. The 5-year survival for stage 1 (T1N0M0) is 92% and for
stage IV (any T, any N, M1) is 14%.
REFERENCES
1. Gerber B, Krause A, Reimer T, et al. Skin-sparing mastectomy with conservation of the
nipple–areola complex and autologous reconstruction is an oncologically safe procedure.
Ann Surg. 2003;238(1):120–127.
2. Ravdin PM, Cronin KA, Howlader N, et al. The decrease in breast-cancer incidence in 2003
in the United States. N Engl J Med. 2007;356:1670–1674.
3. merican Cancer Society. How Many Women Get Breast Cancer? Overview: Breast Cancer.
Atlanta, GA: American Cancer Society; 2009.
4. Gartner R, Kroman N, Callesen T, et al. Multimodal prevention of pain, nausea and
vomiting after breast cancer surgery. Minerva Anesthesiol. 2010; 76(10):805–813.
5. Yeh CC, Yu JC, Wu CT, et al. Thoracic epidural anesthesia for pain relief and postoperation
recovery with modified radical mastectomy. World J Surg. 1999;23(3):256–260.
6. Lewis JW, Shavit Y, Terman GW, et al. Apparent involvement of opioid peptides in stress-
induced enhancement of tumor growth. Peptides. 1983;4:635–638.
7. Gottschalk A, Sharma S, Ford J, et al. The role of the perioperative period in recurrence
after cancer surgery. Anesth Analg. 2010;110:1636–1643.
• Postoperative nausea and vomiting.
• Epidural
CODES
ICD9
174.9 Malignant neoplasm of breast (female), unspecified
ICD10
• C50.919 Malignant neoplasm of unsp site of unspecified female breast
• C50.929 Malignant neoplasm of unsp site of unspecified male breast
CLINICAL PEARLS
• Potential anesthetic interventions that can attenuate the surgical stress response and tumor
genesis include: Use of regional anesthesia, COX inhibition (e.g., celecoxib, indomethacin),
normothermia, and beta-blockers (7).
– Regional anesthesia has been shown to reduce metastasis and optimize post-operative
analgesia in animal studies. Surgical stress and general anesthesia may suppress the
immune system, and activate the neuroendocrine and sympathetic nervous systems.
– Immunosuppression, and thus promotion of cancer progression, is thought to be mediated
by cytokines, chemokines, prostaglandins, and COX. Additionally, pain stimulates the
hypothalamic—pituitary–adrenal axis and can activate the sympathetic nervous system.
This can result in immunosuppression and suppression of natural killer T-cell activity, thus
promoting tumor development in animal studies (6).
MECHANICAL CIRCULATORY ASSIST DEVICES (MCAD)
Jonathan D. Leff, MD
Daniel A. Lazar, MD
BASICS
DESCRIPTION
General
• Mechanical circulatory assist devices (MCADs) can partially or completely support the
circulation of a patient with a failing heart. Indications for its placement include:
– “Bridge to Recovery”: Utilized for acute cardiac decompensation. Considered “rescue”
therapy in cardiogenic shock, myocardial infarction, myocarditis, postcardiotomy, heart
failure.
– “Bridge to Transplant”:Offers support until a donor heart becomes available.
– “Destination Therapy”: Approved by the FDA in 2002 as a permanent alternative to heart
transplantation in patients who are not otherwise candidates.
• Pump classification:
– Pulsatile flow (first generation): Large devices that are volume dependent, have
unidirectional valves, and are pneumatically or hydraulically driven.
– Continuous flow (second and third generations): Have several advantages including a
smaller, simpler design with less mechanical parts to malfunction or replace; as well as
less sheer forces on blood. They can also be implanted in smaller patients (1). There are 3
types:
Axial pump: Utilizes helically shaped blades that propel blood to accelerate along the
axis of the rotor.
Centrifugal: The rotors are shaped to accelerate flow circumferentially and towards the
outside of the pump (2).
Non-contact magnetic bearing: Provides for no-touching parts within the pump since the
rotors are suspended between two magnetic components.
• Anticoagulation with either heparin/warfarin or antiplatelet therapy is needed to prevent
thrombosis with most MCADs. This therapy is initiated soon after implantation of the device
and continued throughout the duration of support.
• The pump and its cannulas/connections are placed during “open heart surgery” after the
institution of cardiopulmonary bypass (CPB). The pump is placed within the abdominal wall
or pericardium. Cardiac inflow and outflow cannulas are positioned as follows:
– Left ventricular assist device (LVAD): Inflow: Left atrium or left ventricle apex. Outflow:
Ascending aorta, descending aorta.
– Right ventricular assist device (RVAD): Inflow: Right atrial appendage. Outflow:
Pulmonary artery.
– Biventricular assist device (BIVAD) have RVAD and LVAD connections.
– Percutaneous: Impella (Abiomed Danvers, Massachusetts)-consist of one cannula that is
inserted via the femoral artery and through the aortic valve; precludes the need for CPB.
TandemHeart (CardiacAssist Inc. Pittsburgh, PA)- consists of two percutaneous cannulas
with the inflow placed across the atrial septum to provide left heart drainage.
Position
Supine
Incision
Median sternotomy or percutaneously in the catheterization lab.
Approximate Time
Variable and dependent on factors such as previous sternotomy.
EBL Expected
• Bleeding following device implantation can be substantial in the perioperative period (~1–3
L).
• Coagulopathy may also be observed immediately after placement secondary to the device’s
damaging effect on platelets and coagulation factors.
Hospital Stay
Median discharge time 27–28 days, ranging from 8 days to 12 months (3).
• Device: The pump and cannula are implanted; the computer controller, power pack/battery,
and a reserve power pack are external.
• Cardiopulmonary bypass circuit.
• Transesophageal echocardiography.
EPIDEMIOLOGY
Incidence
• Heart failure affects 4.8 million Americans; of which ∼250,000 are considered refractory to
medical therapy (4).
• Less than 3,000 available hearts for transplant.
Prevalence
Annually, over 1,000 LVADs are placed.
Morbidity
Related to device malfunction, coagulopathy, reoperation, end-organ dysfunction, right
ventricle failure, pulmonary hypertension, infection, AAPACHE score, center experience, and
the extent of psychosocial support.
Mortality
Most common causes of death post-LVAD implantation: Sepsis, multiorgan failure, right heart
failure, device failure.
• Although patients may present from home, MCADs are often placed on inpatients with
decompensated congestive heart failure (CHF) or acute insults. They usually have multiple
co-morbidities, are catecholamine dependent, and have slow circulation times.
• Careful fluid management is required secondary to pulmonary congestion during the
preoperative period. Post-LVAD implantation, the patient is preload/volume dependent for
their cardiac output.
• Prepare for coagulopathy by administration of antifibrinolytics and have blood products
easily accessible.
• A transesophageal echocardiogram (TEE) is performed, following induction of anesthesia to
assess for MCAD suitability (patent foramen ovale, right ventricular function, tricuspid
regurgitation, aortic insufficiency, left ventricular thrombus) as well to assist with cannula
placement and device management.
• When placing an LVAD, the right ventricle needs special attention and pharmacologic
support.
SYMPTOMS
• Dyspnea, orthopnea, paroxysmal nocturnal dyspnea.
• Chest pain.
History
Ischemic and/or non-ischemic cardiomyopathy.
Signs/Physical Exam
Peripheral edema, elevated jugular venous pressure, S3 gallop
MEDICATIONS
• CHF therapy: Diuretics, angiotensin converting enzyme (ACE) inhibitors, beta blockers,
aldosterone antagonist, nitrates, digoxin, etc.
• Many patients with CHF are on anticoagulation therapy such as: Aspirin, heparin, warfarin,
and clopidogrel. These drugs, while useful in preventing thrombosis and ischemia, increase
the risk of bleeding and may require reversal.
• Intotropes in acute decompensation.
Labs/Studies
• Electrolytes, BUN, Cr.
• CBC, PT, PTT, INR, fibrinogen, D-dimer, etc.
• Type and cross
• Electrocardiogram
• Chest X-Ray, chest radiography, echocardiography, coronary angiography
• Pulmonary hypertension.
• Renal insufficiency, liver failure, peripheral vascular disease, diabetes.
TREATMENT
Premedications
If on vasopressors/inotropes, continue as needed throughout induction and pre-CPB.
Management of defibrillators, pacemakers, and Cardiac Resynchronization Therapy (CRT)
includes disabling shock capabilities and placement of external defibrillator pads.
Pacemakers, if present, should be switched to an asynchronous mode.
• Wide spectrum antibiotics are administered in the preoperative period including:
Vancomycin, rifampin, and fluconazole.
• The most frequent organisms in patients with MCADs are: Staphylococcus epidermidis and
Staphylococcus aureus. Other less common organisms include: faecalis and methicillin-
resistant Staphylococcus epidermidis [MRSE], methicillin-susceptible Staphylococcus aureus
[MSSA] and Corynebacterium striatum, and methicillin-susceptible Staphylococcus epidermidis
[MSSE] and Corynebacterium species.
INTRAOPERATIVE CARE
General anesthesia with endotracheal tube
Monitors
• Preinduction arterial line for beat-to-beat BP monitoring and frequent blood sampling.
• Large bore peripheral intravenous access for fluid resuscitation in patients without central
access.
• Central venous access (8.5 or 9F) with CVP monitoring capability and multiple infusion
ports for the infusion of vasoactive drugs.
• Pulmonary artery catheter (PAC) allows for monitoring of pulmonary artery pressure,
cardiac output, mixed venous analysis, and pacing capability. In the postoperative period, it
is utilized to manage right ventricular function.
• Intra-operative TEE to evaluate for:
– Aortic insufficiency: Can lead to a circulatory loop between the left side of the heart and
the aortic valve as blood from the outflow cannula passes retrograde into the left ventricle
through an incompetent aortic valve rather than flowing in an antegrade manner to the
body.
– Right heart and tricuspid valve functions: Left ventricular decompression leads to an
increase in cardiac output and right ventricular volume overload (increased right
ventricular preload) which may not be tolerated by the right heart.
– Intracardiac shunts: A patent foramen ovale (PFO) can result in left ventricular unloading
and right-to-left shunting.
– Specific to CPB: De-airing as well as assessment of aortic plaques, placement of cannulas,
and left ventricle decompression.
• Near infrared spectroscopy (NIRS) is useful to assess frontal cortex oxygenation. Pulse
oximetry is often difficult, following implantation of a continuous flow device and cerebral
oximetry can provide information in regards to cerebral oxygen saturation. The use of the
technology is variable among institutions.
• Individualized to each patient and slowly titrated to effect and hemodynamic goals;
fentanyl, etomidate, and/or ketamine are commonly utilized. In general, heart failure
patients have slow circulation time and are dependent upon catecholamines to support their
circulation. Excessive blunting of this demand can lead to severe hypotension.
• Emergency drugs such as epinephrine and ephedrine may serve to enhance the impaired
cardiac output during induction. Coronary perfusion pressure should be maintained to
ensure an adequate myocardial oxygen supply.
Maintenance
• Pre CPB.
– Volatile anesthetics as tolerated. Nitrous oxide can increase pulmonary vascular resistance
and is best avoided.
– Opioids: High dose techniques may bestow hemodynamic stability.
– Echocardiographic evaluation of appropriate LV decompression.
– Careful attention to fluid management.
– Heparinization.
• Post CPB:
– Patients may be vasodilated and require vasoactive drugs.
– Patients are preload-dependent; maintenance of an adequate volume status is imperative
for adequate cardiac output.
– Right heart support for LVAD.
– Monitor mechanical assist device flows.
– Echocardiographic evaluation of the heart.
– Pulmonary vasodilators such as nitric oxide or milrinone may be required for pulmonary
hypertension and to decrease RV afterload.
– Address coagulopathies which often require the use of blood products (i.e., FFP, platelets,
and cryoprecipitate). This therapy can be guided with the use of thromboelastography
(TEG). There is always a risk of clotting a device and therefore it is best to utilize guided
therapy for administration of blood products and begin anticoagulation on postoperative
day 1 or 2.
– ICD reactivation.
May be extubated in the ICU when criteria are met.
POSTOPERATIVE CARE
BED ACUITY
• ICU
• Anticoagulation with heparin is started post-operatively when bleeding is stabilized and
transitioned to Warfarin.
• Continue antibiotics.
• Aseptic technique should be maintained around the driveline when changing dressings.
ANALGESIA
Pain is typically moderate to severe and managed with PCAs.
COMPLICATIONS
• Thromboembolism within the pump can lead to malfunction or cerebral vascular events.
• Infections: Occur most commonly in the driveline or the abdominal wall pocket.
• Hemorrhage from coagulopathies.
• Right heart failure.
• Device malfunction.
• Cerebral air embolism.
• GI bleeding.
PROGNOSIS
(LVAD) survival range 86%, 56%, 33% at 30 days, 1 year and 2 years, respectively. More
recent devices continue to show improvement in survival.
REFERENCES
1. Slaughter MS, Rogers JG, Milano CA. Advanced heart failure treated with continuous-flow
left ventricular assist device. NEJM. 2009;361:2241–2251.
2. Hensley FA, Martin DE, Gravlee GP. Cardiac Anesthesia. 4th ed. Philadelphia, PA:
Lippincott Williams and Wilkins, 2008;587–589.
3. Leitz K, Long JW, Kfoury AG. Outcomes of left ventricular assist device implantation as
destination therapy in the post-REMATCH era. Circulation. 2007;116:497–505.
4. Goldstein DJ, Oz MC, Rose EA. Implantable left ventricular assist devices. NEJM.
1998;339:1522–1533.
5. iha H, Netuka I, Kotulak T, et al. Anesthesia management of a patient with a ventricular
assist device for noncardiac surgery. Semin Cardiothorac Vasc Anesth. 2010;14(1):29–31.
• Heart transplantation.
• Congestive heart failure.
• Cardiopulmonary bypass.
• Antifibrinolytics
CODES
ICD9
428.9 Heart failure, unspecified
ICD10
I50.9 Heart failure, unspecified
CLINICAL PEARLS
Patients may present to the operating room with MCADs for noncardiac procedures.
Preoperative care involves consulting with MCAD management personnel, detailed
assessment of end-organ dysfunction, appropriate antibiotic prophylaxis, deactivation of
implantable cardioverter-defibrillator for the time of surgical procedure, and choosing the
anesthesia type. Intraoperative monitoring for pulsatile devices do not require special
monitoring; whereas devices with nonpulsatile blood flow require the placement of an
arterial line (pulse oximetry and noninvasive blood pressure measurement are not reliable).
Patients are exquisitely dependent on preload to maintain adequate cardiac output and need
careful fluid management. Anesthetic agents can decrease systemic vascular resistance and
need to be carefully titrated; vasoconstrictors should be readily available for administration.
Management of anticoagulation needs to be discussed with the surgeon and cardiologist (5).
MEDIASTINOSCOPY
Teresa L. Moon, MD
BASICS
DESCRIPTION
General
• A mediastinoscopy facilitates mediastinal exploration in a less invasive manner than a
sternotomy or thoracotomy.
• The lungs possess a rich lymphatic system that drains into the subcervical, paratracheal, and
supracervical nodes.
• The procedure is mainly performed to biopsy mediastinal lymph nodes to assess the spread
of bronchogenic carcinoma; it is considered as the gold standard for mediastinal lymph
node staging.
– A cervical approach can be employed for pretracheal, paratracheal, and anterior
subcarinal nodes.
– A transthoracic or anterior approach is commonly used for aortopulmonary nodes.
• The procedure entails dissection between the trachea and pretracheal fascia. A
mediastinoscope (lighted instrument) is inserted and advanced along this plane to the level
of the carina; it remains behind the aortic arch, the innominate artery, and the innominate
vein.
– Needle aspiration and biopsy may be performed
– Clips may be placed to facilitate X-ray visualization
– A drain may be inserted to allow for blood, fluid, or air collection
– Often performed in conjunction with a bronchoscopy
• Other indications for mediastinoscopy include:
– Biopsies when sarcoidosis, Hodgkin’s disease, or tuberculosis are suspected
– Excision of mediastinal masses
Position
• Supine
• Reverse Trendelenburg
• Shoulder roll with neck extension
Incision
• Suprasternal transverse for cervical mediastinoscopy; approximately 1–2 cm above the
sternum and 4 cm long.
• Parasternal, usually left second interspace for transthoracic mediastinoscopy (Chamberlain’s
procedure or anterior mediastinotomy).
Approximate Time
Less than one hour
EBL Expected
• Minimal
• Risk of significant hemorrhage if vascular injury occurs.
Hospital Stay
Outpatient versus 23-hour observation.
Mediastinoscope: A handle with a blade that appears similar to a laryngoscope (Miller blade).
The instrument is lighted and can either have a lens that allows for direct visualization or can
be attached to a cable that allows for video-assisted display onto a monitor screen. Biopsy
instruments are passed through a large channel alongside the scope.
EPIDEMIOLOGY
Prevalence
For use in lung cancer evaluation most commonly
Morbidity
• Bleeding (0.73%)
• Pneumothorax (0.66%)
• Recurrent laryngeal nerve injury (0.34%)
• Cerebral ischemia
• Esophageal perforation
• Pleural tear
• Laceration of trachea
• Acute tracheal collapse
• Tension pneumomediastinum
Mortality
Overall: 0.09%
• Airway collapse may result secondary to the presence (and size) of the mediastinal mass.
Patients should be evaluated by history and symptoms as well as imaging or pulmonary
flow volume loops to determine this potential. If airway collapse is likely with muscle
paralysis, it is best to keep the patient spontaneously ventilating.
• The anaesthetist should have a clear understanding of the anatomy of the procedure. There
are multiple large vessels in the mediastinum, and potential vascular injury can be
catastrophic.
SYMPTOMS
• Dyspnea that is positional may suggest an anterior mediastinal mass that is compressing an
airway structure
• Cough
History
• Usually performed for lung cancer with enlarged nodes or mediastinal lymph node
enlargement due to lymphoma, thymoma, or retrosternal goiter.
• Commonly performed for sarcoidosis, tuberculosis, or therapeutic excision of a mediastinal
mass.
• Therapy: Chemotherapy and/or radiation.
Signs/Physical Exam
• Tracheal deviation
• Vein engorgement
MEDICATIONS
Variable
Labs/Studies
• Chest CT: To look for any airway obstruction or distortion, or any vascular (superior vena
cava) obstruction
• Carotid studies: To determine if there is an increased risk for cerebral malperfusion during
surgical manipulation
• Type and cross: Blood should be available in the event of vascular injury
• Lung cancer: Respiratory reserves may be suboptimal
• Eaton–Lambert signs may be present from oat cell carcinoma, leading to resistance to
depolarizing agents and increased sensitivity to nondepolarizing muscle relaxants
• Compression of vascular structures by a mass: Include the heart, pulmonary artery, or
superior vena cava (SVC). SVC obstruction may lead to increased ICP
TREATMENT
Premedications
Anxiolysis may be considered if there is no evidence of airway obstruction.
• Awake fiberoptic intubation may be planned when there is a risk for airway obstruction
(mass is encroaching into the trachea) or potential for anterior mediastinal mass collapse.
Discuss the indications and reasonable sedation goals.
• Massive blood loss, requiring transfusion of blood products.
A third generation cephalosporin for skin organisms
INTRAOPERATIVE CARE
General endotracheal anesthesia with neuromuscular blockade offers a more controlled
environment, especially with surgical manipulation
Monitors
• Standard monitors
• Radial arterial line
• Large bore peripheral IV (14–16G)
• Arterial line and/or pulse oximeter should be placed on the right upper extremity in order to
immediately recognize compression of the innominate artery by surgical manipulation.
• Awake fiberoptic intubation if there is an anticipated difficult airway or risk of airway
obstruction with induction and muscle relaxant. This technique will allow for the
maintenance of airway patency and spontaneous ventilation while securing the airway.
• IV induction with muscle relaxant (short acting) if the patient has no signs or symptoms of
airway compression or obstruction.
• Mask induction to maintain spontaneous ventilation may also be used if there is concern
about airway obstruction with muscle relaxant and no contraindications such as GERD.
Maintenance
• Volatile anesthetic or total intravenous anesthesia may be chosen. Volatile agents are chosen
when spontaneous ventilation is desired and should be considered in patients with reactive
airway disease (potent bronchodilators).
• Muscle relaxants can aid with surgical manipulation and visualization as well as prevent
coughing and venous engorgement in the chest. However, it should be avoided when
attempting to keep the patient spontaneously ventilating.
• Avoid nitrous oxide due to the potential for pneumothorax and pneumomediastinum.
• Plan for extubation in the operating room.
• If the surgeon identifies potential damage to the recurrent laryngeal nerve, assess injury
after extubation by having the patient vocalize the letter “e.”
FOLLOW-UP
BED ACUITY
• Recovery room with discharge either to home or floor.
• ICU if major vascular injury with resulting reconstruction or repair.
• A chest radiograph is performed in all patients to evaluate for a pneumothorax.
ANALGESIA
• Parenteral opioids.
• Ketorolac.
• Local anesthetic can be injected at the skin incision by the surgeon.
COMPLICATIONS
• Vascular injury is more common at the lower right paratracheal node (4R) biopsy site.
• Pneumothorax
• Recurrent laryngeal nerve injury
• Cerebral ischemia due to compression of the innominate artery (especially in those patients
with pre-existing cerebral malperfusion)
REFERENCES
1. Lemaire A, et al. Nine-year single center experience with cervical mediastinoscopy:
Complications and false negative rate. Ann Thorac Surg. 2006;82:1185–1190.
2. McCurdy MD, Philips PA, Marty AT, et al. Mediastinoscopy: Procedure of choice for
diagnosis and determination of operability. Cardiovasc Dis. 1974;1(3):242–250.
3. Cho JH, Kim J, Choi YS. A comparative analysis of video-assisted mediastinoscopy and
conventional mediastinoscopy. Ann Thorac Surg. 2011;92(3):1007–1011.
4. Bulut T, Brutel de la Riviere A. Mediastinoscopy as a therapeutic tool. Ann Thorac Surg.
2011;91(5):1616–1618.
5. Rami Porta R. Surgical exploration of the mediastinum by mediastinoscopy, parasternal
mediastinoscopy and remediastinoscopy: Indications, technique and complications. Ann
Ital Chir. 1999;70(6):867–872.
6. Fernandez A, Campos JR, Filomeno LT, Jatene FB. Mediastinoscopy: Technical aspects and
current indications. Rev Hosp Clin Fac Med Sao Paulo. 1994:49(4):164–167.
CLINICAL PEARLS
• Be prepared for complications including bleeding, pneumothorax, airway collapse.
• Radial arterial line and/or pulse oximeter should be placed on the right upper extremity to
immediately identify innominate artery compression.
• Video-assisted mediastinoscopic lymph node biopsy may be associated with fewer
complications than direct visualization. In addition, it may allow for examination and
removal of more lymph nodes than conventional mediastinoscopy.
MEDICATION ERRORS
Ronnie J. Glavin, MB, ChB, MPhil, FRCA, FRCP (Glas)
BASICS
DESCRIPTION
• The National Coordinating Council for Medication Errors Reporting and Prevention defines a
medication error as any preventable event that may cause or lead to inappropriate
medication use or patient harm while the medication is in the control of the healthcare
professional, patient, or consumer. Such events may be related to professional practice,
health care products, procedures, and systems, including: prescribing order communication;
product labeling; packaging; nomenclature; compounding; dispensing; distribution;
administration; education use.
• This definition emphasizes the complexity of drug preparation and administration and the
many different stages at which something can go wrong.
• A more workable definition is provided by the Institute of Medicine – an adverse drug event
is an injury caused by medical management rather than the underlying condition of the
patient.
• An adverse drug reaction is a response to a drug that is noxious and unintended and occurs
at doses normally used for the prophylaxis, diagnosis, and therapy of disease or for the
modification of physiological functions.
EPIDEMIOLOGY
Prevalence
• Ranges from 0.5 to 1 errors/near misses per 133 patients undergoing anesthesia (1,2)[C].
• In US hospitals, adverse medication events range from 2 to 6 per 100 admissions.
Prevalence
The FDA (3)[C] estimates 3 billion prescriptions are prescribed annually with adverse events
resulting in more than 4 million hospital visits and 117,000 hospitalizations annually.
Morbidity
Medication errors in anesthesia may result in awareness, prolonged anesthesia, and a need for
prolonged ventilation.
Mortality
A UK retrospective study using data from a national voluntary reporting system reported an
incidence of 15 fatal or severely harmful episodes in 1,120 medication errors (1.3%) but did
not define severe harm.
Common errors include:
• Incorrect dose
• Substitution (syringe swap or wrong drug drawn up into syringe)
• Omission (not giving the drug when intended)
• Repetition
• Medication errors can usually be divided into two main categories: Active failures and latent
conditions.
• Active failures
– Slips (failures of attention), for example, picking up the wrong syringe.
– Lapses (failure of memory), for example, being interrupted while programming an infusion
pump and forgetting to complete the program may result in that infusion not being
delivered when expected or in the dose expected.
– Rule-based mistakes in which the wrong rule may be invoked. An example includes
emergency care when the use of amiodarone or magnesium as part of the management of
acute cardiac events may be associated with wrong dilutions or incorrect rates of
administration. The written material accompanying the packaging is not always easily
read during crises.
– Knowledge-based mistakes in which the wrong drug is prescribed or administered, but the
person believes it to be the appropriate choice for that clinical context.
– Violations in which the person administering or prescribing the drug knows what the
correct action should be, but chooses to ignore it. For example, choosing to use an amount
of local anesthetic drug that exceeds the recommended toxicity thresholds.
• Latent conditions refer to components in the system that do not normally contribute to harm
but when the appropriate circumstances apply, they will emerge. For example, if the
electronic dispensing facility in a hospital pharmacy broke down and the doctors could not
access further supplies of emergency drug, then an adverse outcome for the patient could
result. These can contribute to errors or mistakes taking place. Luckily, many errors do not
result in serious or life-threatening episodes because some defensive mechanisms are
present.
• The list of active failures highlights the importance of effective cognitive processes:
Attention, memory, recall of knowledge. Circumstances that interfere with these are more
likely to result in slips, lapses and mistakes and also errors of judgment, which in turn may
influence the performance. Interruptions while preparing drugs may result in the wrong
drug being drawn up into the syringe. Fatigue, hunger, thirst, cold or hot environments may
all contribute to a reduction in attention or the effectiveness of working memory. Busy
periods when many demands are placed on the anesthesia provider and unexpected
emergencies where the solution is not obvious will also place a burden on the cognitive
powers of the anesthesia provider, increasing the likelihood of errors and mistakes.
• General measures
– Creating a working environment where unnecessary distractions are discouraged and
where extra vigilance is encouraged (for example cross checking complex programming of
infusion pumps or calculations of infusions) during conditions of fatigue or stress.
Recognizing the presence of hunger or thirst and taking pre-emptive measures to prevent
them from getting worse. Recognizing one’s own state of health, including the use of any
medication.
– A helpful self-checklist used in aviation is ‘I’M SAFE’, which may also be used to
determine safety when caring for patients.
Illness
Medication
Stress
Alcohol
Fatigue
Emotion
• Specific measures: Jensen (4)[A] described a list of twelve such actions and linked them to
the strength of evidence for their effectiveness. These are, listed by the strength of evidence,
as follows:
– Strongly recommended
The label on any drug or ampule or syringe should be carefully read before a drug is
drawn up or injected.
Legibility and contents of labels on ampules and syringes should be optimized according
to agreed standards.
Syringes should be labeled (always or almost always).
Formal organization of drug drawers and workspaces should be used.
– Recommended
Labels should be checked specifically with a second person or device before a drug is
drawn up or administered.
Errors in IV drug administration during anesthesia should be reported and reviewed.
Management of the drug inventory should focus on minimizing the risk of drug error.
Similar packaging and presentation of drugs should be avoided where possible.
– Possibly recommended
Drugs should be presented in prefilled syringes rather than ampules.
Drugs should be drawn up and administered by the anesthetist who will administer
them.
Color coding by class of drug according to an agreed national or international standard
should be used.
– Unclear
Coding by syringe position or by the needle on the syringe should be used.
• This will depend on the effects of the drug. A useful classification system gives six categories
of drug reaction. These are as follows:
– Augmented (dose-related)
– Bizarre (non-dose-related)
– Chronic (dose-related)
– Delayed (time-related)
– End of use (withdrawal)
– Failure (unexpected failure of therapy)
– Most medication errors seen by anesthesia providers will fall into the first two categories
of the above list.
• It is very important to remember that medication errors affecting the patient may be due to
the actions of other health care workers or even the patient and not confined to the actions
of the individual anesthesia provider. For example, a patient may have been advised to omit
a regular antihypertensive drug before attending surgery under anesthesia. An even more
severe case would be one in which a patient with an acute medical condition had been
charted as having been given a drug but had not actually received that drug. An anesthesia
provider anticipating some therapeutic benefit may then be faced with an adverse outcome,
for example, a patient with heartburn who had not received a scheduled dose of protein
pump inhibitor or H2 blocker could be at greater risk of adverse reaction to aspiration of
gastric contents.
• Many of the adverse outcomes in the prospective studies were related to actions of
anesthetic drugs: Prolonged anesthesia or need for prolonged ventilation. A high index of
suspicion should be maintained if a patient appears to be unduly sensitive or resistant to a
commonly administered anesthetic drug.
There are many ways in which a medication error may present but in the context of
anesthesiology, most will present acutely and so are more likely to fall into the augmented or
bizarre categories of drug reaction.
TREATMENT
• Treatment will be a combination of specific and supportive. The most important component
is awareness on the part of the anesthesia provider that an abnormal response by the patient
may be due to a reaction to a medication error.
• As an example, if a spontaneously breathing patient demonstrated signs of respiratory
depression, then appropriate supportive therapy should begin at once – conversion to
positive pressure ventilation and so on. A quick review of the drug ampules used may
confirm that higher concentration of opioid drug than intended was prepared and
administered. The specific treatment would be consideration of the use of an antagonist
such as naloxone.
FOLLOW-UP
The importance of the use of the generic error system is that it provides a framework that
allows the anesthesia provider to structure a critical incident report. The inclusion of any
latent conditions is particularly important to help identify and eliminate these and so reduce
their possible future contribution to potential adverse outcome (5)[C] .
REFERENCES
1. Webster CS, Merry AF, Larsson L, et al. The frequency and nature of drug administration
error during anaesthesia. Anaesth Intensive Care. 2001; 29(5):494–500.
2. Llewellyn RL, Gordon PC, Wheatcroft D, et al. Drug administration errors: A prospective
study survey from three South African teaching hospitals. Anaesth Intensive Care.
2009;37(1):93–98.
3. U.S. Department of Health and Human Services Food and Drug Administration. FDAs Safe
Use Initiative: Collaborating to reduce preventable harm from medications. 2009 – see
website below (last accessed 27th February, 2011)
4. Jensen LS, Merry AF, Webster CS, et al. Evidence-based strategies for preventing drug
errors during anaesthesia. Anaesthesia. 2004; 59(5):493–504.
5. Glavin RJ. Drug errors: Consequences, mechanisms, and avoidance. Br J Anaesth.
2010;105(1):76–82.
ADDITIONAL READING
• FDA Safe drug initiative – variety of documents and workshops available at
http://www.fda.gov/Drugs/DrugSafety/ucm187806.htm
• Dornan T, Ashcroft D, Heathfield H, et al. An in depth investigation into causes of
prescribing errors by foundation trainees in relation to their medical education. EQUIP
Study. General Medical Council, 2009. Available from http://www.gmc-
uk.org/about/research/research_commissioned.asp (accessed 27th February 2011).
CODES
ICD9
• 960–979—poisoning by drugs, medicinals and biological substances
• 968.0–968.9—poisoning by other central nervous depressants and anesthetics
CLINICAL PEARLS
• Medication errors are common and although the majority of them result in very little patient
harm, the potential for patient death or severe harm is always present.
• If an abnormal patient response occurs in response to an anesthetic intervention, think
“Could this be a medication error?”
• Medication errors are more likely during circumstances in which the cognitive processes of
the anesthesia provider are under pressure.
METABOLIC ACIDOSIS
Kanishka Monis, MD
BASICS
DESCRIPTION
• Metabolic acidosis is defined as a plasma pH <7.35 that results from either an increase in
nonvolatile acid production or loss of bicarbonate ions. It can:
– Be acute, lasting minutes to days (common); or chronic, lasting weeks to months (less
common).
– Results when the body’s multiple buffering and compensatory mechanisms are exhausted.
• Metabolic acidosis is divided into a normal or increased anion gap and is useful in
establishing a differential diagnosis. Anion gap is defined as the unmeasured anions present
in the plasma; it does not imply that anions are missing, but only that they are not directly
measured. It is calculated as follows:
– Anion gap = [Na+] − ([Cl-] + [HCO3-]).
– A normal anion gap is 6–10 mmol/L and is attributed to serum albumin, phosphates, and
sulfates.
– Perioperatively, the base excess is more commonly utilized in determining the extent of
increased acid load. This is because metabolic acidosis is most commonly the result of
anaerobic metabolism (lactic acidosis).
EPIDEMIOLOGY
Incidence
Acute metabolic acidosis is estimated to affect ∼64% of ICU patients (1).
Prevalence
Chronic metabolic acidosis has an increased prevalence in patients with chronic kidney
disease.
Morbidity
Primarily related to the underlying disease
Mortality
Primarily related to the underlying disease
• Increased anion gap metabolic acidosis results from increased nonvolatile acid (2,3).
– Lactic acidosis
– Uremia
– Ketoacidosis
– Intoxication: Methanol, ethylene glycol, salicylates, paraldehyde
• Normal anion gap metabolic acidosis results from the loss of bicarbonate:
– Diarrhea
– Chronic kidney disease
– Adrenal insufficiency
– Drugs: Spironolactone, prostaglandin inhibitors, triamterene, amiloride, cyclosporine
– Hyperkalemic distal renal tubular acidosis (RTA)
– Type I and Type II (Gordon’s syndrome) pseudoaldosteronism
• Normal acid production is 1 mmol/kg/day in adults and 1–3 mmol/kg/day in infants and
children.
• The hydrogen ion concentration is tightly regulated in the body to maintain a physiologic
[H+] of 40 mEq/L. There are 3 key mechanisms:
– Intracellular and extracellular buffering systems are the first-line mechanisms to remove
excessive [H+].
Carbonic acid/bicarbonate system: [H+] + [HCO3−] ←→ H2CO3 carbonic anhydrase
H2O + CO2. When the [H+] increases, the [HCO3−] declines as more H2CO3 forms.
Carbonic anhydrase will convert H2CO3 to CO2 and H2O.
Phosphate: [H2PO4−] [H+] + [HPO44−]. The high intracellular concentration makes it
an important intracellular buffer.
Hemoglobin
Plasma proteins
– Alveolar ventilation and elimination of carbon dioxide (CO2)
Increases in [H+] stimulate chemoreceptors in the carotid body to increase minute
ventilation and exhalation of CO2.
Winter’s formula aids with identifying the presence of a mixed respiratory disorder:
PaCO2 = (1.5 × [HCO3-]) + 8 ± 2. When the calculated and measured PaCO2
correspond, it suggests that the metabolic acidosis is an isolated disorder. If the
measured PaCO2 is greater than the calculated PaCO2, a primary respiratory acidosis is
also present; whereas, if the measured PaCO2 is lower than the calculated PaCO2, a
primary respiratory alkalosis is also present.
– Renal compensation:
Reabsorption and secretion. Filtered HCO3− is converted to CO2 in the lumen of the
renal tubule; it then diffuses into proximal tubule cells and is subsequently reconverted
to HCO3− and returned to the systemic circulation. Thus, for each HCO3− that is
reabsorbed, an H+ is secreted into the urine by the renal tubular cell.
• Effects on organ systems:
– Cardiovascular
Impaired contractility of the myocardium
Increased pulmonary vascular resistance
Decreased systemic vascular resistance
– Respiratory
Hyperventilation (compensatory mechanism)
Shift of oxygen dissociation curve to the right
Decreased 2,3-Diphosphoglycerate (DPG) in red cells leads to a decrease in hemoglobin’s
affinity to oxygen. There is a “left-shift" of the oxyhemoglobin curve.
– Bone
Chronic acidosis, as is seen with renal disease, can result in increased mobilization of
calcium from bone secondary to cellular effects on osteoclasts and osteoblasts and
impaired bone matrix mineralization.
• Close monitoring of blood glucose levels in diabetics to prevent ketoacidosis.
• Lactic acidosis results from tissue hypoxia (anaerobic metabolism) that is due to impaired
perfusion or oxygen delivery
– Maintain adequate volume in burn injuries, trauma, hemorrhage, diarrhea, bowel prep,
third spacing
– Maintain adequate perfusion with inotropes and vasopressors
– Maintain adequate blood oxygen content via increasing the inspired oxygen fraction and
possibly transfusing blood, if appropriate.
DIAGNOSIS
• Symptoms are non-specific in the awake patient:
– Chest pain
– Palpitations
– Nausea and vomiting
– Abdominal pain
– Decreased visual acuity
– Decreased appetite
– Weight loss
– Muscle weakness
• Signs: Kussmaul respirations, tachypnea, cranial nerve damage (ethylene glycol poisoning).
• Arterial blood gas measurements provide values for pH, HCO3−, PaCO2, and base excess and
are assessed in context with one another.
– pH <7.35
– [HCO3−] <24 mmol/L. Decreased from titration of nonvolatile anions or loss.
– PaCO2: Assess for respiratory compensation or concurrent acidosis.
– Base excess: More frequently utilized than the anion gap in the perioperative period; this
is because metabolic acidosis is often the result of lactic acidosis secondary to anaerobic
metabolism. Aids with determining the extent of the increased acid load, as opposed to
aiding in the differential diagnosis.
• Anion gap (AG) calculation aids with narrowing the diagnosis: AG = [Na+] − ([Cl-] +
[HCO3-]). As mentioned above (1):
– Increased AG signifies an accumulation of endogenous or exogenous acids.
– Normal or non-anion gap metabolic acidosis reflects the loss of HCO3− anions from the
kidneys or GI tract, the inability of the kidneys to excrete excess [H+], or overzealous
fluid resuscitation with normal saline (hyperchloremic metabolic acidosis).
• Urinary pH: Normally, the urine pH is less than 5. In patients with metabolic acidosis, urine
pH becomes more acidic as the kidneys attempt to excrete the acid load.
• Plasma glucose: The measurement is necessary to rule out diabetic ketoacidosis, along with
urine ketones and glucose.
• Hyperkalemia: Acidosis leads to intracellular shifting of hydrogen ions in exchange for
potassium. The EKG may reveal peaked T waves, widening of the QRS complex, and
reduction in the size of the P wave.
• Respiratory acidosis:
– Low pH
– Increased PaCO2
– Low [HCO3−]
• Mixed metabolic and respiratory acidosis: Use Winter’s formula as mentioned before.
TREATMENT
• Diabetic ketoacidosis: Fluid and electrolyte replacement and insulin therapy, as well as
inciting cause (e.g., infection, myocardial infarction).
• Uremia: Dialysis, hemofiltration and renal replacement therapy.
• Lactic acidosis: Identify and treat the underlying cause (hypovolemia, hypoxia,
hypoperfusion).
• Sodium bicarbonate administration: In the acidotic patient, inotropes and vasopressors may
have decreased efficacy and hinder therapy aimed at the underlying cause.
– NaHCO3 dissociates into a sodium and bicarbonate ion. The bicarbonate ion can bind with
hydrogen ion to form H2CO3 which can be converted via carbonic anhydrase to water and
carbon dioxide. CO2 can be exhaled via the pulmonary system.
– The bicarbonate deficit can be calculated as follows: ([HCO3-]desired − [HCO3-]measured) ×
0.6 × body weight in kg). Bicarbonate levels should not be corrected >12 mmol/L in the
initial correction to prevent over treatment.
– However, its use remains controversial and has not been shown to improve the outcome,
even in patients in cardiopulmonary arrest. In addition, hyperosmolarity and
hypernatremia can have deleterious effects. An inability to increase minute ventilation can
result in a respiratory acidosis.
REFERENCES
1. Maciel AT, Park M. Differences in acid–base behavior between intensive care unit survivors
and nonsurvivors using both a physicochemical and a standard base excess approach: A
prospective, observational study. J Crit Care. 2009;24(4):477–483.
2. Morris CG, Low J. Metabolic acidosis in the critically ill: Part 2. Causes and treatment.
Anaesthesia. 2008;63(4):396–411.
3. Morris CG, Low J. Metabolic acidosis in the critically ill: Part 1. Classification and
pathophysiology. Anaesthesia. 2008;63(3):294–301.
• ACLS anesthetic management.
• Lactic acidosis
• Anion gap
CODES
ICD9
276.2 Acidosis
ICD10
E87.2 Acidosis
CLINICAL PEARLS
• Acidosis decreases protein binding of local anesthetics; therefore increasing the free fraction
of the drug and its risk of systemic toxicity.
• Propofol infusion syndrome should be suspected when metabolic acidosis develops in
patients on a propofol infusion, combined with rhabdomyolysis and cardiac failure.
METABOLIC ALKALOSIS
Kanishka Monis, MD
Michael Grover, MD
BASICS
DESCRIPTION
• Metabolic alkalosis is a pathophysiologic state of high plasma pH (>7.45) that can be
caused by the:
– Accumulation of base.
– Loss of acid.
– Loss of fluid containing chloride ion than bicarbonate from the extracellular space (1).
• It may be classified as either:
– Acute versus chronic.
– With or without pulmonary compensation: The lungs attempt to blunt the pH change by
decreasing exhalation of carbon dioxide; however, it cannot completely restore
homeostasis.
– Chloride depletion, potassium depletion, volume contraction, or iatrogenic. The literature,
however, discusses several other methods to classify metabolic alkalosis based upon the
etiology (e.g., organ dependent) (2).
• Because pH homeostasis is essential for the proper function of enzymes and protein, organ
dysfunction (e.g., impaired inotropy, decreased cerebral blood flow) and impaired drug
clearance may be seen (3).
EPIDEMIOLOGY
Mortality
• Medical and surgical inpatients with an arterial blood pH of 7.55 have been shown to have a
45% mortality (2).
• Medical and surgical inpatients with an arterial blood pH of 7.65 have been shown to have
an 80% mortality (2).
• Chloride depletion (2,4):
– Gastric losses: Vomiting, nasogastric suctioning, bulimia, or pyloric stenosis
– Diarrheal states: Villous adenoma, congenital chloridorrhea, inflammatory bowel disease
– Use of chloruretic diuretics: Chlorothiazide, bumetanide
– Cystic fibrosis
• Potassium depletion (5)
• Volume depletion: (Often results in, or is secondary to, chloride or potassium depletion).
This is also referred to as “contraction alkalosis” in the literature (2).
• Iatrogenic: Sodium bicarbonate administration.
• Metabolic alkalosis can be classified by the:
– Underlying pathophysiology: Chloride or potassium depletion, volume contraction,
mineralocorticoid excess
– Primary organ system involved (2)
• Hypokalemia can cause or maintain metabolic alkalosis due to:
– Intracellular shifting of hydrogen ions.
– Stimulation of H+/K+ ATPase receptors at the collecting ducts. To re-establish normal
potassium levels, the receptor increases potassium ion reabsorption while secreting
hydrogen ion into the urine.
– An increase in renal ammonia production with resultant net acid excretion as NH4+; the
exact mechanism is unknown (2,6).
• Chloride depletion enhances absorption and impairs excretion of bicarbonate in the kidneys.
– Low levels are sensed by the macula densa and stimulate the renin–angiotensin–
aldosterone system (RAAS). The RAAS functions to increase volume, retain sodium, and
excrete potassium. At the level of the collecting duct, sodium is retained at the cost of
hydrogen secretion into the urine.
– Impairs the Cl−/HCO3− exchanger at the level of the collecting duct (2).
• Decreased volume
– Decreases in glomerular filtration rate (GFR) will decrease the filtered load of bicarbonate
at the glomerulus and hence excretion in urine (2).
– Stimulates the renin–angiotensin–aldosterone system. At the level of the collecting duct,
sodium is retained at the cost of hydrogen secretion into the urine. The maintenance of
volume supersedes pH homeostasis (2).
• Gastrointestinal
– Gastric fluid contains 60–140 mM HCl. It can be quickly depleted with vomiting or
suctioning. In addition, extracellular fluid (ECF) volume contraction, as well as sodium
and potassium loss can stimulate renin and aldosterone production with renal
compensation (4).
– Villous adenomas secrete chloride rather than potassium and bicarbonate (4).
• Skin: Cystic fibrosis is a genetic defect that causes an abnormal chloride channel protein and
impaired cAMP-regulated chloride transport across epithelial cells leading to metabolic
alkalosis by chloride depletion (2).
• Compensation: Increases in pH depress central and peripheral receptors with resultant
hypoventilation/hypercapnia. The ability to compensate, however, is limited due to:
– Hypoxia from rising alveolar carbon dioxide partial pressures can stimulation
chemoreceptors and result in hyperventilation.
– Mechanical ventilation: Unless recognized and adjusted for, ventilator settings can result
in a “relative” hyperventilatory state.
– Pain in patients who are breathing spontaneously.
DIAGNOSIS
• The presence of symptoms such as cardiac arrhythmias, confusion, neuromuscular
irritability or weakness, and hypoventilation (hypoxia and increased PaCO2) may suggest a
metabolic alkalosis (2).
• Arterial blood gases:
– Elevated pH
– Increased bicarbonate concentration
– Differentiate between acute and chronic processes
– Identify the presence of a mixed disorder. The expected PaCO2 = 0.7[HCO3−] + 20,
range ±5; the large range is the result of factors that can impair hypoventilation (see
above). When the expected PaCO2 is increased or decreased, consider the possibility of a
concomitant respiratory acidosis or alkalosis.
• The measurement of urinary chloride and potassium can aid with narrowing the diagnosis
(however, this is not routinely performed in the perioperative setting) (2,4).
– Urinary chloride <10 mEq/L
Chloride depletion alkalosis
Gastric losses
Cystic fibrosis
Colonic villous adenoma
Dietary chloride deprivation
– Urinary potassium concentration >30 mEq/L
Renal potassium wasting
Diuretics
High circulating aldosterone
– Urinary potassium <20 mEq/L
Extrarenal potassium loss
Metabolic alkalosis is a unique disorder that is always a sign of some other underlying
disease; thus, the etiology is, in itself, the differential diagnosis.
TREATMENT
• Treatment should be aimed at the underlying etiology. Replacement of chloride, potassium,

and volume may also be indicated, as appropriate.
• Chloride responsive alkalosis (2)
– Volume depleted/contracted: Administer normal saline ([Cl−] = 154 mEq/L). When
severely dehydrated, reabsorption of chloride takes precedence over acid reabsorption
(also known as paradoxical aciduria). The base is eventually excreted by the kidneys as
volume is replenished and chloride becomes available.
– Normovolemic patients: The chloride deficit can be calculated by: ([0.2 × body weight
(kg)] × [difference between desired and current plasma chloride (mEq/L)]). The deficit
can be replaced intravenously; ensure that chronic electrolyte disturbances are not rapidly
corrected.
– Volume overload: In patients with congestive heart failure, chloride should be repleted
with KCl, instead of NaCl. If hyperkalemia exists, then intravenous HCl may be indicated.
– Potassium concentration must be monitored closely during the course of treatment and
repleted as necessary. Hypokalemia is a common occurrence with rehydration.
– Acetazolamide can be given to patients with normal renal function or when normal saline
infusion is not effective; it promotes diuresis of NaHCO3 by the inhibition of carbonic
anhydrase.
• Chloride-resistant alkalosis/hypokalemia (2):
– Oral or intravenous KCl:
Mild to moderate hypokalemia: oral KCl 40–60 mEq 4–5 times per day.
Severe or life-threatening hypokalemia up to 40 mEq per hour IV potassium may be used
(central line administration). Patients should have continuous EKG monitoring when
high rates of IV KCl are used.
REFERENCES
1. Medarov BI. Milk-alkali syndrome. Mayo Clin Proc. 2009;84(3):261–267.
2. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000;11(2):369–375.
3. Anderson LE, Henrich WL. Alkalemia-associated morbidity and mortality in medical and
surgical patients. South Med J. 1987;80(6):729–733.
4. Gennari FJ, Weise WJ. Acid–base disturbances in gastrointestinal disease. Clin J Am Soc
Nephrol. 2008;3(6):1861–1868.
5. Assadi F. Diagnosis of hypokalemia: A problem-solving approach to clinical cases. Iran J
Kidney Dis. 2008;2(3):115–122.
6. Weinstein AM. A mathematical model of distal nephron acidification: Diuretic effects. Am J
Physiol Renal Physiol. 2008;295(5):F1353–1364.
• Respiratory alkalosis
• Hypokalemia
• Cystic fibrosis
CODES
ICD9
276.3 Alkalosis
ICD10
E87.3 Alkalosis
CLINICAL PEARLS
• Perioperative metabolic alkalosis can be seen with:
– In patients with chronic respiratory failure (respiratory acidosis), a compensatory
metabolic alkalosis may develop.
– Administration of hypernatremic solutions (e.g., normal saline) results in an increased
strong ion deficit due to sodium gain. Sodium is buffered by bicarbonate.
• Metabolic alkalosis can result in:
– Electrolyte disturbances leading to arrhythmias, cardiovascular collapse, altered mental
status, and delayed emergence.
– pH abnormalities can decrease inotropy and increase cerebral blood flow.
– Increased affinity of oxygen to hemoglobin, shifting the oxygen–hemoglobin dissociation
curve to the left.
– Altered efficacy and clearance of medications.
– Increased mortality.
METHEMOGLOBINEMIA
David P. Frey, DO
Adam Thaler, DO
BASICS
DESCRIPTION
• Methemoglobin (MetHb) was first described by Felix Hoppe-Seyler in 1864.
• MetHb is a potentially lethal accumulation of oxidized hemoglobin. Although it is usually
acquired, it can also be congenital.
EPIDEMIOLOGY
Incidence
• Dapsone (used to treat leprosy, or Pneumocystis pneumonia) accounts for 42% of acquired
cases (1).
• Benzocaine spray accounts for the most severe cases (1).
Prevalence
50% of cases involve infants and the elderly, with infants <4 months being particularly
susceptible (2).
Mortality
Death occurs when methemoglobin fractions approach 70%.
• Exposure to an oxidizing agent is the most common cause of MetHb (3).
– Examples of oxidizing agents: Benzocaine, lidocaine, prilocaine, acetaminophen,
methylene blue (high dose), metoclopramide, and nitrates; also aniline, dapsone,
celecoxib, chloroquine, cyclophosphamide, ifosfamide, methanol, phenazopyridine,
phenytoin, primaquine, riluzole, trimethoprim–sulfamethoxazole.
– Other exogenous oxidizing agents are found in teething gels, automobile exhaust,
inhalants, industrial chemicals, smoke, and pesticides.
• Well water and foods containing nitrates can be converted to nitrites (powerful oxidizers) by
intestinal flora (4).
• States of high oxidative stress including systemic infection and cancer (3).
• Anemia (including mild degrees): MetHb is more likely to progress to symptoms when there
is a lower hemoglobin reserve.
• Acidosis: Endogenous reducing enzymes are less efficient at a low pH (4).
• Idiopathic MetHb is commonly seen among infants <4 months old (4).
• Genetic mutation is a rare cause of MetHb. Although usually benign, these patients are at
increased risk of developing acute toxicity when exposed to oxidizers or oxidative states (4).
• Other than the risk factors described herein, it is unknown why some people develop MetHb
while others do not.
• Oxidative toxicity involves the “redox” reaction, or loss of electrons from a substrate;
whereas reduction involves the transfer (gain) of electrons to a substrate.
• Hemoglobin is composed of four heme groups, each with one atom of iron. The iron atom
binds oxygen only in the reduced ferrous (Fe2+) state. Thus, when oxidation occurs (Fe2+
to Fe3+), a ferric heme state is created, known as methemoglobin, that does not bind and
transport oxygen to tissues.
• RBC’s are uniquely susceptible to oxidation and as such, MetHb typically presents before
oxidative injury in other tissues. RBCs:
– Carry O2, and hence are constantly exposed to oxygen free radicals.
– Lack a nucleus and cannot synthesize new proteins; thus “older” cells are more prone to
oxidative injury.
– Lack mitochondria. They are less efficient at generating the cofactors and energy needed
for reducing enzymes.
• Normally, methemoglobin is quickly reduced (gains electrons) back to hemoglobin by
cytochrome-b5 reductase (b5R); it is responsible for 99% of daily methemoglobin reduction.
This keeps methemoglobin levels at around 1% in healthy individuals.
• Methemoglobin is incapable of binding O2, and additionally, the Fe3+ heme creates an
allosteric change that decreases the O2 unloading from any remaining Fe2+ heme groups.
Thus, it produces a combined:
– Decrease in O2 carrying capacity; oxyhemoglobin becomes non-oxygen carrying
methemoglobin.
– Decrease in peripheral O2 delivery (impaired unloading); seen as a left-shift of the oxygen-
dissociation curve.
– These abnormalities result in functional anemia and tissue hypoxia.
• MetHb occurs when there is:
– Increased methemoglobin production.
– Decreased reduction capacity.
– Thus, toxicity and symptoms depend on the methemoglobin level and any concomitant
conditions that impair the ability to deliver O2 to the tissues.
• Methemoglobin can also covalently bind sulfur to form sulfhemoglobin. Endogenous
glutathione can serve as the sulfur donor and many drugs capable of producing MetHb can
also produce sulfhemoglobinemia, which will affect treatment (4).
• Re-exposure, high concentrations (>20%), and liberal use of benzocaine should be avoided.
• Identify those individuals at high risk and make methylene blue (MB) and blood available
for the procedure.
DIAGNOSIS
• Cyanosis is the first sign.
– Develops with 1.5 g/dL of methemoglobin (∼15% total hemoglobin) due to its
spectrographic properties as compared to deoxyhemoglobin that requires 5 g/dL
– Difficult to detect in dark skinned patients
– Maintain a high index of suspicion when cyanosis is refractory to O2 supplementation, and
especially if it develops 20–60 minutes (up to 2 hours) after benzocaine, prilocaine, or
lidocaine administration
• Severity of symptoms is dependent on the level of methemoglobin. MetHb as a % of total
hemoglobin:
– <1.5% – asymptomatic
– 10–20% – cyanosis
– 30–40% – headache, fatigue, weakness, tachycardia, tachypnea, chest pain, and dizziness
– 40–50% – dyspnea, confusion, and lethargy
– 50–60% – acidosis, arrhythmias, hypoxia, seizures, coma, bradycardia, and ventricular
dysrhythmias
– >70% – death
• Concomitant conditions: Anemia, acidosis, respiratory compromise, and cardiac disease may
make patients more symptomatic for a given methemoglobin level.
• Oxidant-induced hemolysis can accompany MetHb.
• Pulse oximeters measure two wavelengths of light: 660 nm (red, oxyhemoglobin) and 940
nm (infrared, deoxyhemoglobin). Methemoglobin absorbs equal amounts of these
wavelengths; a ratio of pulsatile and nonpulsatile absorbances equal to 1 corresponds to a
hemoglobin saturation of 85%. Thus, regardless of the actual oxygen saturation, MetHb will
read at 85% oxygen saturation on pulse oximeter.
• Co-oximeters detect multiple wavelengths of light, and can measure the concentration of
different forms of hemoglobin including reduced hemoglobin, oxyhemoglobin,
carboxyhemoglobin, and methemoglobin. Measurements are accurate and available in <2
minutes.
– Methemoglobin levels rise with storage time
– Both sulfhemoglobin and MB have similar absorbencies and will be reported as
methemoglobin
• Arterial line: Placement allows for frequent arterial blood gas (ABG) measurements (lactic
acidosis), beat-to-beat pressure regulation, and direct measurement of methemoglobin
levels. Because PaO2 refers to dissolved gas, it will reflect true partial pressure values;
however, the SpO2% calculation assumes normal hemoglobin oxygen binding characteristics
and will yield a false value. Thus, the SaO2% should be directly measured by the lab.
• Arterial blood appearance
– High concentrations of methemoglobin appear chocolate brown.
– Deoxyhemoglobin appears dark red and upon exposure to atmospheric O2 will turn bright
red. In contrast, methemoglobin will not change color over time, as it is unable to bind to
oxygen.
– Sulfhemoglobin also appears chocolate brown.
• EKG: Presence of myocardial ischemia indicates decreased O2 delivery to other tissues.
• Potassium cyanide (Drabkin’s reagent) test.
– Distinguishes between sulfhemoglobin and methemoglobin.
– Methemoglobin will react to the addition of potassium cyanide and turns bright red.
– Sulfhemoglobin is inert and will remain chocolate brown.
• Respiratory/cardiac compromise
• Sulfhemoglobinemia
• G6PD deficiency
• Nicotinamide adenine dinucleotide phosphate (NADPH)-methemoglobin reductase
deficiency
• Congenital MetHb
TREATMENT
• MetHb toxicity can be rapidly lethal but with prompt recognition and early initiation of
treatment, outcomes are good.
• Any oxidizing agents should be sought and discontinued.
• Supportive care
– Maintain airway
– Hemodynamic support
• Methylene blue (MB): NADPH-methemoglobin reductase is a generalized reductase found in
the body and has a high affinity for MB dye. If NADPH is available, it will reduce MB, which
in turn reduces methemoglobin back to hemoglobin.
– Treatment is indicated at approximately 20% MetHb in symptomatic patients, 30% MetHb
in asymptomatic patients, and 10–30% MetHb in patients with concurrent problems that
compromise O2 delivery.
– The dose of 1% solution is 1–2 mg/kg or 0.1–0.2 mL/kg over 3–5 minutes intravenously,
followed by 15–30 mL normal saline flush. If symptoms persist after 20 minutes, another
dose of 1 mg/kg can be given 30–60 minutes after the initial dose. Do not exceed a total
of 7 mg/kg because at these doses, MB can cause MetHb.
– Ineffective in the following scenarios:
G6PD deficiency: NADPH is largely generated by glucose-6-phosphate dehydrogenase
(G6PD). MB may also induce oxidant injury or hemolysis
NADPH-methemoglobin reductase deficiency
Sulfhemoglobin emia
• Secondary options if failure to respond to standard treatment or methemoglobin levels
exceed 50%:
– Hyperbaric oxygen administration
– Exchange transfusion
• Dextrose solutions catabolize glucose via glycolysis and replenish NADH and NADPH, which
are both necessary cofactors for the reduction of methemoglobin.
FOLLOW-UP
• An ABG should be obtained to confirm the absence of acidosis and no increase in

methemoglobin.
• Therapeutic MB can cause a false elevation in methemoglobin levels due to the similar
absorbance spectrum. Confirmation should be performed by using the specific Evelyn–
Malloy method which involves adding cyanide and ferricyanide reagents.
• Some drugs like dapsone and aniline have been reported to produce a rebound MetHb 4–12
hours after successful MB therapy because their metabolites are oxidizers.
• Oxidative hemolysis can follow MetHb 12–24 hours after first exposure to the etiologic
agent.
• The future use of oxidizing agents should be avoided in these patients.
REFERENCES
1. Hamilton RJ. Acquired methemoglobinemia: A retrospective series of 138 cases at 2
teaching hospitals. Ann Emerg Med. 2005;46(5):477–478.
2. So T, et al. Topical benzocaine-induced methemoglobinemia in the pediatric population. J
Pediatr Health Care. 2008;22(6):335–339.
3. Kane GC, et al. Benzocaine-induced methemoglobinemia based on the Mayo Clinic
Experience from 28,478 transesophageal echocardiograms. Arch Intern Med.
2007;167(18): 1977–1982.
4. Wright RO, et al. Methemoglobinemia: Etiology, pharmacology, and clinical management.
Ann Emerg Med. 1999;34(5):646–656.
• Pulse oximeter
• Cyanide poisoning
• Hyperbaric oxygen
• Hemoglobin
CODES
ICD9
289.7 Methemoglobinemia
ICD10
D74.9 Methemoglobinemia, unspecified
CLINICAL PEARLS
• Dapsone is the leading cause of drug acquired cases; whereas, benzocaine spray accounts for
the most severely acute elevations.
• MetHb produces a combined decrease in O2 carrying capacity and peripheral O2 delivery.
• The same drugs that cause hemolysis in G6PD deficiency can cause MetHb.
• Methemoglobin binds cyanide to form the nontoxic cyanomethemoglobin and is part of the
treatment for cyanide poisoning.
• Recognition and treatment with IV MB is imperative to save lives. Failure to respond to MB
include:
– Incorrect diagnosis (e.g., sulfhemoglobinemia)
– Ongoing toxin absorption
– G6PD deficiency
– Congenital MetHb
– NADPH-dependent methemoglobin reductase deficiency
– Unique toxin
• Pulse oximetry
– Measures light absorbance at the wavelengths 660 and 940 nm which is the absorbance of
oxy- and deoxygenated blood, respectively. SpO2 is calculated from this ratio
– Methemoglobin is absorbed at both of these wavelengths and will give a false value
– Significant methemoglobin will only be detected as mild to moderate O2 desaturation
MINIMUM ALVEOLAR CONCENTRATION (MAC)
Jeffrey W. Lim, MD, PhD
BASICS
DESCRIPTION
• The “minimum alveolar concentration,” or MAC, is the alveolar fraction/concentration of
volatile anesthetic that is able to prevent 50% of subjects from moving in response to
surgical stimuli (1).
• The concept of MAC is utilized intraoperatively as an index of:
– Depth
– Induction
– Recovery
– As well as for studies to standardize doses for different agents and to measure and assess
potency (1)
• Volatile agents are:
– Halogenated hydrocarbons that are hydrophobic
– Used perioperatively for the induction and maintenance of general anesthesia. Other uses
include bronchodilation during status asthmaticus
– Stored as liquids at room temperature and vaporized for anesthetic delivery via the
inhaled route
– Able to provide loss of consciousness, amnesia, and immobility
• Pharmacodynamics: Their mechanism is unknown, but believed to act on multiple areas
(unlike intravenous medications that act on a single receptor) and disrupt electrical
transmission (via proteins, membrane receptors, intracellular systems) and synapses at a
lower concentration than axonal synapses (2).
• Pharmacokinetics
– The concentration of gases are measured as partial pressures; they are denoted by Plocation
(Pbrain, PA, Pa, etc; units are mmHg). However, volatile agents are denoted as fractions;
Flocation (Fbrain, FA, Fa, etc; units are %). For example, sevoflurane 2% indicates that the
agent comprises 2% of the total inspired gas.
– Tissue groups: The vessel-rich group (brain, heart, liver, kidney, and endocrine organs)
receives significant blood flow and concentrations quickly rise; however, they also have a
small overall capacity. The muscles, fat, and the vessel-poor group (bone, ligaments, teeth,
hair, and cartilage) receive less blood flow (hence volatile agent delivery) and
concentrations take longer to rise; however, they have a very large capacity and function
as a “depot.” When a volatile agent is stored in a “depot,” it is essentially diverted from
the brain (site of action) and decreases the speed of induction and emergence. This effect
is accentuated with increased blood:gas solubility or increased duration of administration
(MAC-hr).
– Partition coefficients: The ratio of the amount of substance present in one phase compared
with another (assumes 2 phases at equal volume and specified temperature). Allows an
assessment of relative solubilities between blood and gas, brain, muscle, or fat (provides a
means to assess and compare the quantity and time needed for uptake and saturation of a
tissue). For example, halothane’s blood–gas partition coefficient is 2.4; thus, at
equilibrium, its concentration in blood is 2.4 times greater than in gas in contact with the
blood (e.g., in the alveoli).
– Fi is the inspired concentration of volatile agents. It is affected by fresh gas flow rates,
concentration of agent delivered, ventilation (rate, tidal volume), volume of the breathing
system (circuit length and diameter), and absorption (circuit, machine). Fi is increased
with increased fresh gas flow rates, concentration delivered, and ventilation as well as
decreased breathing circuit volume and absorption.
– FA is the alveolar concentration of a volatile agent. FA is affected by Fi (input) as well as
factors affecting uptake from the lungs (output). Uptake is affected by the blood:gas
solubility, cardiac output, and the venous–arterial partial pressure difference. At
equilibrium FETagent ∼ FA ∼ Fblood ∼ Fbrain, and an assessment of anesthetic depth
(induction, maintenance, and recovery) can be extrapolated from FA. FA (and rate of
induction) is increased with poorly soluble gases, impaired cardiac output, decreased
alveolar blood flow, and small venous–arterial partial pressure differences. Note that FA is
indirectly measured by end tidal monitors that reflect alveolar concentrations (FETagent).
– FA/Fi ratio: By convention, ratio is <1 due to uptake of the anesthetic agent by the
pulmonary circulation; if no uptake exists, it would equal 1, but it is not possible to
exceed 1 on induction or maintenance. FA/Fi ratio provides a method to assess the speed
of onset.
– Elimination: Recovery depends on lowering the volatile concentration in the brain tissue;
FA is used as a surrogate indicator of Fbrain (FETagent ∼ FA ∼ Fblood ∼ Fbrain). Volatile
agents are eliminated by exhalation, biotransformation, and transcutaneous loss. Factors
that speed up induction can also speed up recovery: Increased fresh gas flow, decreased
anesthesia machine-circuit volume and absorption, decreased solubility, increased
cerebral blood flow, and increased ventilation.
• 1 MAC is the alveolar concentration of the volatile agent, at 1 atmosphere, that is required
to produce immobility in 50% of patients at skin incision.
– Determination of the value: After equilibration of the agent, subjects were exposed to a
single skin incision and then observed for purposeful movement in response to the noxious
stimuli.
– At equilibrium, measurements of expired gases can be extrapolated to alveolar MAC, and
hence, blood and brain tissue levels. Perioperatively, there is no current method to
directly measure brain tissue concentration or alveolar concentration.
– 1 MAC, however, does not reflect an individual’s response, and additionally, it does not
guarantee amnesia.
• Factors increasing MAC.
– Infants: Generally higher, the exception being neonates which have a lower MAC value.
The MAC value peaks at approximately 6 months of age (3).
– Hyperthermia
– Chronic alcoholism
– Thyrotoxicosis
– Hypernatremia
– Genetic factors: Patients with red hair have an approximately 19% increased requirement.
– Sympathetic drugs:
Monoamine oxidase inhibitors (MAOIs)
Tricyclic antidepressants (TCAs)
Acute cocaine
Acute amphetamines
Ephedrine
Levodopa
• No effect on MAC
– Duration of anesthesia
– Gender
– Hypocarbia and mild hypercarbia
• Factors decreasing MAC:
– Increasing age: MAC decreases by approximately 6% per decade (3)
– IV anesthetics such as dexmedetomidine, propofol, ketamine, barbiturates, clonidine
– Anxiolytics
– Narcotics
– IV local anesthetics such as lidocaine
– Hypothermia: For every 10°C decrease, there is a 50% decrease
– Acute alcohol intoxication
– Pregnancy: After ~8 weeks of gestation, decreases are seen. Levels can decrease by up to
30% during pregnancy and return to normal within 3 days postpartum (4).
– Hypotension (MAP <40 mm Hg)
– Hyponatremia
– Metabolic acidosis
– Anemia (hematocrit <10%)
– Hypercarbia (paCO2 >95 mm Hg)
– Hypoxia (paO2 <38 mm Hg)
• MAC is an additive value and provides a point of reference for the varying stages of
anesthesia. The caveat is that MAC is independent of other factors that may or may not be
taken into account and is based on the average individual in the population. As with most
averages, there are outliers (1).
• MAC-95 is the alveolar concentration at which 95% of patients will not move in response to
surgical stimuli (skin incision). It is measured at approximately 1.2–1.3 MAC for isoflurane,
sevoflurane, and desflurane.
• MAC BAR is the alveolar concentration at which 50% of patients do not exhibit a
sympathetic response (heart rate, blood pressure, noradrenaline levels) to surgical
stimulation. It is approximately 1.6 MAC for isoflurane, sevoflurane, and desflurane.
• MAC BAR95 is the alveolar concentration where 95% of patients do not exhibit a
sympathetic response to surgical incision.
• MAC EI is the alveolar concentration to prevent laryngeal response to endotracheal tube
intubation. It is approximately 1.3 MAC for isoflurane, sevoflurane, and desflurane.
• MAC-hour is the MAC time for exposure to the volatile agent; MAC is multiplied by hour
increments. For example, 1.25 MAC for 2 hours represents 2.5 MAC-hours. It is used as a
comparative measure of exposure when calculating adverse effects and setting dose-limits. It
does not account for difference in metabolism, effects at different concentrations, and fresh
gas flow.
• MAC-awake is the alveolar concentration at which 50% of patients voluntarily respond
(open eyes) to verbal command. It is NOT equivalent to MAC aware/recall. It is measured as
approximately 0.3–0.4 MAC for isoflurane, sevoflurane, and desflurane and approximately
0.5 MAC for nitrous oxide and halothane.
• MAC-aware is the MAC value at which 50% of patients are aware of surgical events despite
some anesthetic being on board. MAC-aware is generally 0.4–0.5. However, for 95%
confidence, the MAC value for awareness is generally up to ∼25% higher.
GRAPHS/FIGURES
See Table
REFERENCE
1. Quasha AL, Eger EL II, Tinker JH. Determination and applications of MAC. Anesthesiology.
1980;53:315–334.
2. Yasuda N, Lockhart SH, Eger EI. Kinetics of desflurane, isoflurane, and halothane in
humans. Anesthesiology. 1991;74:489–498.
3. Lerman J, Schmitt-Bantell BI, Gregory GA. Effect of age on the solubility of volatile
anesthetics in human tissue. Anesthesiology. 1986;65:307–311.
4. Chan MTV, Gin T. Postpartum changes in the minimum alveolar concentration of
isoflurane. Anesthesiology. 1995;85:1360–1363.
ADDITIONAL READING
• Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott
Williams & Wilkins; 2006.
• Chestnut DH. Obstetric Anesthesia. 3rd ed. Philadelphia: Elsevier-Mosby: 2004.
• Eger EI, Eisenkraft JB, Weiskopf RB. The pharmacology of inhaled anesthetics, Dannemiller;
2002.
• Awareness under anesthesia
• FAlveolar
CLINICAL PEARLS
• MAC is the minimum concentration of gas where 50% of average patients do not move in
response to a surgical stimulus.
• MAC is affected by many factors including age and concomitant drug administration.
MINUTE VENTILATION
Stephane Ledot, MD
Yoram G. Weiss, MD, MBA, FCCM
BASICS
DESCRIPTION
• Minute ventilation (MV) is the volume of all inhaled or exhaled gas in one minute. It is
calculated by the multiplication of the tidal volume (VT) and respiratory rate (RR): MV =
VT × RR.
• During spontaneous ventilation, MV is under tight control by the respiratory center in the
brainstem.
– Central and peripheral feedback mechanisms adjust MV to deliver adequate oxygen to the
tissues while removing CO2 from the lungs.
– At rest, for an average adult, normal tidal volume is ∼500–600 mL (6–8 mL/kg) and the
respiratory frequency is around 12–22 breaths per minute. This results in a normal MV of
∼7–8 liters per minute.
• Under general anesthesia, the patient can either breathe spontaneously or be mechanically
ventilated. Anesthetic agents have dose-dependent effects on the medullary respiratory
center that affect MV in both the spontaneously ventilating and postoperative patient.
• MV in the spontaneously ventilating (SV) patient is tightly regulated by the respiratory
control center, located in the medulla oblongata. It receives afferent input from
mechanoreceptors, chemoreceptors, baroreceptors, and proprioceptors, as well as voluntary
control from the cerebral cortex and temperature.
• Brainstem respiratory control center is divided into the:
– Inspiratory center: Efferent nerves stimulate spontaneous and rhythmic contraction of the
diaphragm (phrenic nerves) and intercostal muscles.
The apneustic center, located in the pons, provides a constant stimulus to the inspiratory
center and is inhibited by the pneumotaxic center.
The pneumotaxic center, also located in the pons, provides inhibitor impulses that limit
phrenic nerve contraction and overdistension. It antagonizes the apneustic center
(constant stimulus) and decreases tidal volume; the absence of the pneumotaxic center
would result in increased tidal volume and decreased RR.
The Hering–Breuer reflex consists of afferent receptors located in the bronchi and
bronchioles that are activated by stretching and non-stretching. Efferent impulses are
transmitted via the vagus nerve to the respiratory center. Thus, inflation acts to inhibit
inhalation and prevent further inflation. As the expiratory phase begins, the receptors
are no longer stretched, impulses are no longer sent, and inhalation can begin again.
– Expiratory center: Under normal, resting conditions, expiration is a passive process via
relaxation of the diaphragm and intercostals as well as elastic recoil of the lungs; there is
no activity within the expiratory center. With “fight or flight,” the center stimulates
forceful expiration by contraction of the abdominal and internal intercostals.
• Afferent input to the respiratory center.
– Chemoreceptors: Function to maintain carbon dioxide, pH, and oxygen homeostasis by
adjusting the rate, depth, and rhythm of respiration. Central chemoreceptors are cells
located in the ventrolateral medulla (surface of the fourth ventricle) that are sensitive to
the pH of the cerebrospinal fluid (CSF); they provide feedback to the medullary
respiratory center. An acidic CSF stimulates increases in MV, whereas an alkalotic CSF
inhibits the inspiratory center. Peripheral chemoreceptor cells are located in the carotid
bodies and aortic arch and respond to O2 and CO2 concentrations in the arterial blood;
they transmit information via the glossopharyngeal nerve (IX) and the vagus nerve (X),
respectively, to the respiratory center; their feedback regulates the MV on a breath by
breath basis.
– Baroreceptors: The most important groups are situated in the carotid sinus and aortic arch.
An increase in arterial blood pressure can cause reflex hypoventilation or apnea.
Conversely, hypotension elicits a sympathetic baroreceptor reflex.
– Proprioceptors are located in muscles, tendons, and joints that sense movement. During
“fight or flight,” these receptors transmit signals to the respiratory center that increase the
RR and tidal volume.
– Cerebral cortex: Voluntary control can be exerted to take deep, slow breaths.
– Temperature: In hypothermic states, MV decreases via:
Impairment of synaptic transmission.
Decreased velocity of neuronal conduction; the ventral surface of the medulla is
particularly prone.
Respiratory muscles and motor neurons do not appear to be affected by hypothermia.
• Ventilation: The relationship between ventilation and PaCO2 is described as follows: PaCO2
= (k) (VCO2)/VA, where k is a constant that corrects for the units (k = 0.863), VCO2 is the
metabolic production of carbon dioxide, and VA is alveolar ventilation. To maintain
homeostasis, increases or decreases in the PaCO2 are met by respective increases or
decreases in VA.
• Composition of the MV is equal to the sum of alveolar ventilation and dead space
ventilation.
– Alveolar ventilation (VA): The volume of inspired gases reaching the alveoli and taking
part in gas exchange in one minute.
– Dead space (VD): The volume of inspired gas that does not participate in gas exchange. It
comprises gases in non-respiratory airways (conducting airways also known as anatomic
dead space) and alveoli that are not perfused (alveolar dead space).
• A progressive increase in MV starts soon after conception and peaks at 50% above normal
levels around the second trimester.
– Oxygen consumption increases gradually in response to the needs of the growing fetus,
culminating in a rise of at least 20% at term. During labor, oxygen consumption is further
increased (up to 60%) as a result of the exaggerated cardiac and respiratory work load.
– Progesterone stimulates ventilation by lowering the CO2 threshold of the respiratory
center and may also act as a primary stimulant.
– There is a 40% rise in TV and 15% rise in RR. Since dead space remains unchanged,
alveolar ventilation is about 50% higher at the end of gestation.
– Because the increase in MV exceeds the CO2 production, the normal PaCO2 decreases to
∼32 mm Hg. The increased secretion of renal bicarbonate partially compensates for the
hypocarbia so that pH increases only slightly (from 7.42 to 7.44).
• The increased MV is in response to the increased metabolic demands of growth.
– In neonates, the oxygen consumption is 4–6 mL/kg (compared to 2 mL/kg in adults).
– MV is 200 mL/kg/min in the newborn compared to 100 mL/kg/min at puberty. Alveolar
ventilation is also double of that of an adult.
– Tidal volume remains constant at 7 mL/kg throughout life, with the increase in MV
primarily from an increase in RR. In neonates, the RR is ∼ 3 times that of an adult (∼30
breaths/minute) and progressively falls to adult values at adolescence.
– Immature respiratory control is responsible for an increased risk of postoperative severe
hypoventilation and apnea in preterm infants.
• In the elderly patients, MV at rest is maintained despite decreases in tidal volume secondary
to increased RR. These changes are due to decreases in chest wall compliance as well as
changes in the function of central chemoreceptors and peripheral mechanoreceptors in the
chest wall and lung parenchyma. A reduction of 50–60% in the ventilatory response to
hypoxia and hypercapnia is observed.
• Alveolar hypoventilation: Normal and continued removal of CO2 from the blood is
dependent on adequate MV. In the event that VA is affected, or does not adequately
complement changes in PaCO2, a respiratory acidosis or alkalosis may result.
• Obesity hypoventilation syndrome (OHS) or Pickwickian syndrome: Defined as a
combination of obesity (BMI >30 kg/m2) and awake arterial hypercapnia (PaCO2 >45 mm
Hg) in the absence of other known causes of hypoventilation. Although the precise
mechanism is unknown, it is believed to result from the combination of:
– Impaired respiratory mechanics reflective of a restrictive ventilatory defect: OHS patients
have decreased total lung capacity, vital capacity, functional residual capacity, and
compliance as well as increased residual volume, work of breathing, and airway
resistance.
– Abnormal medullary respiratory center control: OHS patients appear to lack a
compensatory increased ventilatory drive to offset the effects of the mechanical
restrictions of obesity. Conversely, obese patients without OHS appear to have an
augmented ventilatory response.
– Neurohormonal aberrancies: Leptin is normally produced by the adipose tissue and acts on
the central respiratory center to stimulate ventilation. In OHS patients, there appears to be
a leptin deficiency that results in hypoventilation.
• COPD: Hypoventilation is secondary to multiple mechanisms. Patients usually present with
severe airway obstruction as well as a decreased responsiveness to hypoxia and
hypercapnia. In advanced stages, or periods of decompensation, tidal volume is decreased,
RR is increased, and work of breathing is increased resulting in a rapid shallow respiratory
pattern. In addition, diaphragmatic dysfunction may result from muscle fatigue and limited
movement, leading to an increased VD/VA. In patients with airflow obstruction,
inhomogeneities in ventilation are responsible for the increase in dead space.
• General anesthesia.
– Equipment or apparatus dead space is increased and can be clinically relevant in low MV
ventilation states or in pediatrics. To avoid hypercarbia and acidosis, measures to decrease
the dead space volume or increase MV need to be adjusted accordingly.
– Inhaled anesthetics produce dose-dependent and drug-specific effects on the breathing
pattern, ventilatory response to CO2 and hypoxemia, and airway resistance. The net effect
is a rapid and shallow pattern of breathing, a net decrease in MV, and increase in the
PaCO2.
Tidal volumes are decreased via direct depression of the medullary respiratory center
(central effect), as well as impaired intercostal muscle and diaphragm function
(peripheral effect).
There is reduced activity of the pre-Bötzinger complex situated in the ventrolateral
medulla of the brainstem; this area is assumed to be the core of the respiratory rhythm
generation (respiratory pacemaker).
The GABA agonist effect inhibits both inspiratory and expiratory neurons.
– Intravenous anesthetics: Propofol, barbiturates, and benzodiazepines, with the exception
of ketamine, produce central nervous system depression via their ability to enhance the
effects of the inhibitory neurotransmitter GABA and depress the respiratory centers. These
agents block mechanoreceptor transmission to the respiratory centers and provoke an
apneustic breathing pattern. They also cause a depressant effect on bulbospinal expiratory
neurons due to their inhibition of the NMDA receptor.
– Opioids produce dose-dependent depression of the respiratory rate with compensatory
increases in the tidal volume; apnea results at high doses. Effects are primarily through:
An antagonist effect on the medullary respiratory center (mediated by the μ opioid
receptors) as well as the pre-Bötzinger complex in the ventrolateral medulla.
Also affects the Kölliker-Fuse and parabrachial nucleus of the dorsolateral pons
(pneumotaxic centre).
• Neuraxial anesthesia: Spinal and epidural anesthesia have very little effect on the pulmonary
function (lung volumes, resting MV, dead space, and shunt fraction). In the event of a high
block, active inspiratory volumes could be affected by abdominal muscle paralysis. This
effect may be more pronounced in patients with pulmonary disease (e.g., COPD) that rely
on accessory muscles to maintain the MV. In addition, neuraxial opioids (intrathecal and
epidural) can result in immediate or delayed respiratory depression.
EQUATIONS
• MV = VT × RR; where MV is minute ventilation, VT is tidal volume, and RR is respiratory
rate.
• PaCO2 = (k)(VCO2)/VA; where PaCO2 is the partial pressure of carbon dioxide in the
arterial blood, k is a constant that corrects for units (k = 0.863), VCO2 is the metabolic
production of carbon dioxide, and VA is alveolar ventilation.
REFERENCES
1. Quanjer PH, et al. Lung volumes and forced ventilatory flows. Report Working Party
‘Standardization of Lung Function Tests’. European Community for Steel and Coal. Eur
Respir J Sippl. 1996;16:5–40.
2. Powell FL, et al. Comparative physiology of lung complexity: Implications for gas
exchange. News Physiol Sci. 2004;19:55–60.
3. Hendenstierna G, et al. The effects of anesthesia and muscle paralysis on the respiratory
system. Intensive Care Med. 2005;31:1327–1335.
4. Yamakaye M, et al. Changes in ventilatory pattern and arterial oxygen saturation during
spinal anesthesia in man. Acta Anaesthesia Scand. 1992;35:569–571.
5. Douglas NJ, et al. Respiration during sleep in normal man. Thorax. 1982;37:840–844.
6. Hegewald MJ, et al. Respiratory physiology in pregnancy. Clin Chest Med. 2011;32:1–13.
7. Barnes PJ, et al. Chronic obstructive pulmonary disease. N Engl J Med. 2000;343(4):269–
280.
8. Berger AJ, et al. Regulation of respiration. N Engl J Med. 1977;297(4):194–201.
9. Olson AL, Zwillich C. The obesity hypoventilation syndrome. Am J Med. 2005;118:948–
956.
ADDITIONAL READING
• Guyton and Hall. Textbook of Medical Physiology. 12th ed. Saunders Elsevier; 2011.
• John B West. Respiratory physiology: The essentials. 8th ed. Lippincott Williams and
Wilkins; 2008.
• Dead space
• Mechanical ventilation
• Tidal volume
• Carotid body
CLINICAL PEARLS
• MV is the product of tidal volume and respiratory rate and is ∼7–8 liters per minute for a
normal adult.
• Alveolar ventilation is the volume of inspired gases reaching the alveoli and taking part in
gas exchange in one minute.
• Volatile and intravenous agents, including opioids, have direct and indirect effects on the
tidal volume and the respiratory rate.
• Physiological and pathophysiological changes in MV produced by induction and
maintenance of anesthesia must be understood and addressed to safely maintain adequate
gas exchange. Elderly and pregnant patients demonstrate changes in normal physiologic
respiratory patterns as do obese and COPD patients.
MITRAL REGURGITATION
BASICS
DESCRIPTION
• The mitral valve, normally consists of two leaflets (bicuspid valve) that open during
ventricular diastole and close during systole. During systole, the mitral valve closes and
prevents the backflow of blood from the left ventricle (LV) to the left atrium (LA). Closure
of the valve helps maintain LV diastolic pressure and volume and thus systemic and
coronary perfusion pressure.
• Mitral regurgitation (MR) is the presence of a backflow leak through the valvular apparatus
during systole.
– Ranges in severity from trace, mild, moderate, to severe. Severity is classified by the
amount of regurgitant volume, regurgitant orifice area size, and regurgitant fraction by
echocardiography.
– Acute MR is the sudden onset of symptoms usually due to an acute event such as
myocardial infarction and valvular apparatus trauma or disruption.
– Chronic MR has a gradual onset and may be sustained for many years and may be
compensated or uncompensated.
EPIDEMIOLOGY
Incidence
• Rheumatic heart disease is the most common cause of MR world-wide; mitral valve prolapse
is the most common cause in the US (accounts for 45%).
• Mean age of rheumatic MR is 36 years old.
• Following a myocardial infarction, 20–30% of patients develop MR.
Prevalence
• Mitral valve prolapse is present in ~4% of the population
• Under 20 years of age, males > females
• Males >50 years of age have more severe disease
Morbidity
• Acute MR has a higher rate of morbidity and mortality due to the pathophysiology. Acute
congestive heart failure (CHF) and cardiogenic shock may occur. Operative mortality is near
80%.
• Chronic MR may be asymptomatic for years. Chronic severe MR will lead to eventual
decompensation with diastolic and systolic dysfunction and CHF.
• Surgical management becomes the common end point to both acute and chronic MR.
• Global and regional left atrial (LA) functions are altered in patients with chronic MR
secondary to myxomatous mitral valve disease (1)[C].
• Left ventricular dysfunction may be present with MR and may be underestimated in severe
MR. The decreased after load on the LV with backward flow through the mitral valve gives
the false appearance of normal function. In severe MR, a low LV ejection fraction carries a
very poor prognosis.
Mortality
• MR due to flail leaflets and LA diameter of >55 mm is associated with increased mortality
under medical management (2)[B].
• Mild MR is an independent predictor of post-MI mortality.
• Atrial fibrillation was identified by multivariate logistic regression analysis as a predictor of
in-hospital death after non-cardiac surgery; OR 11.579 (3)[B].
May be associated with any condition that alters mitral valve closure. Organic, also known as
intrinsic valve disease, may be due to myxomatous changes, rheumatic heart disease, mitral
valve prolapse, or calcific valve disease. Functional MR results from a non-valvular disease
such as dilated cardiomyopathy, causing incomplete closure of the mitral valve.
PATHOPHYSIOLOGY
• Acute MR is often due to ruptured chordae or papillary muscle resulting in an acute increase
in LV diastolic volume, LA volume, LV ejection fraction (EF), and aortic systolic pressure.
Acute fulminant CHF may ensue and is marked by a decrease in contractility and EF. Mitral
valve prolapse and tissue diseases (e.g., rheumatic heart disease, myxomatous disease) may
present with an acute phase that is often milder in onset and leads to chronic MR.
• Chronic MR has a more insidious onset and may take months to years to become
symptomatic. Eccentric left ventricular hypertrophy, atrial enlargement, and increased heart
rate compensate for the extra volume of regurgitation; ejection fraction is maintained and
symptoms typically do not appear without exertion or positional changes. As regurgitant
volume and MR worsen over time, the left ventricle decompensates. The ventricle becomes
too enlarged and the increased wall stress and decreased myocardial perfusion lead to
diminishing EF and CHF, end organ hypoperfusion, decreased coronary perfusion pressure,
increased myocardial oxygen demand, and cardiogenic shock. In addition, increases in LA
pressure lead to pulmonary congestion and eventually chronic decompensated CHF with
right ventricular failure. LA enlargement leads to atrial fibrillation which diminishes
forward flow and increases the risk of thrombus formation. Sympathetic stimulation
increases systemic vascular resistance to maintain pressure but worsens MR. Without timely
surgical repair, the heart may not be able to significantly recover.
• Maintain high-normal sinus rhythm to minimize regurgitant time and excessive left
ventricular filling.
• Systemic vascular resistance may be decreased, but should be balanced between facilitating
forward flow (decreasing regurgitation) and maintaining adequate coronary and systemic
perfusion pressure.
• Careful fluid management and inotropic support to prevent cardiovascular overload or
collapse.
• Decrease pulmonary hypertension by avoiding increased pulmonary vascular resistance from
hypoxia, hypercapnia, acidosis, and pulmonary vasoconstrictors.
• Maintain contractility with inotropes if unresponsive to volume and afterload changes.
SYMPTOMS
• Fatigue
• Palpitations
• Orthopnea
• Angina
History
• Family history of cardiac valvular disease, collagen or connective tissue disease, or
congenital malformations.
• History of rheumatic disease or risk factors for endocarditis.
• Commonly diagnosed after symptomatic exercise or during work up for diastolic or systolic
CHF.
• May be discovered early after detailed physical exam and heart auscultation of murmur.
• Usually classified by echocardiographic measurement of color Doppler flow across the valve.
Signs/Physical Exam
• Systolic murmur
• Signs of congestive heart failure
• Endocarditis
• Cyanosis
TREATMENT HISTORY
• Medical management of angina, CHF, diabetes, hypertension, and hyperlipidemia, if
associated.
• Balloon mitral valvuloplasty or valve replacement.
• Previous treatment of infective endocarditis.
• Anticoagulation or ablation for atrial fibrillation.
MEDICATIONS
• Antihypertensives including calcium channel blockers and avoiding beta-blocker
bradycardia.
• Anti-anginals including nitrovasodilators.
• Heart failure treatments including digoxin, ACEI/ARB, and diuretics.
• Statin therapy if indicated.
Labs/Studies
• Basic metabolic profile: Monitoring electrolytes and the kidney function.
• Complete blood count: Monitoring for preoperative infection and hematocrit and platelet
counts adequate for surgery.
• Basic coagulation studies: Evaluation of liver function and adequate levels for surgery.
• Electrocardiogram: Diagnosis of arrhythmia and ischemic changes.
• Chest X-ray: Cardiopulmonary status
• CT scan for evaluation of aorta.
• Echocardiogram: Diagnosis and classification of disease severity and ventricular function.
• Concomitant mitral stenosis or aortic valve disease in rheumatic heart disease
• Ischemic cardiomyopathy or hypertrophic cardiomyopathy
• Hypertension
• Pulmonary hypertension, congestion, and pleural effusion
• Severe decompensated symptomatic MR with decreased left ventricular function for non-
cardiac surgery
• Recent MI or stroke
• Unrelated end organ failure
CLASSIFICATIONS
Severe mitral regurgitation criteria:
• >60 mL regurgitant volume
• >50% regurgitant volume
• Effective regurgitant orifice area >0.4 cm2
• Color Doppler vena contracta >0.7 cm
• Pulmonary vein flow reversal on ventricular systole
• Severe LA enlargement
• MR jet ‘V’ wave and PCWP cannon “V” wave
TREATMENT
Premedications
Midazolam to prevent anxiety and increased sympathetic tone.
Risk for intraoperative stroke, myocardial infarction, and death should be discussed.
INTRAOPERATIVE CARE
• Depends on the procedure; sedation, general (endotracheal tube or laryngeal mask airway),
and regional anesthesia may be utilized.
• Neuraxial techniques can result in a sympathectomy and facilitate forward flow (reduce
regurgitation), but may reduce coronary perfusion pressure.
Monitors
• Invasive monitors may be chosen based upon the severity of MR and the surgical procedure:
5 lead EKG, arterial line, central venous catheter, pulmonary artery catheter,
transesophageal echocardiogram or less invasive cardiac output monitors.
• Smooth controlled induction to maintain vital signs within normal limits.
• Anticholinergic medications may be administered to maintain high-normal heart rate.
Maintenance
• Volatile anesthetics, intravenous, or a combination may be utilized. Reductions in systemic
vascular resistance are desirable to facilitate forward flow; however, adequate cerebral and
coronary perfusion should be ensured. Total intravenous techniques may be associated with
bradycardia, particularly if utilizing high doses of remifentanil.
• Fluid balance includes maintaining normal preload and a hematocrit >24–30% to optimize
forward flow and myocardial oxygen balance. Excessive preload may add to regurgitant
volume and cause LV failure.
No additional concerns
POSTOPERATIVE CARE
BED ACUITY
Depends on surgical procedure and severity of underlying disease.
Standard postoperative fluid and electrolyte management and related laboratory studies.
COMPLICATIONS
Perioperative arrhythmia
REFERENCES
1. Moustafa SE, et al. Global left atrial dysfunction and regional heterogeneity in primary
chronic mitral insufficiency. Eur J Echocardiogr. 2011; 12(5):384–393.
2. Rusinaru D, et al. Left atrial size is a potent predictor of mortality in mitral regurgitation
due to flail leaflets: Results from a large international multicenter study. Circ Cardiovasc
Imaging. 2011; 4(5):473–481.
3. Lai HC, et al. Mitral regurgitation complicates postoperative outcome of noncardiac
surgery. Am Heart J. 2007;153(4):712–717.
4. Grigioni F, et al. Ischemic mitral regurgitation: Long-term outcome and prognostic
implications with quantitative Doppler assessment. Circulation. 2001;103:1759–1764.
ADDITIONAL READING
• 2006 American College of Cardiology/American Heart Association guidelines.
CODES
ICD9
• 394.1 Rheumatic mitral insufficiency
• 424.0 Mitral valve disorders
• 746.6 Congenital mitral insufficiency
ICD10
• I05.1 Rheumatic mitral insufficiency
• I34.0 Nonrheumatic mitral (valve) insufficiency
• Q23.3 Congenital mitral insufficiency
CLINICAL PEARLS
• Etiologies of mitral regurgitation are either:
– Organic from intrinsic valvular causes such as myxomatous, rheumatic, or calcific disease.
– Functional from non-valvular causes such as dilated cardiomyopathy that result in
incomplete closure.
• Mitral regurgitation is described based upon onset:
– Acute: life-threatening and may require immediate surgical management.
– Chronic: requires medical or surgical management and may be asymptomatic until late
stages.
• Severity is classified by echocardiographic criteria. Severe MR will have a regurgitant
volume that is >60 mL or >50%, or an effective regurgitant orifice area >0.4 cm2.
Significant signs and symptoms are present (shortness of breath, systolic and diastolic
congestive heart failure).
MITRAL STENOSIS
BASICS
DESCRIPTION
• Mitral valve stenosis (MS) is a narrowing of this area at the valve itself. New criteria for
diagnosis of severe mitral stenosis includes an open area of <1.0 cm2 with a transvalvular
mean gradient of >10 mm Hg, although symptoms may begin at much earlier stages of
stenosis.
EPIDEMIOLOGY
Incidence
Most common after rheumatic fever with a latency period of 10–25 years in under-developed
countries to 20–40 years in developed countries.
Prevalence
• Women: 1.6%
• Men: 0.4% (1)[B]
Morbidity
• Risk for congestive heart failure, atrial fibrillation, thromboembolism, stroke, pulmonary
hypertension, right-sided heart failure, and pulmonary edema.
• Mitral stenosis with atrial fibrillation increases the risk of stroke 7–15% per year (2)[B].
• Mild to moderate MS may be asymptomatic except during exertion, while severe MS
symptoms occur at rest.
• LV dysfunction may occur in 30% of MS patients.
Mortality
2-year mortality for infants with severe congenital MS is 40% (3)[B].
• Majority of cases are due to rheumatic fever and resultant rheumatic heart disease.
• Severe mitral calcification and congenital mitral stenosis are uncommon causes.
PATHOPHYSIOLOGY
• The basic pathophysiology of MS stems from obstruction of left ventricular filling with a
highly resistant valve opening. The disease process progresses as follows:
– Initially, the resistance to left ventricular filling is compensated by left atrial hypertrophy
(enhanced atrial kick).
– With time, the left atrium begins to dilate to handle the increase in volume
– However, the volume overload eventually overwhelms the left atrium and LV filling
becomes impaired. Fluid backs up into the pulmonary vasculature leading to pulmonary
congestion, left congestive heart failure, and resultant right heart failure.
• Left atrial enlargement increases the risk for developing atrial fibrillation. In addition, the
decreased flow state increases the risk for thrombus formation.
• Normal sinus rhythm and a slow rate are desired to allow time for forward flow and filling
of the left ventricle
• Primary goals are the maintenance of:
– Cardiac output
– Coronary perfusion (diastolic perfusion pressure)
– Normal and slow sinus rhythm
– Volume status
– Prevention of cardiac decompensation
• Inotropic support may be necessary to prevent cardiovascular overload or collapse.
Vasopressor support and fluid maintenance may help maintain preload and coronary
perfusion pressure.
• Pulmonary hypertension is a major concern and may persist after mitral valve repair.
Resulting right ventricular (RV) dysfunction may be a greater concern than left ventricular
(LV) dysfunction.
SYMPTOMS
• Severity of symptoms may be classified by NYHA I–IV.
• Exertional shortness of breath, orthopnea, fatigue, palpitations, and rarely chest discomfort.
• Severe symptoms occur from pulmonary edema, pulmonary hypertension, and decreased
cardiac output with resultant dyspnea, angina, cough, and hemoptysis.
History
Commonly diagnosed after symptomatic exercising, during work up for diastolic or systolic
CHF, or new onset atrial fibrillation.
Signs/Physical Exam
• Mid-diastolic murmur with opening S2 snap.
• Congestive heart failure (jugular venous distention, pitting edema, shortness of breath) and
increased sympathetic tone (cool extremities, hypertension, etc.).
• In infants: Cyanosis, poor growth, shortness of breath.
TREATMENT HISTORY
• Balloon mitral valvuloplasty or valve replacement
• Atrial fibrillation: Ablation
MEDICATIONS
• Beta blockers to maintain a slow normal sinus rhythm.
• Heart failure treatments including digoxin and ACEI/ARBs, diuretics, nitrates.
• Anticoagulants to prevent or treat thrombus.
• Atrial fibrillation: Amiodarone, beta blockers, calcium channel blockers.
Labs/Studies
• Basic metabolic profile: Electrolytes and kidney function aid with perioperative management
and risk stratification (renal failure carries an increased risk of mortality).
• Complete blood count: Preoperative infection, hematocrit, and platelet counts adequate for
surgery.
• Basic coagulation studies
• Chest X-ray: Active congestive heart failure.
• Transesophageal echocardiogram: Diagnosis and classification of disease severity and
ventricular function.
• Cardiac catheterization: Cardiac function and pulmonary pressure evaluation.
• Cardiac: Left ventricular dysfunction, hypertension; mitral regurgitation (due to poor valve
closure); aortic stenosis or regurgitation in rheumatic heart disease.
• Pulmonary: Hypertension, congestion, and pleural effusion.
• Decompensated congestive heart failure
CLASSIFICATIONS
• Based upon echocardiographic or cardiac catheterization measurements of valve area and
transvalvular pressure gradients.
• Mitral stenosis severity by valve area.
– Normal: 4–6 cm2
– Mild stenosis: <2.5 cm2
– Moderate stenosis: 1.0–1.5 cm2
– Severe stenosis <1.0 cm2
• Mitral stenosis severity by mean pressure gradient (PG)
– Mild stenosis: <5 mm Hg
– Moderate stenosis: 5–10 mm Hg
– Severe stenosis: >10 mm Hg
• Mitral stenosis severity by pressure half time (PHT)
– Mild stenosis: 100–150 milliseconds
– Severe stenosis: >220 milliseconds
TREATMENT
Premedications
Benzodiazepines may be useful to prevent anxiety and tachycardia.
• Risk for intraoperative stroke, acute congestive heart failure, myocardial infarction, and
death, if increased risk, should be discussed.
• Access and monitoring line placement, if needed.
INTRAOPERATIVE CARE
• Depends on the procedure; sedation, general anesthesia (endotracheal tube or laryngeal
mask airway (LMA), and regional techniques may be utilized.
• Neuraxial techniques can result in a sympathectomy and decreased systemic vascular
resistance that can impair coronary perfusion and decrease venous return (preload). It may
be considered in mild or moderate MS. Epidurals allow for slow bolusing and time for fluid
loading and treatment of hypotension with vasopressors. Carefully confirm appropriate
anticoagulation status and profile before proceeding.
Monitors
• 5 lead EKG: Arrhythmia, ischemia
• Arterial line: Beat-to-beat BP monitoring
• Invasive monitors may be chosen based on the severity of MS and the surgical procedure.
Smooth, controlled induction to maintain vital signs within normal limits (heart rate and
systemic vascular resistance) and allow time for treatment.
Maintenance
• Volatile anesthetics, intravenous, or a combination may be utilized. The specific drug is less
important than the overriding goal: maintain normal sinus rhythm, systemic vascular
resistance, contractility, and preload. Anesthetic agents can decrease vascular resistance and
need to be titrated appropriately, co-administered with phenylephrine, or co-administered
with other adjunctive agents (e.g., opioids) to decrease the total dosage.
• Adequate preload is essential to maintaining a stable cardiac output. Left ventricular filling
is impaired with right ventricular and left atrial dysfunction thus predisposing to pulmonary
edema.
• Maintenance of normal sinus rhythm is achieved by minimizing cardiac stress and avoiding
pro-arrhythmic drugs.
– Caution should be exercised when administering powerful chronotropes or
anticholinergics. Tachycardia increases myocardial oxygen consumption, decreases
diastolic time, and decreases LV filling.
– Hypotension and hypertension should be managed with rate and rhythm in mind. All
inotropes and vasopressors may be used with caution.
– Ischemia usually occurs with arrhythmia, tachycardia, or hypotension, and the treatment
usually lies in the reversal of those conditions.
• Hyperoxia, hypocarbia and pulmonary vasodilators may improve pulmonary resistance.
• Avoid tachycardia and hypotension; consider having rapid onset and short-acting beta
blockers and antihypertensives immediately available.
• Standard extubation criteria.
POSTOPERATIVE CARE
BED ACUITY
Depends on the surgical procedure, severity of underlying disease, and intraoperative events.
Cardiology consultation may be considered in severe diseases if ischemic events occur
intraoperatively.
COMPLICATIONS
• Mental status changes and stroke
REFERENCES
1. Movahed MR, et al. Increased prevalence of mitral stenosis in women. J Am Soc
Echocardiog. 2006; 19:911–913.
2. Carabello BA. Modern management of mitral stenosis. Circulation. 2005;112:432–437.
3. Moore P, et al. Severe congenital mitral stenosis in infants. Circulation. 1994;89:2099–
2106.
ADDITIONAL READING
• Nishimura RA, et al. ACC/AHA 2008 Guideline update on valvular heart disease: Focused
update on infective endocarditis: A report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines endorsed by the Society of
Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions,
and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;52(8):676–685.
• Mitral valve replacement
• Left ventricular end diastolic pressure (LVEDP)
CODES
ICD9
• 394.0 Mitral stenosis
• 424.0 Mitral valve disorders
• 746.5 Congenital mitral stenosis
ICD10
• I05.0 Rheumatic mitral stenosis
• I34.2 Nonrheumatic mitral (valve) stenosis
• Q23.2 Congenital mitral stenosis
CLINICAL PEARLS
• Mitral stenosis is most commonly an acquired disease but may be related to congenital
malformations and rheumatic heart disease.
• Significant signs and symptoms include shortness of breath, fatigue, palpitations, diastolic
and systolic congestive heart failure, and thromboembolism.
• Severity is classified by valve area and transvalvular gradients. Severe disease is defined as a
valvular area <1.0 cm2 and mean PG of >10 mm Hg
• Maintenance of general anesthesia includes supporting cardiac diastolic function, optimizing
fluid management, sustaining a normal and slow sinus rhythm, and monitoring for
arrhythmia and pulmonary edema.
MITRAL VALVE PROLAPSE
Alain A. Salvacion, MD
James D. Boone, MD
BASICS
DESCRIPTION
• Mitral valve prolapse (MVP) is the systolic displacement of varying portions of one or both
of the mitral, bicuspid leaflets above the mitral annulus into the left atrium.
• Echocardiographic MVP is defined as single or bileaflet prolapse at least 2 mm above the
annular plane, with or without leaflet thickening.
EPIDEMIOLOGY
Incidence
Equally distributed between men and women; more common in young women, but higher
incidence of complications in men.
Prevalence
• Most commonly diagnosed cardiac valvular abnormality.
• 2–3% of the general population based on current criteria.
• MVP in Marfan syndrome is reported to be between 40 and 80%
Morbidity
• Most patients are asymptomatic.
• MVP syndrome includes atypical chest pain, dyspnea, palpitations, syncope, and anxiety.
• Serious complications, such as endocarditis, cerebrovascular events, progressive mitral
regurgitation (MR), arrhythmias, and sudden cardiac death, are uncommon but related to
higher morbidity.
• Moderate to severe MR and depressed left ventricular (LV) function are major risk factors
for complications.
• Mild MR, flail leaflet, left atrial enlargement, atrial fibrillation, and age older than 50 are
minor risk factors for complications.
Mortality
• Usually has a benign course and excellent prognosis.
• Survival rate is similar to that in an age-matched and sex-matched population without MVP.
• Well-recognized association with connective tissue disorders such as Marfan syndrome
(∼90% prevalence), Ehlers–Danlos, and osteogenesis imperfecta.
• Most cases are sporadic, but can also be familial.
PATHOPHYSIOLOGY
• Related to histological valve tissue abnormalities, geometric discrepancies between the LV
and MV, or several connective tissue disorders.
• Myxomatous degeneration, characterized by leaflet thickening and redundancy, is the most
common and clinically important abnormality.
• Distinguish patients with functional MVP from those with advanced disease and associated
hemodynamically significant MR.
• Patients with functional MVP are younger and have fewer risk factors for anesthesia. In
these patients, increased LV emptying should be avoided because this will accentuate MVP
and lead to increased MR; therefore, hemodynamic goals should include avoiding the
following:
– Decreases in LV preload
– Decreases in systemic vascular resistance (SVR)
– Increases in contractility
– Tachycardia
• Patients with significant mitral degeneration and associated hemodynamically significant
MR are usually older and more likely to have congestive heart failure (CHF). These patients
will benefit from hemodynamics that improve forward flow, such as mildly increased heart
rate, increased preload, and decreased SVR.
• Patients with CHF will benefit from an anesthetic plan that preserves myocardial function.
SYMPTOMS
• Assess for symptoms of MVP syndrome.
• Assess for symptoms of heart failure such as dyspnea, orthopnea, and paroxysmal nocturnal
dyspnea.
• Assess for symptoms of arrhythmias such as palpitations.
History
• Age of diagnosis
• Complications from MVP, such as endocarditis, cerebrovascular events, MR, and
arrhythmias
• Associated disorders
• Exercise tolerance
Signs/Physical Exam
• Mid-systolic click, often accompanied by a late systolic murmur in mild MVP.
• Holosystolic murmur in severe MR; click may also disappear.
• S3 and rales seen in CHF.
• Other signs of CHF, such as pulmonary edema, JVD, and lower extremity edema.
• Look for signs of connective tissue disorders.
TREATMENT HISTORY
• Previous treatment for complications of MVP
• Other treatment for associated disorders
MEDICATIONS
• Beta blockers or anti-arrhythmics for arrhythmias
• Anti-coagulation, such as aspirin or warfarin for history of CVA
• Heart failure medications
Labs/Studies
• Echocardiography for diagnosis, as well as assessment of LV function and severity of MR.
• EKG if there is concern for arrhythmias.
• CXR may show pulmonary congestion if the patient is in heart failure.
• Other studies dictated by medications and other comorbidities.
• Send blood cultures if there is concern for endocarditis.
• There is potential for cerebrovascular events.
• Other organs (e.g., lungs, liver, and kidneys) can be affected if the patient is in heart failure.
• Optimize serum electrolytes to reduce risk of intra-operative arrhythmias.
• Optimize volume status if patient is in CHF.
CLASSIFICATIONS
Thickening of leaflets:
• >5 mm: Classic prolapse
• <5 mm: Regarded as non-classic
TREATMENT
Premedications
• Ensure sufficient anxiolysis to avoid tachycardia, which may reduce LV size and possibly
worsen prolapse and regurgitation.
• Give premedication judiciously in patients with hemodynamically significant MR and
depressed LV function.
• Bacterial endocarditis prophylaxis should be considered in patients with mitral valve “click”
and regurgitation or high-risk features including:
– Prosthetic cardiac valve
– Previous endocarditis
– Cyanotic congenital heart disease that is unrepaired (including those with palliative shunts
and conduits).
– Completely repaired congenital heart disease with prosthetic material or device for the
first 6 months post-procedure (either surgical or catheter intervention).
– Repaired congenital heart disease with residual defects at the site or adjacent to the site of
a prosthetic patch or prosthetic device.
– Cardiac transplantation recipients with cardiac valvular disease.
Parental consent if a minor.
INTRAOPERATIVE CARE
• Dependent on procedure, provider preference, and patient preference.
• Functional MVP without significant MR or LV dysfunction will tolerate all forms of
anesthesia. However, those with significant LV dysfunction should be considered for local or
peripheral nerve blocks when possible or appropriate.
Monitors
• Dependent on the extent of procedure.
• Patients with functional MVP usually do not require invasive monitoring.
• Patients with significant MR and LV dysfunction may benefit from an arterial line for
continuous blood pressure monitoring and a central line for vasopressor support. Consider a
pulmonary artery catheter and/or transesophageal echocardiography (TEE) for cases
involving large volume shifts.
• In patients with functional MVP, avoid hemodynamics that will enhance MVP such as
decreases in LV end-diastolic volume, decreases in SVR, increases in contractility, or
tachycardia.
• In patients with significant MR, hemodynamic goals should promote forward flow such as
mildly increased heart rate, increased preload, and decreased SVR while avoiding
myocardial depression.
Maintenance
• Minimize sympathetic stimulation and undesirable decreases in LV emptying that may
worsen prolapse, as above.
• Patients with significant MR will benefit from hemodynamic goals that improve forward
flow, as above.
• Intra-operative arrhythmias may occur especially in head up positions (presumably due to
decrease in preload and accentuation of MVP). Consider beta blockers or lidocaine.
• Fluids: Maintenance of a positive fluid balance will help with decreases in preload that may
accentuate prolapse or MR.
Avoid excessive sympathetic stimulation which may worsen prolapse or MR.
POSTOPERATIVE CARE
BED ACUITY
• Routine post-operative care in majority of patients.
• ICU care for patients with high-risk procedure, hemodynamically significant MR, or poor LV
function.
• Majority of patients with MVP do not require post-operative studies or consults
• Repeat echocardiogram in patients undergoing mitral valve repair or replacement
COMPLICATIONS
• Monitor for fluid overload and worsening LV function in patients with poor myocardial
reserve.
• Patients are at risk for arrhythmias.
REFERENCES
1. HayekE, et al. Mitral valve prolapse.Lancet.2005;365:507–518.
2. Sutton MJ, Weyman A. Mitral valve prolapse prevalence and complications: An ongoing
dialogue. Circulation. 2002;106:1305–1307.
3. Freed L, et al. Prevalence and clinical outcome of mitral-valve prolapse. NEJM.
1999;341:1–7.
4. Hanson E, et al. Mitral valve prolapse. Anesthesiology. 1996;85:178–195.
ADDITIONAL READING
• www.americanheart.org
• www.mayoclinic.com/health/mitral-valve-prolapse
• Mitral valve regurgitation
CODES
ICD9
424.0 Mitral valve disorders
ICD10
I34.1 Nonrheumatic mitral (valve) prolapse
CLINICAL PEARLS
• It is important to distinguish between patients with functional MVP from those with
hemodynamically significant MR and LV dysfunction in order to formulate an appropriate
anesthetic plan.
MITRAL VALVE REPLACEMENT
Daniel Castillo, MD
BASICS
DESCRIPTION
General
• Surgical procedure in which the diseased mitral valve is replaced by a mechanical or
biological tissue valve, commonly due to mitral stenosis, regurgitation, or severe prolapse.
• Mitral valve (MV) repair, when feasible, is usually preferred over replacement for the
surgical treatment of mitral regurgitation (1,2)[A]. Retrospective studies of MV repair
appear to demonstrate lower operative mortality, greater improvement in LV function, and
higher overall survival at 10 years as compared with MV replacement.
• Most often, mitral valve surgery is performed in conjunction with either coronary bypass
surgery or another valvular surgery; less frequently, the mitral valve abnormality is an
isolated problem requiring cardiac surgery.
• Following sternotomy and opening of the pericardium, venous and arterial cannulations are
performed. The patient is then taken onto full cardiopulmonary bypass (CPB). After the
heart is arrested, the left atrium is opened to expose the mitral valve. The valve leaflets are
excised and the annulus is debrided. If feasible, chordae are preserved. The annulus is then
measured to properly match the prosthetic valve. Interrupted sutures are placed through the
annulus for its entire circumference and then passed through the sewing ring. The prosthesis
is securely tied in place.
• Systemic warming is initiated during the final stages of the valve implantation. After closure
of the left atriotomy, the patient is placed in the head-down position and all remaining air is
vented from the left heart through the LV vent. The cross-clamp is removed. Chest tubes are
placed and the patient is weaned from bypass.
• Minimally invasive mitral valve surgery through smaller incisions with specialized
instruments is being explored; for surgery on the valve itself, conventional instruments and
techniques are used. Only selected patients are eligible for these approaches. There are, as
yet, no randomized comparisons of conventional and minimally invasive approaches with
regard to clinical outcome, complications, and cost.
Position
• Supine with the arms positioned next to the body.
• The patient may be temporarily placed in Trendelenburg at the time of de-airing of the
ventricles before coming off bypass.
Incision
• Median sternotomy is the standard incision.
• Alternative incision sites (e.g., via a right mini-thoracotomy) are used as part of “minimally
invasive mitral valve surgery.”
Approximate Time
Time typically varies between 4–8 hours depending on the experience of the team, the type of
approach (standard versus minimally invasive approach), and technical difficulties.
EBL Expected
• Cardiopulmonary bypass machine leads to dilution.
• Blood loss typically ranges between 1,000–2,000 cc.
Hospital Stay
Surgical intensive care unit for 1–3 days; 7–10 days total in the hospital.
• Cardiopulmonary bypass machine (operated by a perfusionist).
• Standard equipment for open heart surgery.
• Minimally invasive approaches require special equipment.
• Transesophageal echocardiography probe (intraoperative examination performed by echo-
trained anesthesiologists or cardiologists).
EPIDEMIOLOGY
Incidence
N/A
Prevalence
About 65,000 MV repairs and replacements are performed in the US each year.
Morbidity
• Bleeding, reoperation, stroke, renal failure, prolonged ventilation, and infection are known
complications.
• The incidence varies depending on preoperative status, length, and type of operation.
• The 2008 ACC/AHA valvular disease guidelines refer to risk stratification models to estimate
the risk of in-hospital mortality and morbidity of valve surgery with or without coronary
artery bypass surgery (2)[B].
– US based registry by the Society of Thoracic Surgeons (STS) (3)[B]. Includes data from
nearly 90% of cardiac surgery providers in the US and may provide the most accurate risk
stratification for valve replacement.
– European system for cardiac operative risk evaluation (“Euro Score”)
– Scoring system developed from Great Britain’s and Ireland’s national data base
Mortality
• Varies significantly with age, co-morbidities, type of valvular lesion, ventricular function,
concomitant valvular surgery, and/or bypass surgery.
• Risk stratification models are useful to predict mortality risk for the individual patient (see
under morbidity).
• Hemodynamic stability throughout the induction period until initiation of bypass.
Management depends on the type of lesion (stenosis versus regurgitation), right and left
ventricular functions, pulmonary pressures, and other clinical factors.
• After successful repair/replacement and completion of bypass, the goal is to maintain
adequate cardiac output and blood pressure. Inotropes may be required if the left
ventricular function is depressed.
SYMPTOMS
• Symptoms vary depending on the type of lesion (stenosis versus regurgitation) and the time
course (acute versus chronic).
• Chronic mitral regurgitation often remains asymptomatic for years.
• Typical symptoms include shortness of breath, fatigue, palpitations, and heart murmur.
History
• See chapters on mitral stenosis, regurgitation, and prolapse.
• Determine if there is a history of esophageal strictures or other abnormality that would
prohibit placement of a transesophageal echocardiography probe during the procedure.
Signs/Physical Exam
Detailed description available in chapters on MV regurgitation, MV stenosis, and MV
prolapse.
MEDICATIONS
• Medical management depends on the type of lesion and other co-morbidities.
• Initiation of statins may reduce the incidence of atrial fibrillation and mortality.
Labs/Studies
• Preoperatively, a transthoracic echocardiography and sometimes a transesophageal
echocardiography are obtained.
• Coronary angiography is also routinely performed to determine whether the patient requires
concurrent coronary bypass grafting.
• Pre-existing renal dysfunction is of concern since further deterioration may be precipitated
by catheterization prior to the valve replacement and by prolonged pump times.
• Chronic pulmonary disease may worsen acutely secondary to bypass and lead to hypoxemia
when coming off bypass.
• Pre-existing neurologic deficits put the patient at great risk for further deterioration
postoperatively.
TREATMENT
Premedications
Consider gentle anxiolysis with benzodiazepines.
Morbidity and mortality risks vary with the extent of surgery (e.g., coronary bypass surgery
in addition to valve replacement) and preexisting comorbidities.
Skin flora is the greatest concern. Cefazolin may be utilized within 60 minutes prior to
incision if the patient is not a carrier of multi-resistant bacteria and does not have an allergy;
repeat every 3–4 hours until chest closure. Alternatively, vancomycin may be considered.
INTRAOPERATIVE CARE
• General anesthesia in the US.
• There are case reports of open heart surgery performed under epidural with sedation in
other parts of the world.
Monitors
• ASA standard monitoring.
• Arterial line, most often, placed prior to induction; non-pulsatile flow during bypass does
not allow for accurate non-invasive blood pressure measurement.
• Central venous access is usually obtained after induction; pulmonary artery catheter
placement may be considered.
• Transesophageal echocardiography is frequently used intraoperatively to guide and assess
MV repair/replacement.
• The goal is to provide hemodynamic stability throughout the induction period; gentle
administration of propofol with pressors or etomidate is most often used in combination
with fentanyl.
• Mask ventilation prior to endotracheal tube placement is performed except in cases of
increased aspiration risk when a rapid-sequence induction is chosen.
Maintenance
• Patients are usually maintained with oxygen/volatile agents and intermittent doses of
opioids and non-depolarizing muscle relaxants.
• During bypass, a volatile agent is added to the blood by the perfusionist through the bypass
machine.
• The management of patients during bypass varies substantially by institution and
practitioner.
• On bypass, the target mean arterial blood pressure is typically between 50–80 mm Hg.
• On bypass, the patient’s body temperature is cooled at the beginning and warmed to normal
body temperature before the termination of bypass.
• Patients remain intubated and are transferred to the intensive care unit.
• Postoperative sedation is typically provided with propofol infusion or most recently with
dexmedetomidine infusion. The latter appears to have a lower risk for the development of
postoperative delirium.
POSTOPERATIVE CARE
BED ACUITY
• Surgical intensive care unit.
• The time to extubation varies from a few hours to 24 hours. However, it can be several days
depending on the patient’s hemodynamic status, respiratory status, bleeding/coagulation,
and other organ systems.
ANALGESIA
• Analgesia is usually provided by intravenous opioids either as intermittent boluses or as
continuous infusion until extubation.
• Once the patient is extubated and the bowel function has returned, oral opioids can be
given.
COMPLICATIONS
• Atrial fibrillation: Patients often present preoperatively but also have a high risk of
developing it intraoperatively or postoperatively.
for complications that are unique to the prosthetic valve (3)[A]. A variety of complications
can occur:
– Structural failure (not uncommon with bioprosthesis, very rare with mechanical valve).
– Severe and recurrent bleeding due to anticoagulant therapy. Note: Mechanical valves
require long-term anticoagulation therapy, most often with warfarin, while patients with
bioprosthetic valves usually receive anticoagulation with warfarin only for 6 weeks to 3
months postoperatively and then aspirin life-long.
– Valvular thrombosis and thromboembolic events, especially in patients with mechanical
valves and inadequate anticoagulant therapy.
– Severe hemolysis mostly in mechanical valves.
– Endocarditis.
• Complications associated with open heart surgery and cardiopulmonary bypass (see chapter
Cardiopulmonary Bypass).
PROGNOSIS
As survival after a first valve replacement has improved, more patients require a second
operation for replacement.
REFERENCES
1. Bonow RO, Carabello BA, Chatterjee K, et al. Focused update incorporated into the
ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A
report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. Circulation. 2008;118:e523–e661. Vahanian A, Baumgartner H, Bax J,
et al. Guidelines on the management of valvular heart disease: The task force on the
management of valvular heart disease of the European Society of Cardiology. Eur Heart J.
2007;28:230–268.
2. Ruel M, Chan V, Bedard P, et al. Very long-term survival implications of heart valve
replacement with tissue versus mechanical prostheses in adults <60 years of age.
Circulation. 2007;116:I294–I300. Bolman RM, 3rd. Survival after mitral valve replacement:
Does the valve type and/or size make a difference? Circulation. 2007;115:1336–1338.
3. Salem DN, O’Gara PT, Madias C, et al. American College of Chest Physicians. Valvular and
structural heart disease: American College of Chest Physicians Evidence-Based Clinical
Practice Guidelines (8th Edition). Chest. 2008;133:593S.
• www.sts.org/quality-research-patient-safety/quality/risk-calculator-and-models/risk-
calculator
• www.euroscore.org
• www.ucl.ac.uk/research/riskmodel/index.html
• Mitral stenosis
• Mitral valve prolapse
CODES
ICD9
• V42.2 Heart valve replaced by transplant
• V43.3 Heart valve replaced by other means
ICD10
• Z95.2 Presence of prosthetic heart valve
• Z95.4 Presence of other heart-valve replacement
CLINICAL PEARLS
• Mitral valve repair is preferred over replacement when feasible.
• Risk stratification models are useful to predict morbidity and mortality risks for the
individual patient.
for complications that are unique to the prosthetic valve.
• There is a significant rate of structural failure of bioprosthetic valves within the first 10–15
years, requiring reoperation.
MIXED VENOUS OXYGEN SATURATION (MVO2)
BASICS
DESCRIPTION
• Mixed venous oxygen saturation (MvO2) is the measurement of oxygen remaining in the
blood after passing through the body’s tissue capillary beds; it measures what is not used.
• A true “mixed” venous sampling is taken from the distal port of the pulmonary artery
catheter; it is comprised of blood from the superior and inferior vena cava and coronary
sinuses.
• MvO2 is the product of the starting arterial blood oxygen, how efficiently oxygen is
transported or delivered throughout the body, and the amount of oxygen used by the body.
Because oxygen delivery is dependent upon cardiac output (CO), hemoglobin (Hg), and
oxygen saturation (O2 sat%), MvO2 can also serve as a surrogate to assess these factors. In
addition, it reflects dynamic functioning of the pulmonary and cardiac systems.
• Whereas blood pressure, O2 sat%, and other monitoring tools provide information about
large scale circulation, MvO2 is one of the clinician’s (limited) resources to assess the
efficacy of the microcirculation and cell oxygenation.
• (O2 starting) – (O2 consumed) = O2 remaining. MvO2 represents the unused O2 returning to the
heart by modification of the Fick principle.
• MvO2, or the O2 remaining in venous blood after perfusing the body, can serve as an
indicator of oxygen supply (O2 sat%, Hg, CO), oxygen demand (metabolic requirements of
tissues/cells), and tissue oxygenation (efficacy of O2 delivery to the demand).
• Under normal, resting conditions, MvO2 = 75% (PaO2 of 40 mm Hg). O2 supply >O2
demand, with only 25% of O2 utilized or extracted from the blood, which leaves a safety
reserve of 75%.
• Train station analogy: O2 (cargo) is delivered to the lungs (train station) from the
atmosphere. O2 (cargo) is uploaded by the blood (train) that passes by, onto Hg molecules
(boxcars). The heart pump (engine) delivers the oxygenated blood/oxyhemoglobin (cargo-
filled boxcars) to the tissues/cells (towns). The Hg (boxcars) is loaded to capacity with the
O2 (cargo) at the lungs (train station) and the blood (train) returns unused O2 (cargo) to the
lungs (train station). Because there is no reliable method to calculate all the O2 (cargo) that
is utilized by the tissues/cells (towns), it is indirectly determined by how much is loaded
onto the blood (train) and what is returned. Under normal conditions, the cells/tissues
(towns) utilize approximately 25% of what is loaded at the lungs (train station); thus 75%
of the Hg (boxcars) capacity returns to the lungs (train station).
• Oxygen demand: Describes the amount of O2 necessary to satisfy the body’s metabolic
requirements. O2 is required at the cellular level to maintain normal cell function and the
basal metabolic rate of each organ differs. In addition, it is dependent on factors such as
temperature, metabolic conditions, and muscle work. Direct measurement is difficult, but by
applying the Fick principle, it can be assessed indirectly by measuring the O2 consumption
(MvO2).
• Oxygen consumption: Describes the amount of O2 used by the tissues, and is equal to the O2
demand in the healthy patient. When demand increases (increased metabolic requirement),
the body compensates by increasing CO (SV, HR) or O2 extraction in order to avoid
tissue/cellular hypoxia.
• Oxygen supply: Because the body cannot store O2 (unlike glucose), its supply is entirely
dependent on the dynamic and sustained function of the pulmonary (O2 sat%) and
circulatory (Hg, CO) systems.
– Pulmonary: With inspiration, the patient receives an FIO2 of 21%, resulting in an alveolar
partial pressure (FA) of 100 mm Hg. FA = (Pbaro – PH20) (FIO2) – (PaCO2/0.8) = (760 –
47)(0.21) – (40/0.8) = 100 mm Hg. Because the capillary venous blood
lacing/enveloping the alveoli has a PaO2 of 40 mm Hg (aka MvO2), a pressure gradient
exists that allows for simple diffusion from a higher to lower partial pressure (alveoli to
capillary venous).
– Blood oxygen content: The O2 from the alveoli is transported in the blood in two forms:
Dissolved in plasma (2%) and attached to Hg (98%). O2 blood content = O2 dissolved + O2
bound to Hg = PaO2(0.003) + Hg(1.39)(SaO2). Under normal conditions, a Hg molecule
becomes completely saturated after traversing the alveoli.
– Cardiovascular: The heart provides the pumping force that delivers the oxygenated blood
to the tissues where it is consumed. Arterial blood oxygen content multiplied by CO
equals O2 delivery. [(Hg)(1.39)(SaO2) + PaO2(0.003)] * CO * 10. An abnormality in any
of these factors can result in reduced O2 delivery.
ANATOMY
• A true mixed venous sample is taken at the pulmonary artery (distal tip of pulmonary artery
catheter). This allows for adequate mixing of blood from the superior vena cava (SVC),
inferior vena cava (IVC), and coronary sinus. Technology for continuous monitoring of
MvO2 has been developed and is built into special pulmonary artery catheters (precludes
aspirating and sending samples).
• At rest, venous return from the SVC (brain, heart), has a lower saturation (more tissue
consumption) than from the IVC (lower extremities).
• Whether SVC O2 sat% (ScO2) can be utilized to monitor global tissue hypoxia is a matter of
controversy. The benefit of ScO2 is that it can be attained from an upper body central
venous line sample, which is less invasive and may already be in place; in addition, it may
allow a surrogate assessment of CO. Technology for continuous monitoring has been
developed in special central line catheters (1).
• If the PAC is wedged or partially wedged, the sample will reflect the composition of arterial
blood.
• A left-to-right intracardiac shunt (e.g., ventricular septal defect), results in “arterialized”
blood, causing a “step up” in the saturation of the MvO2 as it passes through the right
ventricle.
• Pathophysiologic states can result in O2 demand > O2 delivered. An increase in demand
(increased metabolic requirement) is met by an increase in CO (increased HR, SV) or oxygen
extraction (75% reserve). However, after the compensatory mechanisms are exhausted,
demand > consumption, the tissue/cell resorts to anaerobic metabolism (without oxygen)
in order to maintain cellular function.
• Low MvO2 states: Potential increase in O2 demand/consumption, or reduced CO, Hg, or
arterial saturation
– Increased O2 demand/consumption: Fevers, seizures, shivering, fighting ventilator,
malignant hyperthermia, thyroid storm. If the patient has adequate cardiac reserve, the
body will compensate by increasing CO, to preserve tissue oxygenation. With increasing
demand above that, the body will compensate by increasing O2 extraction from the
arterial blood.
– Reduced CO: Ischemia, infarction, negative inotropes, increased afterload, acute failure,
reduced SV or hypovolemia, shock, arrhythmias, tamponade. When this occurs, the only
available mechanism is to increase O2 extraction. Poorly tolerated compared to other
causes of reduced MvO2.
– Reduced Hg: Hemorrhage, anemia, surreptitious blood loss. Mild reductions can often be
met by increased CO in a patient with adequate cardiac reserve. Significant blood loss is
met by an increase in CO and O2 extraction from the arterial blood. If the patient has
reduced cardiac reserve, they are at risk of tissue/cell hypoxia.
– Arterial desaturation: Atelectasis causing reduction in FRC from positioning, insufflations,
fluid overload, retractors, or other V/Q mismatch such as pulmonary embolism. Met by
increased CO, followed by O2 extraction and does not necessarily result in anaerobic
metabolism or lactic acidosis if compensated for.
• High MvO2 states: Potential reduced O2 demand/consumption, increased O2 sat%, Hg, or
CO; arterialized venous sample.
– Reduced O2 demand/consumption: Hypothermia, anesthesia, pharmacologic paralysis.
– Sepsis results in inappropriate shunting of blood away from cells/tissues that need O2,
leaving them poorly oxygenated and resorting to anaerobic metabolism. This is a
maladaptation, given that the shunted blood returns to the heart highly oxygenated or
unused (increased MvO2) (2,3).
– AVMs and other large shunts can also create a similar clinical scenario (increased MvO2
despite oxygen deprivation, secondary to inappropriate shunting of blood away from
tissues).
– Cyanide poisoning prevents utilization of O2 at the cellular level because oxidative
enzymes are blocked or only partially functional; prevents Hgb unloading from capillary
blood. Blood returns highly oxygenated, (increased MvO2), despite cell hypoxia.
– Increased arterial saturation: Increased FIO2, increased FRC (alveolar recruitment from
PEEP, larger tidal volumes, positioning such as reverse Trendelenburg, removal of
abdominal retractors), improved V/Q matching.
– Increased Hg: Blood transfusion.
– Increased CO: Increased inotropy from medication, sympathetic stimulation, reduced
afterload, increased preload (Starling curve), resolution of arrhythmia, increased heart
rate (4).
– A wedged PAC samples blood from surrounding alveoli that has been oxygenated; referred
to as “arterialized” sample.
• When there is an imbalance of O2 supply to demand, the body mobilizes its compensatory
mechanisms to ensure adequate availability; increased O2 extraction and CO.
• Intraoperatively, O2 is usually at steady state consumption, and a reduction should prompt a
search for reduced tissue delivery, often from reduced CO, but also from low Hg or O2 sat%
(4). Reduced CO is problematic, as it removes one of the body’s compensatory mechanisms
for tissue/cell oxygenation.
• Studies have demonstrated that a decrease in MvO2 generally precedes or indicates
imminent cardiac failure (10–15 minutes prior) as well as poor overall prognosis. In
addition, consequent lactic acidosis is presumptive evidence of tissue hypoxia and is also
associated with a poor prognosis.
• In the ICU, it can be utilized to monitor, assess, and guide therapy during sepsis.
• ScVO2 may be utilized, as it is less invasive and is more routinely inserted in critically ill
patients. Values should be evaluated with caution as it reflects the degree of O2 extraction
from the brain and upper body (1).
• PAC migration often occurs in cardiac surgery when the heart is being manipulated. Deflate
the balloon and pull the catheter back 1–3 cm.
EQUATIONS
•
13.9 = K factor (derived from 1.39 × 10, see below)

• MvO2 normal values:
– Mixed venous oxygen saturation = 60–80%
– Mixed venous partial pressure = 35–45 mm Hg
• Venous oxygen content; CvO2 = 15.5 mL/dL
– O2 dissolved + O2 bound to Hg {Hg × 1.39 × MvO2) + PvO2(0.003) = 15.5 mL/dL.
– 1.39 = mL of O2 that can bind to 1 g of Hb
– 0.003 = solubility coefficient of O2 in plasma
– (15 × 1.39 × 0.75) + 40(0.003) = 15.5 mL/dL
• Venous O2 transport = DvO2 = 775 mL O2/min.
– CvO2 × CO × 10 = 775 mL O2/min
– 15.5 mL/dL × 5 L/min × 10 = 775 mL O2/min
– Multiplying by 10 allows to convert from dL to mL
• Arterial oxygen content; CaO2 = 20.1 mL/dL
– Arterial O2 Saturation = SaO2-95–98%
– Arterial O2 partial pressure = 80–100 mm Hg
– O2 dissolved + O2 bound to Hg
– [Hg × 1.39 × SaO2] + [PaO2(0.003)] = 20.1 mL/dL
– (15 × 1.39 × 0.97) + 100(0.003) = 20.1 mL/dL
• Arterial O2 transport = DO2 = 1005 mL O2/min
– CaO2 × CO × 10 = 1005 mL O2/min
– 20.1 mL/dL × 5 L/min × 10 = 1005 mL O2/min
• VO2 = Arterial O2 transport – Venous O2 transport
– = (CO × CaO2 × 10) – (CO × CvO2 × 10)
– = CO (CaO2 – CvO2) × 10
– = CO × [(Hg × 1.39 × SaO2)−(Hg × 1.39 × SvO2)] ×10
– = CO × Hg ×1.39 × (SaO2−SvO2) × 10
– = CO × Hg × 13.9 × (SaO2 – SvO2)
– = (5 L/min × 15 g/dL × 13.9) × (0.97−0.75)
– Note that the O2 dissolved in plasma is excluded because it is miniscule
– = 230–250 mL O2/minute
– Extraction = 250/1005 mLO2 = 25%
REFERENCES
1. Ho KM, Harding R, Chamberlain J, Bulsara M. A comparison of central and mixed venous
oxygen saturation in circulatory failure. J Cardiothoracic Vasc Anesth. 2010;24(3):434–
439.
2. Edwards JD. Oxygen transport in cardiogenic and septic shock. Crit Care Med.
1991;19(5):658–663.
3. Shoemaker WC, Appel PL, Kram HB, Bishop M, Abraham E. Hemodynamic and oxygen
transport monitoring to titrate therapy in septic shock. New Horiz. 1993;1(1):145–159.
4. Cariou A, Monchi M, Dhainaut JF. Continuous cardiac output and mixed venous oxygen
saturation monitoring. J Crit Care. 1998;13(4):198–213.
ADDITIONAL READING
• Kelly KM. Does increasing oxygen delivery improve outcome? Yes. Crit Care Med.
1996;12(3):635–644.
• Yu M, Levy MM, Smith P, Takiguchi SA, Miyasaki A, Myers SA. Effect of maximizing oxygen
delivery on morbidity and mortality in critically ill patients: A prospective, randomized
controlled study. Crit Care Med. 1993;21(6):830–838.
• Pulmonary artery catheter
• Cardiac output
• Sepsis
CLINICAL PEARLS
• Mixed venous oxygenation saturation provides a measurement and tool to assess tissue
oxygenation in the perioperative and intensive care unit period. Most of the current
monitors of perfusion are on a global level.
• The venous oxygen saturation is directly measured and inferences about the contributing
factors can be made (hemoglobin levels, oxygen consumption, and cardiac output).
MULTIPLE MYELOMA
Keyuri Popat, MD
BASICS
DESCRIPTION
• Multiple myeloma describes the abnormal, excessive growth of a single clone of plasma cells
with a resultant monoclonal immunoglobulinopathy.
• These abnormal plasma cells grow in the bone marrow resulting in extensive skeletal
destruction with osteolytic lesions, osteopenia, and/or pathologic fractures.
• Patients with multiple myeloma may present for interventional pain therapy, spinal cord
decompression, bone marrow transplant, pathological fracture repair, or other non-related
procedures.
EPIDEMIOLOGY
Incidence
Approximately 1% of all cancers.
Prevalence
• Approximately 10% of all hematologic malignancies
• Age adjusted incidence has remained stable at 4 per 100,000 persons
• Median age of onset 66 years
• Men > women
• African Americans > Caucasians
Morbidity
Incurable disease
Mortality
Responsible for approximately 20% of deaths from hematologic malignancies; 2% of deaths
from all cancers
• First degree relatives have a 3.7-fold increase in incidence
• More common in farmers, miners and those with wood dust exposure
PATHOPHYSIOLOGY
• Multiple myeloma is a clonal B cell malignancy. While some steps of replication of the
malignant clone have been discovered, many remain unknown. Almost all myeloma cases
are preceded by a premalignant plasma cell proliferative disorder known as monoclonal
gammopathy of undertermined significance (MGUS). MGUS is present in over 30% of the
population above the age of 50 years, and progresses to myeloma or a related malignancy at
a rate of 1% per year.
• The disease is characterized by the aberrant expansion of plasma cells within the bone
marrow as well as extramedullary sites. The most common sites are the back and chest;
extramedullary plasmacytomas can be found in the oronasopharynx and paranasal sinuses
and rarely throughout the gastrointestinal system, lung, and central nervous system.
• Bone lesions: The abnormal proliferation of the plasma cell line results in overcrowding and
encroachment of normal progenitor cells. This results in classic bone pain with lytic lesions
that can present on routine skeletal films.
• Hypercalcemia may be either symptomatic or discovered incidentally. This is due to
increased bone resorption, which in turn is due to the release of osteoclast activating factors
such as lymphotoxin, interleukin-6, hepatocyte growth factor, and receptor activator of
nuclear factor kappa B ligand (RANK ligand).
• Immune system: Patients with myeloma are prone to infection due to a combination of
immune dysfunction and physical factors. Immune dysfunction results from impaired
lymphocyte function, suppression of normal plasma cell function, and
hypogammaglobulinemia (due to suppression of normal gamma globulin). Physical factors
that predispose to pulmonary infection include hypoventilation secondary to pathologic
fractures and pain involving the rib cage.
• POEMS syndrome (osteosclerotic myeloma): Polyneuropathy, Organomegaly,
Endocrinopathy (hypogonadism, adrenal insufficiency), Monoclonal protein, Skin changes is
a rare presentation of monoclonal cell disorder due to chronic overproduction of pro-
inflammatory and other cytokines (e.g., vascular endothelial growth factor).
Microangiopathy, edema, effusions, increased vascular permeability, neovascularization,
polyneuropathy, and pulmonary hypertension are also features of this syndrome.
• Assessment of concomitant organ dysfunction should be performed, with the anesthetic
tailored as needed (e.g., renal disease requiring adjustments to medication doses).
• Patients may have significant pain and be on chronic analgesia; appropriate pain
management should be provided.
• Careful patient positioning should be performed given the possibility of skeletal destruction,
radiculopathy, and cord compression.
• Macroglossia can result from amyloid deposition in approximately 15% of patients and may
present difficulty with airway management.
SYMPTOMS
• Pain
• Fatigue
• Paralysis/paraparesis
History
• Bone pain
• Neuropathy secondary to chemotherapy
• Thrombosis secondary to thalidomide
• Renal failure
• Anemia
• Infection
• Spinal cord compression
Signs/Physical Exam
• Fracture
• Kyphosis
• Motor and sensory neurologic deficit
• Macroglossia
MEDICATIONS
• Thalidomide, bortezomib, and lenalidomide (are at higher risk for thrombosis and rarely of
interstitial lung disease)
• Vincristine, doxorubicin, and dexamethasone
• Analgesics
• Erythropoietin
TREATMENT
• Stem cell transplantation

• Blood, platelet, plasma transfusions
• Plasma exchange (patient’s plasma is removed on a cell separator and replaced with
transfusions of human albumin or synthetic plasma)
Labs/Studies
• Electrolytes, including calcium level
• BUN/Creatinine
• Complete blood count
• Urinalysis for proteinuria: Plasma cell proliferation increases total serum proteins and
results in “spillage” into the urine.
• Nervous system: Most commonly includes radiculopathy and cord compression. This can
occur due to direct plasma cell proliferation in the spinal cord or due to bone collapse.
Rarely, peripheral neuropathy due to amyloidosis and central nervous system plasmacytoma
is also seen. Hyperviscosity from monoclonal immunoglobulins may result in stroke or
confusion.
• Cardiovascular: Amyloid deposition can result in restrictive cardiomyopathy and reduce
chamber filling and contractility, as well as cause capillary fragility.
• Renal disease can be glomerular (amyloidosis, immunoglobulin deposition), tubular (cast
nephropathy), or interstitial (interstitial nephritis, plasma cell infiltration). This can be the
presenting feature of myeloma.
• Skeletal destruction commonly involves the spine and can cause vertebral collapse or cord
compression.
• Anemia is due to the involvement of the bone marrow which replaces normal hematopoietic
tissue and by the disruption of the bone marrow microenvironment.
• Airway: Macroglossia may result from amyloid deposition and can occur in 15% of patients.
• Hypercoagulability occurs due to the disease itself, as well as from treatment with
thalidomide. There is increased risk of both venous and arterial thrombosis.
• Acute infection due to poor immunity as discussed above
• Acute thrombosis
• Need for plasmapheresis
CLASSIFICATIONS
• Based on bone marrow biopsy and cytogenetics.
• Broadly classified as:
– Monoclonal gammopathy of unknown origin (MUGUS); asymptomatic.
– Multiple myeloma (MM): End organ damage maybe present.
– Smoldering multiple myeloma (SMM); asymptomatic
TREATMENT
Premedications
Analgesics as needed; patients may have developed a tolerance and require higher dosages.
INTRAOPERATIVE CARE
• General: Be aware of possible renal failure and thus the choice of agents used for induction
and maintenance of anesthesia. Use of certain muscle relaxants cleared by the kidney may
have a longer than desired duration of action.
• Regional anesthesia as the sole technique or for postoperative pain may also be used. If a
neuraxial technique is considered, evaluate the spine carefully for fractures and any
anticoagulation issues that may contraindicate placement.
• Thromboprophylaxis should be discussed with the surgeon and appropriately planned.
Monitors
• Consider arterial line placement in patients with concomitant organ failure
• Any neck manipulation should be done cautiously due to the possibility of lytic spine
lesions.
• Macroglossia may make ventilation or intubation challenging.
• Pharmacokinetics of anaesthetic drugs may be unpredictable due to an altered volume of
distribution, drug clearance, and plasma albumin/globulin ratio. The possibilities of change
in protein binding have been alluded to in the past but no studies have proven this to be
clinically significant (3).
Maintenance
• Analgesia may be challenging as patients may be on high dose or chronic narcotics.
Requirements should be increased accordingly.
• Adequate hydration is important to avoid the precipitation of hyperviscosity syndrome and
renal failure.
• Careful and meticulous positioning and padding of pressure points should be performed.
No special consideration; routine extubation criteria apply.
POSTOPERATIVE CARE
BED ACUITY
• Consider supplemental oxygen (nasal cannula, face mask).
• Pain management may be challenging in opioid tolerant patients; consider an acute pain
consultation or the placement of regional/neuraxial blocks if appropriate.
COMPLICATIONS
• Inadequate analgesia
• Fluid overload
• Perioperative thrombosis
REFERENCES
1. Rajkumar SV. Multiple myeloma: 2011 update on diagnosis, risk-stratification, and
management. Am J Hematol. 2011;86(1):57–65.
2. Mahindra A, Hideshima T, Anderson KC. Multiple myeloma. Blood Rev. 2010;24(Suppl
1):S5–11.
3. Walder AD. Failure of anaesthesia with etomidate. Eur J Anaesthesiol. 1995;12(3):325–
327.
4. Dabrowska DM, Gore C, Griffiths S, et al. Anaesthetic management of a pregnant patient
with multiple myeloma. Int J Obstet Anesth. 2010;19(3):336–339.
ADDITIONAL READING
• Falanga A, Marchetti M. Venous thromboembolism in the hematologic malignancies. J Clin
Oncol. 2009;27(29):4848–4857.
• Bone marrow harvest
• Intrarenal failure
• Vertebroplasty/kyphoplasty
CODES
ICD9
• 203.00 Multiple myeloma, without mention of having achieved remission
• 203.01 Multiple myeloma, in remission
ICD10
• C90.00 Multiple myeloma not having achieved remission
• C90.01 Multiple myeloma in remission
CLINICAL PEARLS
• Assess for the severity of disease in order to appropriately formulate an anesthetic plan.
• Pain control may be a challenge due to multiple lytic lesions. Consider acute pain consult,
regional block.
• Adequate hydration can reduce the occurrence of hypercalcemia and possible renal damage.
• Careful patient positioning to avoid nerve injury.
• Rarely, abnormal pharmacokinetics may be present secondary to changes in the
albumin/globulin ratio.
• If a transfusion is needed or anticipated perioperatively, a discussion with the surgeon and
possibly a hematologist should be conducted.
MULTIPLE SCLEROSIS
BASICS
DESCRIPTION
• Multiple sclerosis (MS) is a polygenic, organ specific autoimmune disease of unknown
etiology. There exist evidentiary signs of tissue destructive activity of humoral and/or
cellular immune system in the myelin components of the central nervous system (CNS).
• It was first described by Dr. J. M. Charcot (1825–1893) and named in accordance with the
widespread “scars” seen in the CNS.
• MS is the most common demyelinating disorder of the CNS and is the leading cause of
acquired neurological disability in young adults.
EPIDEMIOLOGY
Incidence
Female > males in a 2.3:1 ratio.
Prevalence
• In the US, it is present in 30–80 per 100,000 persons.
• Peaks around the age of 30.
• Regional differences exist. In the north–south gradient, there is a higher risk in northern,
industrialized countries. It is rare in Asians and Africans.
• There appears to be a genetic component, with a 10- to 50-fold greater occurrence in
relatives of MS patients.
Morbidity
In 20–40% of patients, it is considered benign with minimal permanent disability
Mortality
• Survival is linked to the extent of disability/secondary complications (lungs, renal).
• Life-expectancy is slightly shortened in most patients.
• Higher risk for suicide.
• Complex interaction of genetic and environmental factors: Related to certain HLA types and
over-expression of human endogenous retroviruses (HERVs), resulting in an altered immune
response.
• Multiple genetic loci have been identified; however, the penetrance of risk only has a
maximum of 25%.
• Involvement of infectious factors include: Viruses (EBV, HHV-6), hepatitis B vaccination,
chlamydia pneumonia.
• Hygiene related factors, low levels of vitamin D, production of melanoma-like melanin.
• MS is a neurodegenerative, primary inflammatory disease that affects both white and gray
matter. It is classically considered a disease of demyelination; however, histopathology also
demonstrates neuroaxonal damage.
• There is a proliferation of CD4 helper T-cells with the formation of cytokines resulting in
blood brain barrier (BBB) damage, production of antibodies, and perforins.
• Exacerbations are dependent on oxidative/nitrosative stress mitochondrial alterations, and
stressful life-events.
• Decrease perioperative stress and maintain body homeostasis to avoid exacerbations.
• The response to non-depolarizing muscle relaxants is variable. Succinylcholine should be
avoided.
• Medications for the treatment of multiple sclerosis may result in co-morbidites with
anesthetic implications as well as interactions with anesthetic medications.
SYMPTOMS
• Depression
• Paresthesias
• Paresis
• Ataxia, dystonia, vertigo (cerebellar symptoms)
• Pain (in 30–50%): Neuropathic and neurogenic pain, trigeminal neuralgia
• Chronic fatigue (>75%), emotional changes
History
• Remissions and relapses: Determine course of disease and neurological function.
• Determine the effects of heat
• Determine if there are side effects of therapies
Signs/Physical Exam
• Nystagmus
• Spasticity with dysfunctional reflexes
• Muscle atrophy
• Respiratory distress, use of accessory muscles, small tidal volumes, one-sided diaphragm
impairment
• Hypotonia, bradycardia (autonomic nervous system)
TREATMENT HISTORY
• Stem cell transplantation
• Plasmapheresis
MEDICATIONS
• General principle: Anti-inflammatory and neuroprotective therapy targeting neuronal
processes and cell bodies.
• Medications for the prevention of relapse:
– First-line treatment:
Interferon-β1α: May be administered IM or SC depending on the formulation. Can result
in hepatic failure/elevated LFTs, leukopenia.
Glatiramer acetate can result in a self-limited, post-injection systemic reaction with chest
tightness, flushing, anxiety, dyspnea, and palpitations in 15% of patients. This may be
mistaken for cardiac ischemia or hives.
– Second-line agents:
Mitoxantrone is an immunosuppressive, chemotherapeutic agent. May result in AML,
leukopenia, congestive heart failure and decreased LVEF, nausea/vomiting.
Natalizumab is a specific mAb. Side-effects include infections (e.g., UTIs, URIs),
arthralgias.
Fingolimod is an immunomodulator.
• Medications for exacerbation:
– High dose methylprednisolone (5–15 mg/kg/d for3–10 days).
– Immunosuppressants: Azathioprine, cyclophosphamide
• Symptom-oriented medication
– Baclofen for spasticity (intrathecal, oral)
– Amantadine for fatigue
– Antidepressants for depression
– Carbamazepine and phenytoin for pain syndromes
– Anticholinergics for neurogenic bladder
Labs/Studies
• When significant respiratory insufficiency is present, consider pulmonary function testing
and an arterial blood gas.
• Imaging studies: MS is primarily a clinical diagnosis. An MRI (T2-weighted) can show
multifocal lesions involving periventricular white matter, optic nerve, brainstem, and spinal
cord white matter.
• CSF analysis: Intrathecal IgG synthesis and oligoclonal bands with lymphocytic pleocytosis.
• Evoked potentials: Visual evoked potentials (VEP) and somatosensory evoked potentials
(SSEPs).
• Plasma: Endothelial microparticles.
• Depression, emotional changes, optic neuritis (70%), nystagmus, paresthesias, spasticity
with dysfunctional reflexes, and atrophy. Cerebellar symptoms include ataxia, dystonia, and
vertigo.
• Autonomic nervous system dysfunction may manifest as hypotonia or bradycardia.
• Respiratory: Muscle weakness can result in a decreased FRC, as well as maximal inspiratory
and expiratory efforts. Diaphragmatic palsy may be seen in cervical cord involvement. If
central control of ventilation is impaired, there may be a decreased response to PaCO2.
• Pain (in 30–50%): neuropathic and neurogenic pain, trigeminal neuralgia.
• Chronic fatigue (>75%)
• GERD
• Current exacerbation
• Acute cardiotoxic effects of mitoxantrone
CLASSIFICATIONS
• McDonald criteria: Diagnostic criteria with clinical findings to prove dissemination in time
and space of lesions supported by MRI, VEP, and CSF
• Relapsing-remitting (RRMS): 80%
• Secondary progressive (SPMS): 50% of RRMS after 10–15 years
• Primary progressive (PPMS): 15% and carries the worst prognosis
• Progressive relapsing (PRMS): 5%
TREATMENT
Premedications
• Consider high-dose glucocorticoids above the antiemetic dose after discussion with a
neurologist.
• In patients with respiratory dysfunction at baseline, benzodiazepines and opioids should be
cautiously titrated if needed. Patients should be monitored with pulse oximetry.
• Patients should be informed about the potential for postoperative exacerbations.
• Depression might make informed consent difficult.
• Pregnancy may cause partial remission; however, in the postpartum period, there is an
increased risk of exacerbation.
INTRAOPERATIVE CARE
• General anesthesia is considered safe.
• Regional anesthesia is possible after carefully weighing the risks and benefits.
– Respiratory dysfunction may be decreased. Avoid intubation, ventilation, and sedation;
beneficial in patients with central nerve involvement or respiratory muscle weakness.
– “Double-crush” phenomenon due to involvement of the peripheral nervous system, which
may be subclinical. Peripheral nerve damage has been reported after peripheral nerve
blocks.
– Epidural anesthesia may be preferred over spinal anesthesia, which is associated with
exacerbations as well as profound hypotension that is resistant to vasopressors.
– Because neurons are demyelinated, they may be more susceptible to local anesthetic
neurotoxicity, which can aggravate conduction blockade. To that extent, consider lower
concentrations and decreased exposure.
Monitors
• Standard ASA monitors; careful attention to temperature
• Neuromuscular monitoring when neuromuscular blocking agents are utilized
• Good pre-oxygenation
• Consider a rapid sequence induction if the patient has dysphagia. There is an increased risk
of aspiration if the cranial nerves are involved (decrease in pharyngeal and laryngeal
reflexes). However, avoid succinylcholine, because up-regulation of acetylcholine (ACh)
receptors may lead to hyperkalemia. The response to non-depolarizing drugs is variable. The
patient may be resistant due to upregulation of ACh receptors or co-medication with
anticonvulsants. However, muscle atrophy and baclofen can render the patient more
sensitive to its effects.
Maintenance
• No studies exist that demonstrate a benefit with any particular technique. However,
inhalational agents have been shown to increase the risk of hypotension due to defects in
the autonomic nervous system.
• Maintain at a “deep” level of anesthesia to avoid stress (MAC-BAR).
• Neuromuscular blockade has an unpredictable response. Utilization of a nerve stimulator
can aid with dosing
• Temperature: Meticulously avoid increases in body temperature as this can slow nerve
conduction in demyelinated nerves.
• Goals include reducing stress/distress while ensuring sufficient respiratory function.
• Consider administering pre-emptive analgesia to minimize postoperative pain (needs to be
balanced against its respiratory effects).
POSTOPERATIVE CARE
BED ACUITY
Depends on the surgery and baseline condition. The patient should be placed in an ICU if they
have respiratory muscle weakness, diaphragmatic palsy and hypoventilation, or dysphagia
due to cranial nerve involvement.
Neurological assessment by the anesthesia team, and in the event of any uncertainties, by a
formal neurologic consult.
COMPLICATIONS
• Respiratory failure/aspiration
• Exacerbations of MS, primarily due to inappropriate pain management, hyperthermia, and
psychological distress
• Potential drug interactions of anesthetics with immunosuppressants, antispasticity and
antiepileptic drugs, and anticholinergics
REFERENCES
1. Dickerman RD, Schneider SJ, Stevens QE, et al. Prophylaxis to avert exacerbation/relapse
of multiple sclerosis in affected patients undergoing surgery. Surgical observations and
recommendations. J Neurosurg Sci. 2004;48(3):135–137.
2. Dorotta IR, Schubert A. Multiple sclerosis and anesthetic implications. Curr Opin
3. Koff MD, Kohen JA, McIntyre JJ, et al. Severe brachial plexopathy after an ultrasound-
guided single-injection nerve block for total shoulder arthroplasty in a patient with
multiple sclerosis. Anesthesiology. 2008;108(2):325–328.
4. Krone B, Grange JM. Paradigms in multiple sclerosis: Time for a change, time for a
unifying concept. Inflammopharmacology. 2011;19(4):187–195.
5. Stadelmann C. Multiple sclerosis as a neurodegenerative disease: Pathology, mechanisms
and therapeutic implications. Curr Opin Neurol. 2011;24:224–229.
6. Vercauteren M, Heytens L. Anaesthetic considerations for patients with pre-existing
neurological deficit: Are neuroaxial techniques safe? Acta Anaesthesiol Scand.
2007;51(7):831–838.
• Epidural
CODES
ICD9
340 Multiple sclerosis
ICD10
G35 Multiple sclerosis
CLINICAL PEARLS
• The primary goal is to avoid any perioperative stress, especially hyperthermia.
• Monitor neuromuscular blockade closely or consider alternatives such as topicalization with
lidocaine or deep anesthesia with remifentanil.
• Interestingly, in patients with MS, there are no exacerbations seen during pregnancy.
However, there is a threefold increase in exacerbations postpartum; this is independent of
whether the patient had anesthesia or not. It may be explained by infection, emotional
lability, and hyperpyrexia.
MYASTHENIA GRAVIS
Fabrizio Racca, MD
BASICS
DESCRIPTION
• Myasthenia gravis (MG) is an autoimmune postsynaptic neuromuscular junction (NMJ)
transmission disorder. In the majority of cases (85%), MG is associated with auto-antibodies
against the acetylcholine (ACh) receptor.
• The hallmark of the disorder is weakness and fatigability in ocular, bulbar, limb, and
respiratory muscles.
EPIDEMIOLOGY
Prevalence
In the US, 10–20 new cases of MG per million annually
Prevalence
• In the US, 150–200 cases of MG per million population
• Bimodal distribution of MG tending to affect:
– Young woman: 20–40 years of age
– Older men: 50–70 years of age
Morbidity
• Intermittent impairment of muscle strength, which may cause aspiration and increased
incidence of pneumonia and falls.
• Medications used to control the disease may produce adverse effects.
Mortality
• In the past, untreated MG had a mortality rate of 30–70%; now most patients have a near-
normal life expectancy.
• Myasthenic crisis: Even with prompt diagnosis and treatment, the mortality rate of a
myasthenic crisis is <5%.
• Cause remains unknown. It is an autoimmune disorder and does not appear to have a
genetic predisposition. In some cases, it may be associated with a thymoma or other
autoimmune disorders.
• Myasthenic crisis:
– Infection
– Hypothermia
– Hypokalemia, hypophosphatemia
– Surgical intervention
– Pregnancy, childbirth
– Tapering of immunosuppressive medications
– Drugs that may worsen the muscular weakness: Aminoglycosides, fluoroquinolones,
macrolides, beta-blockers, diuretics, procainamide, magnesium salts, calcium channel
blockers, intravenous iodinated contrast agents, glucocorticoids
• Normal muscle contraction is the result of pre-synaptic release of ACh into the NMJ. ACh
binds to acetylcholine receptors (AChR) on the postjunctional membrane; when both α
subunits of the AChR are bound, it undergoes a conformational change that allows sodium
and calcium to flow intracellularly and increase the voltage (make positive). The membrane
resting potential is ∼−90 mV, and when a membrane threshold of −30 mV is attained
(∼10–20% of AChR are opened), voltage-gated ion channels open and fully depolarize the
membrane, producing an action potential.
• MG is the result of an antibody-mediated attack against ACh postsynaptic receptors of the
NMJ, leading to a reduction in the number of ACh receptors. Consequently, there is a
decrease in the agonist effect of ACh on the postsynaptic NMJ; therefore, the membrane
threshold is less easily attained.
• This results in a characteristic pattern of progressively reduced muscle strength with
repeated use of the muscle and recovery of muscle strength following a period of rest.
• Myasthenic crisis is an exacerbation and can result in a life-threatening condition,
characterized by neuromuscular respiratory failure. Severe bulbar muscle weakness often
accompanies the respiratory muscle weakness or may be the predominant feature.
Myasthenic crisis may be precipitated by a variety of factors (see Risk Factors). In addition,
it can occur spontaneously as part of the natural history of MG itself.
• Cholinergic crisis results from an excess of anticholinesterase drugs. Excessive ACh
stimulation produces flaccid muscle paralysis and pupil constriction.
• Assess the severity of disease, evaluate pulmonary function, and optimize medications.
• Continue anticholinesterase drugs in the preoperative period. In the postoperative period,
anticholinesterase drugs should be administered slowly and cautiously. Patients may have a
decreased requirement of these drugs in the first 48 hours.
• Avoid muscle relaxants in MG patients, if possible. MG patients have an abnormal response
to depolarizing (i.e., relative resistance) and non-depolarizing (i.e., more prolonged action)
blocking agents.
• The anesthetic plan should consider the use of ultra-short–acting anesthetics in order to
avoid postoperative respiratory depression and hypoventilation.
• Avoid postoperative mechanical ventilation (MV), whenever possible. Most patients may be
safely extubated at the end of the procedure, but those with severe MG may benefit from a
period of MV.
SYMPTOMS
• Fatigable weakness that worsens after exercise and improves with rest
• Chronic, fixed weakness may also be present
History
• Age of onset
• Clinical course
– Early in MG, the symptoms may be absent upon awakening
– Often as the disease progresses, the symptom-free periods are lost; symptoms are
continuously present but fluctuate from mild to severe.
• Intubations and ICU admissions
Signs/Physical Exam
• Ptosis and/or diplopia (>50% of patients with MG)
• Bulbar symptoms including dysarthria, dysphagia, fatigable chewing (about 15% of patients
with MG)
• Proximal limb weakness
• Facial muscles are frequently involved and make the patient appear expressionless
• On physical examination, the findings are limited to the motor system, without loss of
reflexes or alteration of sensation or coordination.
• Careful assessment of respiratory function, ability to cough, and bulbar function
MEDICATIONS
Evaluate the adequacy of drug therapy
• Anticholinesterases
• Immune suppression (steroids, azathioprine, cyclosporine)
• Thymectomy (for patients with generalized MG with thymoma or who are less than age 60
without thymoma)
• Plasmapheresis and intravenous immune globulin.
Labs/Studies
• Pulmonary function tests (negative inspiratory pressure and forced vital capacity)
• Arterial blood gasses (ABGs): The paCO2 and paO2 can help to predict the need for
postoperative MV.
• Chest x-ray may be indicated to rule out aspiration or other pneumonias.
• Thymoma: The majority of patients with AChR antibody-positive MG have thymic
abnormalities; hyperplasia in 60–70% and thymoma in 10–15%.
• Other autoimmune disorders that may be present include systemic lupus erythematous,
rheumatoid arthritis, pernicious anemia, thyrotoxicosis.
CIRCUMSTANCES TO DELAY/CONDITIONS THAT NEED OPTIMIZATION
If the patient is poorly controlled, a course of plasmapheresis may be of benefit in the
preoperative period. There should a 24-hour delay between the last plasmapheresis and
surgery to restore clotting factors.
CLASSIFICATIONS
• Grades
– Grade I: Only eyes affected
– Grade IIa: Mild generalized MG responding well to therapy
– Grade IIb: Moderate generalized MG responding less well
– Grade III: Severe generalized disease
– Grade IV: Myasthenic crisis requiring MV
• Preoperative factors associated with need for prolonged postoperative MV include: FVC
<2.9 L, history of MG >6 years, major surgery, co-existing lung disease, and grades III and
IV MG
TREATMENT
Premedications
• Continue all the doses of medications preoperatively to avoid aggravation of symptoms and
muscle weakness.
• Steroid-dependent patients will require steroid stress dose (hydrocortisone up to 100 mg IV
bolus before induction, then 100 mg q8h × 24h).
• Avoid sedatives as they can cause respiratory compromise.
Inform the patient of the potential requirement for prolonged MV.
INTRAOPERATIVE CARE
• Use of regional or local anesthesia should be utilized, whenever possible.
• Since local anesthetic agents may block neuromuscular transmission, it is better to use
techniques which involve the use of small quantities of these agents; therefore, sub-
arachnoid block is preferable to the use of epidural or caudal anesthesia.
Monitors
• Consider an arterial line in high-risk patients and for thymectomy (ABGs, electrolyte
analysis, and invasive arterial pressure monitoring): Monitoring of neuromuscular
transmission (nerve stimulator).
• Airway should be secured with an appropriate size ET tube using a non-paralyzing
technique. Sevoflurane often provides adequate relaxation for tracheal intubation.
• When muscle relaxant use is indicated, it is better to use small doses (1/10th of the usual
dose) of non-depolarizing rather than depolarizing relaxant drugs.
• The presence of a thymoma (anterior mediastinal mass) can result in intrathoracic airway or
vascular obstruction and may occur upon the induction of anesthesia.
Maintenance
• Several general anesthetic techniques have been proposed (balanced anesthetic technique or
TIVA), although none has been proven to be superior to the other.
• Avoid muscle relaxants, if possible. Volatile anesthetics may provide adequate relaxation
during surgery; however, intermediate and short-acting non-depolarizing agents can be
used. It is best to use small doses with careful monitoring of neuromuscular transmission.
• Preferentially utilize ultra-short–acting anesthetics (propofol, sevoflurane, remifentanil).
• Avoid factors which can enhance neuromuscular blockade (hypothermia, hypokalemia,
hypophosphatemia, and certain drugs).
• Criteria for extubation include:
– Head lift (5 sec)
– Negative inspiratory force of >25 cm of H2O
– Tidal volume >5 mL/kg
– Adequate muscle power evidenced by nerve stimulator
• Adequate postoperative pain control, pulmonary toilet, and the avoidance of drugs that
interfere with neuromuscular transmission facilitate tracheal extubation.
• Anticholinesterases therapy should be restarted in the immediate postoperative period. The
dose is based on the preoperative pyridostigmine dose (2 mg IV neostigmine is equivalent to
60 mg PO pyridostigmine) and titrated to effect.
FOLLOW-UP
BED ACUITY
• Postoperative care should take place in the ICU with monitoring of respiratory function as
well as chest physiotherapy for 12 hours.
• Meticulous attention to pulmonary toilet is required, particularly since respiratory secretions
may be increased by anticholinesterase drugs
• Good pain control, especially after thymectomy
• Avoid drugs that may exacerbate MG.
COMPLICATIONS
• Weakness after surgery presents a special problem in MG patients. The differential diagnosis
includes myasthenic crisis, residual effects of anesthetic drugs, non-anesthetic drugs
interfering with neuromuscular transmission, and cholinergic crisis. For these reasons, many
clinicians prefer to avoid the use of muscle relaxants, or if they use muscle relaxants, allow
the neuromuscular block to recover spontaneously. Tensilon (edrophonium) challenge test is
useful in distinguishing myasthenic crisis from cholinergic crisis.
• Aspiration, pneumonia, inadequate cough, atelectasis
• Need of ventilatory assistance in the postoperative period due to respiratory failure
• Rule out pneumothorax and phrenic nerve damage in case of thymectomy.
REFERENCES
1. irsch NP. Neuromuscular junction in health and disease. Brit J Anaesth. 2007;99(1):132–
138.
2. O’Neill GN. Acquired disorders of the neuromuscular junction. Int Anesthesiol Clin.
2006;42(2):107–121.
3. Tripathi M. The effect of the use of pyridostigmine and requirement of vecuronium in
patients with myasthenia gravis. Journal of Postgraduate Medicine. 2003;49:311–315.
CODES
ICD9
• 358.00 Myasthenia gravis without (acute) exacerbation
• 358.01 Myasthenia gravis with (acute) exacerbation
ICD10
• G70.00 Myasthenia gravis without (acute) exacerbation
• G70.01 Myasthenia gravis with (acute) exacerbation
CLINICAL PEARLS
• Assess severity of the disease.
• Evaluate the adequacy of drug therapy and optimize the patient’s condition.
• Use of regional or local anesthesia, whenever possible
• Avoid muscle relaxants and use ultra-short–acting anesthetics.
• Avoid postoperative ventilation, whenever possible.
• Admission to ICU for postoperative monitoring.
• MG may worsen during the course of pregnancy. The first trimester and the month
postpartum are the periods of highest risk of exacerbation.
MYASTHENIC SYNDROME
Fabrizio Racca, MD
BASICS
DESCRIPTION
• Lambert–Eaton myasthenic syndrome (LEMS) is an autoimmune presynaptic neuromuscular
junction (NMJ) disorder. It results from antibodies against voltage-gated calcium channels
which are involved with acetylcholine (ACh) release.
• The clinical picture is characterized by:
– Weak proximal limb muscles
– Depressed tendon reflexes
– Respiratory failure
– Abnormal autonomic function such as dry mouth, gastrointestinal slowing, postural
hypotension
– Oropharyngeal and ocular muscles are usually spared.
– Weakness that improves with sustained contraction
• Approximately one-half of LEMS cases are associated with a malignancy, mainly small-cell
lung cancer.
EPIDEMIOLOGY
Incidence
• The true incidence of LEMS is unknown, but the condition is uncommon and occurs much
less frequently than myasthenia gravis.
• In a population-based study from a region of Holland with 1.7 million inhabitants, 220 cases
of myasthenia gravis and 10 of LEMS were identified over a 9-year period.
Prevalence
• Cancer is present or later found in ∼40% of patients; clinical manifestations frequently
precede cancer identification.
• LEMS is most commonly seen with small-cell lung cancer (∼3%).
• More common in middle aged patients.
• Male:female 2:1 ratio.
Morbidity
• Respiratory failure
• Mostly associated with the underlying disease or cancer
Mortality
Mostly associated with the underlying disease or cancer
• Cancers: Small-cell lung cancer, as well as non-SCLC, lymphosarcoma, malignant thymoma,
cancer of the breast, stomach, colon, or prostate.
• Drugs that may worsen the muscular weakness include aminoglycosides, fluoroquinolones,
macrolides, beta blockers, diuretics, procainamide, magnesium salts, calcium channel
blockers, intravenous iodinated contrast.
PATHOPHYSIOLOGY
• LEMS is an autoimmune disorder that reduces ACh release from the presynaptic nerve
terminals. Antibodies directed against the voltage-gated calcium channel interfere with the
release of Ach, resulting in muscle weakness. ACh binding and its effect on the postsynaptic
membrane are not impaired, neither is the ACh receptor.
• In patients with cancer, antigens that mimic voltage-gated calcium channels are believed to
induce antibodies. In patients without cancer, antibodies to voltage-gated calcium channels
are believed to result from an autoimmune state.
• Consequently, muscle weakness improves with use as more Ach becomes available in the
NMJ. This phenomenon is referred to as postexercise or postactivation facilitation.
• Assess severity of disease and evaluate pulmonary function.
• Patients show extreme sensitivity to both depolarizing and nondepolarizing blocking drugs
and these should be avoided if possible.
• Other non-anesthetic medications may worsen the muscular weakness by inhibiting
neuromuscular transmission (see risk factors).
• Postural hypotension may be exacerbated by anesthetic induction agents and mechanical
ventilation (MV).
• Whenever possible, the use of ultra-short acting anesthetics should be administered to avoid
postoperative respiratory depression and hypoventilation.
SYMPTOMS
Weakness that improves with activity
History
• Clinical course
• Intubations and ICU admissions
Signs/Physical Exam
• Proximal limb motor weakness
• Depressed tendon reflexes
MEDICATIONS
• 3,4-diamimopyridine increases ACh release
• Guanidine hydrochloride increases ACh release
• Pyridostigmine decreases ACh metabolism and resultantly increases the amount of ACh that
is available.
• Immune suppressors (steroids, azathioprine, cyclosporine)
• Plasmapheresis and intravenous immune globulin
Labs/Studies
• Pulmonary function tests to help predict the need for postoperative mechanical ventilation;
specifically, the negative inspiratory pressure and forced vital capacity (FVC).
• Arterial blood gases to assess the pCO2 and pO2.
• Chest radiograph if aspiration or pneumonia is suspected.
• Cancer; see risk factor section
• Other autoimmune disorders:
– Systemic lupus erythematosus
– Rheumatoid arthritis
– Pernicious anemia
– Thyrotoxicosis
CIRCUMSTANCES TO DELAY/CONDITIONS THAT NEEDED OPTIMIZATION
If the patient is poorly controlled, a course of plasmapheresis may be of benefit in the pre-
operative period. There should be a 24-hour delay between the last plasmapheresis and
surgery in order to restore clotting factors.
TREATMENT
Premedications
• Continue medications preoperatively to avoid aggravation of symptoms and muscle
weakness.
• Steroid-dependent patients may require steroid stress dose (hydrocortisone up to 100 mg IV
bolus before induction, then 100 mg q8h × 24h).
• In general, sedation is avoided as it may cause respiratory compromise.
Inform the patient of the potential requirement for prolonged MV.
INTRAOPERATIVE CARE
• Use of regional or local anesthesia should be warranted whenever possible.
• Because local anesthetic agents may block neuromuscular transmission, it is better to use
techniques which involve the use of small quantities of these agents; therefore, a sub-
arachnoid block is preferable to the use of epidural or caudal anesthesia.
Monitors
• Monitoring of neuromuscular transmission (nerve stimulator)
• The airway should be secured with an appropriate size ET tube using a non-paralyzing
technique (i.e., without the use of muscle relaxant and after adequate topical analgesia of
the pharynx and larynx). Sevoflurane often provides adequate relaxation for tracheal
intubation.
• When muscle relaxant use is indicated, it is better to use small doses (1/10th of the usual
dose) of non-depolarizing drugs.
Maintenance
• Several general anesthetic techniques have been proposed (balanced anesthetic technique or
TIVA), although none have been proven to be superior to the other.
• Avoid muscle relaxants and use ultra-short acting anesthetics (propofol, sevoflurane,
remifentanil) or volatile agents to achieve the relaxation required for surgery. If using non-
depolarizing agents, it is best to use small doses with careful monitoring of neuromuscular
transmission.
• Avoid drugs that can enhance neuromuscular blockade (beta blockers, diuretics, magnesium,
calcium channel blockers).
• Criteria for extubation include:
– Head lift (5 seconds)
– Negative inspiratory force of >25 cm of H2O
– Tidal volume > 5 mL/kg
– Adequate muscle power evidenced by nerve stimulator
• Adequate post-operative pain control, pulmonary toilet, and the avoidance of drugs that
interfere with neuromuscular transmission facilitate tracheal extubation.
POSTOPERATIVE CARE
BED ACUITY
• Post-operative care should be done in the ICU with monitoring of respiratory function as
well as chest physiotherapy.
• Avoid drugs that may exacerbate motor weakness (see risk factors).
COMPLICATIONS
• Aspiration, pneumonia, inadequate cough, atelectasis
• In addition to postoperative pulmonary complications, laryngeal and respiratory muscle
weakness may warrant ventilatory assistance in the post-operative period.
REFERENCES
1. Hirsch NP. Neuromuscular junction in health and disease. Br J Anaesth. 2007;99(1):132–
138.
2. O’Neill GN. Acquired disorders of the neuromuscular junction. Int Anesthesiol Clin.
2006;42(2):107–121.
• Myasthenia gravis
CODES
ICD9
• 358.1 Myasthenic syndromes in diseases classified elsewhere
• 358.30 Lambert-Eaton syndrome, unspecified
ICD10
• G70.80 Lambert-Eaton syndrome, unspecified
• G73.3 Myasthenic syndromes in other diseases classified elsewhere
CLINICAL PEARLS
• Assess severity of the disease.
• Evaluate the adequacy of drug therapy and optimize the condition of the patients. Patients
may require plasmapheresis or stress dosing of steroids.
• Use of regional or local anesthesia, whenever possible.
• Avoid muscle relaxants and use ultra-short acting anesthetics.
• Avoid post-operative ventilation, whenever possible.
• Admission to ICU for post-operative monitoring.
MYOCARDIAL CONTUSION
BASICS
DESCRIPTION
• Myocardial contusion is an injury that usually results from blunt trauma.
• It does not have a standardized diagnostic criteria; clinical presentation is variable and can
range from minor cardiac bruises to severe insults such as cardiac rupture and death.
• Unlike much of cardiac disease managed by anaesthetists, the right ventricle tends to be
predominantly affected due to its anterior location. Thus right-sided failure takes a
predominant place in the pathophysiology of myocardial contusions.
EPIDEMIOLOGY
Incidence
• The lack of clear clinical diagnostic criteria makes determining the exact incidence difficult.
• A very wide range has been reported across the literature following blunt chest trauma: 9.4–
76%.
Morbidity
Associated with a higher incidence of perioperative hypotension, arrhythmias, and death.
This risk may persist for one month post trauma, but the magnitude of risk has not been
clearly defined.
Mortality
• Overall mortality is approximately 15%.
• One study found that a myocardial contusion in patients with thoracic trauma was
associated with a higher operative mortality (e.g., 54% vs. 4.6%), but this seemed to be
related to more severe injuries as most of the deaths were attributed to non-cardiac causes
(1).
Blunt trauma can result in myocardial contusions due to a variety of mechanisms:
• Energy transfer to the underlying heart from direct impact to the thorax.
• An injury due to deceleration of the heart.
• Compression of the heart within the thorax (e.g., between the spine and sternum).
• Trauma to the abdomen or lower extremities (without direct thoracic trauma) has been
implicated via upward displacement of the viscera.
PATHOPHYSIOLOGY
• Histopathology of the affected heart muscle can show hemorrhage, edema, necrosis, and
polymorphonuclear infiltrates.
• Animal models suggest that the pathogenesis is distinct from ischemic heart disease.
Although there is an initial fall in coronary arterial blood flow, it recovers quickly (over a
20-minute period), and the extent of ventricular dysfunction appears to be proportional to
direct myocyte injury and necrosis.
• The most common complication is arrhythmia and can occur even after mild trauma
(leading to the dilemma as to the need for, and the duration of, cardiac monitoring in many
trauma patients).
• As the right heart lies anterior, it is most commonly involved. As a result, frank cardiac
failure from left ventricular failure is less common. Increased pulmonary artery pressure
(from lung contusions, ARDS, etc.) may occur concurrently in this setting and can
complicate a right ventricular contusion, resulting in right ventricular failure.
• Commotio cordis is a cardiac arrest as a result of a low energy impact, often during sports,
resulting in a cardiac arrest.
– Distinct from a myocardial contusion, as there are no histological findings of trauma to the
heart.
– Also called a myocardial concussion.
– If the impact occurs shortly before the peak of the T wave, the result can be ventricular
fibrillation.
– Impact during the QRS complex can result in complete heart block.
• Anesthetic management should take into account the manifestations of myocardial
contusions (which may have presented preoperatively or declare themselves during the
case).
– Arrhythmias may need to be treated pharmacologically or via cardioversion/
defibrillation.
– Recognition that cardiac failure is likely to be right sided: Adequate preload is essential,
and thus TEE may be more useful than PA catheter measurements, especially in the
setting of concomitant pulmonary contusions, mechanical ventilation, and elevated
pulmonary artery pressures.
SYMPTOMS
• Often masked by other injuries or intubation in the severely injured.
• Chest pain and shortness of breath (though this may be secondary to chest wall trauma or
CPR).
• Palpitations.
• Evidence indicating high impact injuries:
– Rib fractures (especially upper) and clavicle fractures
– Pulmonary contusions
– Pneumothorax and/or hemothorax
– Flail chest
– Great vessel injuries
History
Any trauma history consistent with the possibility of myocardial injury should prompt further
investigation. Myocardial contusion should be considered in high-speed motor vehicle
accidents with blunt force trauma (especially chest trauma), auto versus pedestrian trauma,
falls, and other deceleration injuries as well as after cardiopulmonary resuscitation.
Signs/Physical Exam
• Irregular pulse indicating arrhythmias.
• Distended neck veins may indicate right ventricular failure or tamponade.
• Muffled heart tones, pulsus paradoxus may further indicate tamponade.
• Cardiovascular deterioration (decreased blood pressure, poor peripheral perfusion).
• Respiratory failure could represent further deterioration.
TREATMENT HISTORY
• Intubation and mechanical ventilation
• Increased oxygen requirement
• Temporary pacing for complete heart block
MEDICATIONS
• Antiarrhythmics
• Pharmacologic support of cardiac failure
Labs/Studies
• EKG, though as the right ventricle is the most commonly affected, this test may have very
limited utility (low negative predictive value).
– ST and T wave changes are frequent, Q waves are rare.
– Sinus tachycardia is the most common arrhythmia, as would be expected in trauma (i.e.,
low specificity).
– Arrhythmias, right bundle branch block (RBBB), and interventricular conduction defects
should be sought.
– Ventricular tachycardia is very concerning, but may not be captured on a 12-lead EKG
(continuous cardiac monitoring is suggested).
• Creatinine kinase MB is generally not considered helpful due to frequent concurrent skeletal
muscle injuries.
• Troponin levels: Troponin I is more specific than troponin T. However,
– Injury, especially small areas that may predispose to arrhythmia, may occur without
release of troponin.
– Hemorrhage or shock without myocardial contusion can result in troponin release.
• Echocardiography.
– Transthoracic method may be limited by mechanical ventilation, pneumothorax, and
difficulty in positioning the patient.
– Transesophageal might have some difficulty in imaging the right ventricle (the chamber
most often involved) but is still useful for the diagnosis of myocardial contusions and its
complications as well as to assist with cardiovascular management of the patient.
• Cardiac catheterization is indicated in the very few cases where coronary lesions are
suspected.
• Other blunt force injuries: Rib and clavicle fractures, flail chest.
• Pulmonary injuries such as pulmonary contusions, ARDS, aspiration, and pneumothorax
and/or hemothorax can potentially complicate the diagnosis and management of
myocardial contusions, particularly if pulmonary hypertension occurs.
• Associated cardiac injuries include:
– Myocardial infarction as either a complication, or the cause, of the trauma is a definite
and increasing possibility, given the changing population demographics. This can further
complicate the diagnosis and management of myocardial contusion.
– Coronary artery injury.
– Myocardial rupture: The right ventricle is most commonly involved.
– Ventricular and atrial septal defects.
– Valvular lesions: Most often affects the aortic and mitral valves due to the higher
intracavitary pressures.
– Pericardial effusion or hemopericardium.
– Pericardial rupture with the potential for myocardial herniation.
– Aortic rupture.
• Ideally the diagnosis of myocardial contusion should be established, including the extent of
the lesion and the related complications prior to surgery. The nature of much of trauma
injuries and surgery, however, does not frequently allow this luxury. Diagnostic effort may
need to occur in the operating room (e.g., via TEE), although this may prove difficult due to
the demands of merely caring for an unstable trauma patient.
• Further workup, however, may be possible in the more elective subsequent procedures that
are often part of the care of the trauma patient.
CLASSIFICATIONS
Not established
TREATMENT
Premedications
In the setting of confirmed or suspected myocardial contusion, caution with any
premedication may be warranted to avoid compromising the patient’s hemodynamic status.
If applicable, informing the patient and/or their family of the increased risk due to a possible
or confirmed myocardial contusion may be warranted. This might include possible additional
monitors that might be needed during the surgery.
INTRAOPERATIVE CARE
• Usually dictated by concomitant injuries and necessary surgery.
• In rare circumstances, sedation may be utilized to avoid general anesthesia and positive
pressure ventilation, if right ventricular function is compromised.
Monitors
Depending upon the extent of the contusion and its complications, additional monitoring
might be considered, including arterial, central, and pulmonary pressure monitoring as well
as cardiac output monitoring and TEE.
Careful consideration with regard to hemodynamic changes may dictate a “slow careful
induction”; however, a full stomach and potentially unstable cervical spine may complicate
this consideration.
Maintenance
• While no specific anesthetic is indicated, the goal should be to optimize hemodynamics in a
setting of potentially impaired cardiac function.
• Increased FIO2 is often administered.
• Consider the use of an ICU ventilator to allow for additional modes of ventilation (high
frequency, etc).
As per the extent of injury and the course of the surgery.
POSTOPERATIVE CARE
BED ACUITY
• Dependent upon the acuity of the patient’s overall condition and extent of the injury.
• Strongly consider a monitored setting if there is a suspicion of a myocardial contusion in an
otherwise stable (lower acuity) patient due to the potential for developing arrhythmias.
• Continued surveillance for, and support of, the manifestation of myocardial contusion as
outlined above may be indicated.
• Cardiology consult, if not already obtained, should be considered.
COMPLICATIONS
• Pericardial effusions and hemopericardium can occasionally lead to late constrictive
pericarditis (at times with significant calcifications) and may require pericardiectomy.
• Ventricular aneurysms are also occasionally seen as a late complication with variable
significance.
REFERENCES
1. Devitt JH, McLean RF, McLean BA. Perioperative cardiovascular complications associated
with blunt thoracic trauma. Can J Anesth. 1993;40:197–200.
2. Baxter BT, Moore EE, Synhorst DP, Reiter MJ, Harken AH. Graded experimental
myocardial contusions: impact on cardiac rhythm coronary artery flow, ventricular
function, and myocardial oxygen consumption. J Trauma. 1988;28(10):1411–1417.
ADDITIONAL READING
• Orliaguet G, Ferjani M, Riou B. The Heart in Blunt Trauma. Anesthesiology. 2001;95:544–
548.
• Schultz JM, Trunkey DD. Blunt cardiac injury. Critical Care Clinics. 2004;20:57–70.
• Pneumothorax
• Trauma
• Ventricular septal defect
CODES
ICD9
• 861.01 Contusion of heart without mention of open wound into thorax
• 861.11 Contusion of heart with open wound into thorax
ICD10
• S26.91XA Contusion of heart, unsp w or w/o hemopericardium, init
• S26.91XD Contusion of heart, unsp w or w/o hemopericardium, subs
• S26.91XS Contusion of heart, unsp w or w/o hemopericardium, sequela
CLINICAL PEARLS
• While most of our thinking about the heart (diagnosis and treatment) relates to the left
ventricle, much of the pathophysiology of myocardial contusions relates to the right side.
This is due to the orientation of the heart in the chest; the heart lies rotated, thus the right
ventricle is closest to the sternum and is most vulnerable to blunt trauma.
• In at least two scenarios, trauma patients may present with more traditional appearing
cardiac events (with coronary-based pathophysiology) that would dictate angiography with
possible stenting or bypass.
– A young trauma patient with classic findings of a myocardial infarction (on EKG, enzymes
and possibly echo) should be considered for the possibility of having a coronary injury.
– Older patients may have suffered atherosclerotic-related myocardial infarction as either
the cause of the trauma or as a result of the injury. With the aging trauma population, this
added consideration only indicates how much more complex the differential diagnosis will
become in the future.
MYOCARDIAL OXYGEN DEMAND
Emily Gordon, MD
BASICS
DESCRIPTION
• The balance between myocardial oxygen supply and demand is critical to the proper
function of the heart. If myocardial oxygen demands are not met, myocardial ischemia,
infarction, arrhythmias, or death may result.
• Oxygen demand is not equivalent to oxygen consumption. Demand is related to need.
Consumption is the actual amount of oxygen used per unit time.
• The myocardium uses oxygen primarily for effective contraction. Requirements for basal
metabolism comprise only 10–20% of total O2 consumption. Requirements of the electrical
conduction system are even less.
• The major determinants of myocardial oxygen demand are:
– Heart rate
– Contractility
– Myocardial (systolic) wall tension
• Myocardial oxygen consumption (VO2): Large amounts of ATP are needed for the proper
function of the myocardium. Aerobic metabolism (most efficient source) of fatty acids is the
primary mechanism by which ATP is regenerated at rest.
• Oxygen extraction: The myocardium is a tightly regulated tissue which excels in its ability to
extract oxygen from the blood that enters the coronary arteries. In the non-stressed state,
the myocardium extracts 70–75% of the oxygen from the red blood cells/hemoglobin that
flow through the coronary arteries. Venous saturation thus equals ∼25–30%.
• Coronary blood supply is comprised of coronary blood flow and blood oxygen carrying
capacity. Furthermore, because coronary oxygen extraction is near maximal under resting
conditions, the primary mechanism to meet increased oxygen demand is through enhanced
delivery; thus, it is a dynamic process that is modulated by multiple parameters.
– Autoregulation is the intrinsic mechanism to maintain a constant blood flow over a range
of perfusion pressures (60–160 mm Hg); changes in pressure are met by reciprocal
changes in resistance. Local metabolic and myogenic factors appear to play a role.
Myogenic factors describe the response of smooth muscles to the shear forces of perfusion
pressure. Metabolic factors (e.g., oxygen and carbon dioxide tension and adenosine) affect
vascular smooth muscle tone as their concentrations vary. In other words, an increase in
the PaCO2 would stimulate vasodilation and “washout.”
– Humoral factors include circulating agents such as angiotensin II, serotonin, thromboxane,
prostacyclin, and bradykinin that effect coronary resistance.
– Neural control describes autonomic innervation such as alpha, beta, and parasympathetic
activity.
– Diastolic time: The left ventricle’s systolic pressures exceed the coronary artery’s diastolic
perfusion pressure; thus extravascular compressive forces prevent perfusion during systole.
– Blood oxygen–carrying capacity is the sum of oxygen bound to hemoglobin and dissolved
in blood. It is primarily determined by the hemoglobin level (capable of binding 1.39 mL
of oxygen per gram); dissolved oxygen is poorly soluble in blood (0.003), thus, its
contribution is minimal. This serves as the physiologic basis for blood transfusions.
• Oxygen demand: Heart rate has the greatest effect on myocardial work and oxygen demand.
– Heart rate: For every heartbeat, the myocardium undergoes electrical depolarization and
repolarization, generates contractility, ejects blood against the wall tension (preload or
volume work and afterload or pressure work), and undergoes relaxation. Note:
Tachycardia will decrease the diastolic perfusion time which primarily affects the left
ventricle’s blood supply.
– Cardiac contractility or inotropy is the intrinsic ability of the cardiomyocyte to shorten
from its individual resting fiber length; it is independent of preload and afterload.
Contraction results from myosin and actin filament binding and is dependent upon
intracellular calcium ion concentration. Increases in sympathetic tone or catecholamine
state, calcium levels, heart rate, as well as inotropic drugs (beta agonists, calcium,
glucagon, phosphodiesterase inhibitors) have a positive effect on contractility.
– Myocardial wall tension: The law of LaPlace states that wall tension is directly
proportional to the chamber radius and pressure; it is inversely proportional to the wall
thickness.
Radius is primarily determined by preload (changes in blood volume or chamber size).
Pressure is primarily determined by the afterload which is a function of systemic
vascular resistance, the aortic valve, and blood viscosity.
Myocardial wall thickness is responsible for long-axis function secondary to endocardial
and midwall fractional shortening. However, wall thickness is not responsible for short-
axis function.
Tension is dynamic (aside from wall thickness) and can vary with each heartbeat and
throughout the contraction (chamber size decreases with ejection).
ANATOMY
• Coronary arteries: The presence of a stenotic lesion results in a pressure drop that is
proportional to the fourth power of the radius, the length of the plaque, and the magnitude
of flow.
• The subendocardium (inner one-third to one-fourth of the myocardium) is most susceptible
to the effects of CAD or to a reduction in perfusion pressure. This is secondary to:
– Adjacent intraventricular pressures (left ventricular end-diastolic pressure)
– Limited maximal vasodilator response
– Blood flow only occurs during diastole; during systole, extravascular compressive forces
(mechanical forces that compress coronary vasculature) are greatest
• Heart rate is increased by:
– Pain or inadequate anesthesia
– Postoperative shivering
– Catecholamines
– Hypovolemia
– Anemia
– Hypoxia
– Fever
– Hyperthyroidism
– Administration of vagolytic drugs (e.g., atropine, glycopyrrolate)
• Cardiac contractility is increased by:
– Catecholamines
– Increased heart rate: The Treppe or Bowditch effect describes an autoregulatory method
by which myocardial contractility increases with an increase in heart rate. This
mechanism is believed to result from an inability of the sodium–potassium ATPase (moves
sodium extracellularly) to keep up with the sodium–calcium exchanger (moves sodium
intracellularly) during tachycardia. This results in increased intracellular levels of calcium.
• Myocardial wall tension is increased by:
– Increased ventricular diameter (volume overload, impaired ejection fraction, dilated
cardiomyopathy).
– Increased aortic pressure: Hypertension, aortic stenosis, and hemoconcentration increase
the pressure that needs to be generated in order to eject blood from the left ventricle.
• Induction of anesthesia
– Laryngoscopy and airway instrumentation can result in excessive catecholamine release.
The goal is to pre-empt with opioid or anti-hypertensive administration, decrease
laryngoscopy time, ensure an adequate depth of anesthesia (and time for onset), and be
prepared to treat hemodynamic perturbances (esmolol, nitroglycerin, additional anesthetic
agents such as propofol or volatile agents).
• Maintenance of anesthesia
– Pain and awareness under anesthesia can result in tachycardia; ensure an adequate depth
of analgesia and anesthesia. This may become challenging in the hypotensive patient.
Consider the use of nitrous oxide and decrease of volatile agent, volume administration, or
phenylephrine infusion to maintain adequate mean arterial pressures.
– Perioperative beta-blockade may be titrated to a heart rate of 50–80 beats/min or bolused
during catecholaminergic states.
– Changes to desflurane concentrations can result in sympathetic discharge and tachycardia.
– Normothermia may be maintained with blankets or warming devices (convective blankets,
warming fluids, etc.)
– Optimize volume status: Hypovolemia can result in a reflex tachycardia, whereas
hypervolemia increases the myocardial chamber radius (preload).
• Postoperative/PACU care
– Provide adequate pain control: A multimodal approach may include anti-inflammatory
medications, regional nerve blocks, and opioids, as appropriate.
– Optimize volume status: The postoperative period may be marked by fluid flux between
the intracellular and extracellular compartments as well as continued bleeding.
– Treat postoperative shivering (warming techniques, meperidine, clonidine).
– Ensure adequate oxygenation: Residual sedatives or narcotics can decrease the functional
residual capacity and result in hypoxia (increased sympathetic state). Consider nasal
cannula, facemask, deep breathing, coughing or CPAP/BIPAP when indicated.
EQUATIONS
• MVO2 = CBF × (CaO2 – CvO2); where MVO2 is mixed venous oxygen saturation, CBF is
cerebral blood flow, CaO2 is the arterial blood oxygen content, and CvO2 is the venous
blood oxygen content
• A-VO2 = (CaO2 – CvO2) is the arterial-venous oxygen content difference (mL O2/mL blood)
• CO = O2 consumption/A-VO2 difference
• Law of LaPlace: T = ΔPr/2h, where T is tension, ΔP is change in pressure, r is radius, and h
is myocardial wall thickness
REFERENCES
1. DeFily DV, Chilian WM. Coronary microcirculation: autoregulation and metabolic control.
Basic Res Cardiol. 1995;90(2):112–118.
2. Duncker DJ, Bache RJ. Regulation of coronary blood flow during exercise. Physiol Rev.
2008;88(3):1009–1086.
3. Duncker DJ, Merkus D. Regulation of coronary blood flow. Effect of coronary stenosis.
Arch Mal Coeur Vaiss. 2004;97(12):1244–1250.
4. Ardehali A, Ports TA. Myocardial oxygen supply and demand. Chest. 1990;98(3):699–705.
• Chronic angina
• Hypothermia
• Preload
• Afterload
CLINICAL PEARLS
• The myocardial oxygen demand cannot be easily measured in the perioperative period. To
that extent, a clear understanding of the various factors that affect demand, as well as
supply, are critical to optimize an adequate balance and avoid ischemia.
NARCOTIC WITHDRAWAL
Angela T. Hsu, MD
BASICS
DESCRIPTION
• Sudden opioid abstinence or administration of an opioid antagonist in a narcotic-dependent
individual may induce a traumatic reaction in the body, collectively characterized as opioid
withdrawal syndrome.
• Opioid withdrawal is rarely life-threatening, but is highly unpleasant and may complicate
care in the perioperative period.
EPIDEMIOLOGY
Incidence
• Narcotic pain medications are the most frequent class of medications that are misused or
abused; they accounted for 397,160 ED visits in 2009.
• In a 2009 US survey of ER departments, heroin accounted for 213,118 visits.
Prevalence
• In 2002, the prevalence of heroin dependence was estimated at 0.14% of the US population.
• Although ED visits from heroin usage has not changed significantly from 2004 to 2009,
narcotic painkiller related visits have risen dramatically.
• According to recent estimates, >2 million people in the US are abusing prescription opioids.
Morbidity
• Narcotic withdrawal is uncomfortable and associated with sympathetic nervous system
hyperactivity.
• Patients with underlying cardiac risk factors may be predisposed to arrhythmias, ischemia,
and subsequent cardiovascular collapse during withdrawal.
Mortality
Fatality is rare.
In chronic opioid-dependent patients, withdrawal may be precipitated by:
• Abrupt cessation or a significant decrease in the regular dosing of opioids
• Administration of an opioid antagonist: Nalmefene, naltrexone, naloxone
• Administration of an opioid agonist–antagonist: Pentazocine, butorphanol, nalbuphine,
buprenorphine
• Opioid receptors were once thought to be found exclusively in the CNS, but recent studies
show that they are found in virtually all organ systems.
• Endogenous opioids not only modulate the perception of pain, but also help regulate many
other physiologic functions, including:
– Respiration
– Blood pressure
– Shock and stress states
– Vasopressin release and free water clearance by the kidneys
• Neuroadaptation results from the regular use of opioids.
– There is a downregulation of opioid receptors with the continuous presence of high levels
of opioid agonists.
– At the cellular level, there are changes in several components of cyclic adenosine
monophosphate (cAMP) signal transduction cascades.
– Physical dependence usually occurs 1–4 weeks after continuous opioid usage.
• Withdrawal from opioids can result in a sudden increase in cAMP levels in many organ
systems. The sympathetic nervous system is one of the most prominent systems affected by
opioid withdrawal.
– Epinephrine levels increase ∼30 times and norepinephrine levels increase ∼3 times,
leading to restlessness, rhinorrhea, lacrimation, diaphoresis, myosis, piloerection, and CV
changes.
– Explains the benefit of clonidine in attenuating withdrawal symptoms
Management of heroin abusers and chronic opioid-dependent patients
• Maintain opioids during the perioperative period to avoid withdrawal. Long-acting opioids
such as methadone or buprenorphine formulations may be used in combination with short-
acting opioids to decrease troughs in opioid levels and treat breakthroughs, respectively.
• Avoid opioid antagonists and opioid agonist–antagonists in these patients since they can
precipitate acute withdrawal.
DIAGNOSIS
• History: As narcotic withdrawal is not associated with altered mental status (AMS), patients
can often tell you if they are undergoing withdrawal secondary to opioids. They can also tell
you their usual opioid dosing schedule and the timing of their last dose.
• Signs and symptoms
– Manifest between 5 and 24 hours from the last dosing. Methadone withdrawal may take
longer to present, but is usually between 24 and 48 hours.
– Peak withdrawal is 36–72 hours after the last dose. For methadone, it is 72–96 hours after
the last dose.
– Duration is usually 5–10 days. Methadone withdrawal typically lasts 2–3 weeks,
sometimes longer.
– Signs: Pupillary dilation, sweating, piloerection, tachycardia, ventricular dysrhythmias,
vomiting, diarrhea, hypertension, yawning, fever, rhinorrhea
– Psychological withdrawal symptoms, such as dysphoria and insomnia, may last weeks to
months.
– Symptoms: Craving for opioids, restlessness, irritability, increased sensitivity to pain,
nausea, abdominal cramps, myalgia, dysphoria, insomnia, anxiety
• Labs: Urine or blood toxin screen confirms opioids and/or other illicit substances.
• Other substances that cause autonomic instability. AMS, disorientation, hallucinations, and
seizures are not found in narcotic withdrawal but may be found when withdrawing from:
– Alcohol
– Benzodiazepines
– Barbiturates
• Other sedatives/hypnotics
TREATMENT
For patients undergoing anesthesia for emergency procedures:

• Abort withdrawal symptoms by administering opioid agonists.
• Check electrolytes, BUN, and creatinine if there has been significant dehydration, vomiting,
or diarrhea. Give fluids or replete electrolytes, as indicated.
• Consider regional anesthesia when possible.
• For general anesthesia, a balanced technique with volatile anesthetics +/– nitrous is
recommended.
• Beware of perioperative hypotension as intravascular volume depletion is common, given
the fevers, malnutrition, chronic infection, and adrenocortical deficiency often associated
with opioid addiction and withdrawal.
• Clonidine, a central acting alpha-2 agonist, may be given orally or applied via a transdermal
patch to help with sympathetic nervous system hyperactivity found in narcotic withdrawal.
• NSAIDs, such as ibuprofen, are given to attenuate muscle aches.
• Benzodiazepines are sometimes used for anxiety, insomnia, and muscle cramps. However,
given the potential for abuse and high risk of physical dependence, this is not considered
first-line therapy.
• For patients undergoing procedures or for acute pain consultation where narcotic
detoxification is desired:
– Consider administering the original opioid dosing and planning a gradual taper.
– Alternatively switch to long-acting methadone or buprenorphine for gradual
detoxification. Note: Patient must be in full withdrawal prior to starting buprenorphine.
As an agonist/antagonist, buprenorphine can precipitate more severe withdrawals if given
prematurely.
• Ultra-rapid opiate detoxification in which patients are given large doses of opioid antagonist
and placed under general anesthesia for the most severe stages of withdrawal, has become
popular. However, compared to buprenorphine- or clonidine-assisted opioid detoxification,
it is not as effective or safe. Several serious adverse events, including possibly fatal cardiac
and pulmonary complications, have been linked to ultra-rapid opioid detoxification.
• Instead of detoxification, consider lifelong maintenance on methadone or buprenorphine
since these have been associated with much higher rates of long-term program retention.
Studies on methadone maintenance programs have shown decreased medical comorbidity,
transmission of HIV, mortality, and increased social functioning.
FOLLOW-UP
The relapse rate for opioid addiction is high. Significant psychosocial support is needed
beyond the withdrawal period to prevent relapse.
REFERENCES
1. Administration SAaMHS. Results from the 2007 National Survey of Drug Use and Health:
National Findings. Rockville, MD: Administration SAaMHS, 2008.
2. Collet BJ. Opioid tolerance: The clinical perspective. Br J Anaesth. 1998;81:58–68.
3. Collins ED, Kleber HD, Whittington RA, et al. Anesthesia-assisted vs. buprenorphine- or
clonidine-assisted heroin detoxification and naltrexone induction: A randomized trial.
JAMA. 2005;294:903–913.
4. Kaye AD, Gevirtz C, Bosscher HA, et al. Ultra-rapid opiate detoxification: A review. Can J
Anaesth. 2003;50(7):663–671.
5. Kosten TR, O’Connor PG. Management of drug and alcohol withdrawal. N Engl J Med.
2003;348:1786–1795.
6. Substance Abuse and Mental Health Services Administration, Center for Behavioral Health
Statistics and Quality. The DAWN Report: Highlights of the 2009 Drug Abuse Warning
Network (DAWN)—Findings on Drug-Related Emergency Department Visits. Rockville,
MD, December 28, 2010.
• Drug abuse in pregnancy
• Alcohol withdrawal syndrome
CODES
ICD9
292.0 Drug withdrawal
ICD10
F11.23 Opioid dependence with withdrawal
CLINICAL PEARLS
• Opioid withdrawal is rarely life-threatening, but may complicate care in the perioperative
period.
• Clonidine may attenuate the sympathetic nervous system hyperactivity found in withdrawal.
• Consider the possibility of abuse of other illicit substances in patients who abuse opioids.
• Consider comorbid psychiatric conditions in narcotic withdrawal patients.
• When caring for opioid addicts, particularly the intravenous abuser, beware that these
patients often have associated infectious problems: hepatitis, HIV, endocarditis, septic
thrombophlebitis, cellulitis, abscesses, aspiration pneumonitis, malnutrition.
NEGATIVE PRESSURE PULMONARY EDEMA
Agnes Miller, MD
BASICS
DESCRIPTION
• Negative pressure pulmonary edema (NPPE) is an uncommon, but well-recognized clinical
entity that results from the negative intrathoracic pressure generated during spontaneous
ventilation with concurrent upper airway obstruction.
• The pulmonary edema results from either:
– “Pulling” of fluids from the pulmonary capillary bed into the alveoli (Starling forces), or
– Injury to the pulmonary microvascular membranes from severe mechanical stress that
results in capillary “leaking” of fluid.
• NPPE can result from laryngospasm or biting, commonly at induction or extubation, as well
as from epiglottitis, tumors, obesity, hiccups, or obstructive sleep apnea.
• Clinical manifestations result from ventilation and perfusion difficulties (V/Q mismatching
or shunt) with a frequent need for reintubation and temporary ventilatory support.
EPIDEMIOLOGY
Prevalence
• All anesthetic practices: 0.05–0.1%.
• Laryngospasm post-extubation or biting of the endotracheal tube (ETT): 74%
• Initial airway management secondary to laryngospasm or obstruction from large head and
neck tumors: 26%.
Prevalence
Development of pulmonary edema following active intervention for acute upper airway
obstruction: 11%
Morbidity/Mortality
• In undiagnosed cases it can range between 11% and 44%.
• If diagnosed and treated promptly, it is less than 1%.
• Etiology
– Laryngospasm
– ETT biting
– Airway trauma
– Upper airway collapse
– Bronchial obstruction
– Foreign body aspiration
– Postoperative residual curarization (impairs the upper airway dilator muscle strength
while preserving inspiratory muscle function)
• Patient characteristics
– Young, healthy, athletic (capable of generating large negative intrathoracic pressures
during an obstructive event)
• Surgical procedures
– Oropharyngeal surgery, particularly for tumors or other potentially obstructing masses
• The pathogenesis of NPPE is related to the development of high negative intrapleural
pressure by vigorous inspiratory efforts against an obstructed upper airway.
• 2 different mechanisms may explain the development of pulmonary edema during airway
obstruction:
– Starling forces: High negative intrathoracic pressures draw fluid out of micro-vessels into
the peri-microvascular interstitium. Cardiogenic pulmonary edema states (CHF, fluid
overload) have a similar presentation but result from positive capillary pressures that
“push" fluid out of micro-vessels. During upper airway obstruction and forceful
inspiration, pressure in the trachea and lower airways will decrease markedly (become
more negative). The pressure in the pleural space decreases (becomes more negative) by
exactly the same amount. The pressure in the pulmonary vessels decreases by much less,
thus increasing the pressure difference between the inside and the outside of the
capillaries and accelerating the formation of interstitial fluid.
– Disruption of the alveolar epithelium and pulmonary microvascular membranes from
severe mechanical stress occurs, leading to increased pulmonary capillary permeability
and protein-rich pulmonary edema (this resembles non-cardiogenic pulmonary edema
states such as acute respiratory distress syndrome).
– Starling equation: Q = K [(Pmv − Ppmv) − (πmv − πpmv)], where
Q = Net transcapillary flow of fluid
K = Transcapillary permeability
Pmv = Hydrostatic pressure in microvessels
Ppmv = Perimicrovascular interstitium
πmv = Plasma protein osmotic pressure in the peripheral vessels
πpmv = Protein osmotic pressure in the perimicrovascular interstitium
• Respiratory dynamics:
– Pulmonary edema is the pathologic accumulation of fluid in the lung interstitium, and
later alveoli, producing impairment in gas exchange.
– Pulmonary edema leads to V/Q mismatching since less alveoli are participating in gas
exchange. The severity of V/Q mismatch correlates with the severity of the pulmonary
edema.
– Lung edema leads to decreased lung compliance, which leads to an increased work of
breathing.
• Bite block to prevent biting on the ETT
• In patients prone to upper airway obstruction, consider prophylactic placement of an oral
airway or nasal trumpet.
• Treat laryngospasm aggressively with positive pressure ventilation or succinylcholine.
• History: Acute upper airway obstruction in spontaneously ventilating patients
• Signs and symptoms: Onset can occur within minutes after the relief of obstruction. Can
present as stridor, wheezing, decreased SaO2%, or frothy or pink sputum.
• Studies: EKG is typically normal, but may demonstrate right heart strain.
• Laboratory findings: None that are specific
• Radiographic findings: Peripheral or central asymmetric peribronchial infiltrates
• Neurogenic pulmonary edema
• Fluid overload
• Non-cardiogenic pulmonary edema (e.g., acute respiratory distress syndrome).
TREATMENT
• The goal is to maintain a patent upper airway and administer supplemental oxygen.
• Consider a trial of CPAP or pressure support as an alternative to intubation. The aim of
noninvasive respiratory support is to:
– Partially compensate for the increased work of breathing
– Improve alveolar recruitment with better gas exchange
– Reduce left ventricular afterload
– Increase cardiac output and improve hemodynamics
• In severe cases, consider re-intubation. Ventilation mode should be similar to the mode used
during acute lung injury (i.e., small tidal volumes [6 mL/kg], increased respiratory rate
[14–18 breaths/minute], and attempt to keep peak pressures <30 cm H2O).
• Pharmacologic management:
– Bronchodilators may be used to treat bronchospasm and possibly increase the rate of
alveolar fluid clearance.
– Diuretic use is controversial and may not be necessary.
• Extubation criteria:
– Ensure resolution of pulmonary edema.
– General extubation criteria are met.
FOLLOW-UP
• Generally, a benign condition that resolves in 24–48 hours when recognized early and
necessary supportive measures are instituted.
• If NPPE develops at iInduction:
– An elective case should be postponed.
– An emergent case should proceed after the airway has been secured. Implement smaller
tidal volumes, increased respiratory rate, and maintain low peak pressures.
REFERENCES
1. rodel DJ. Casescenario: Acute postoperative negative pressure pulmonary
edema.Anesthesiology.2010;113:200–207.
2. oldenberg JD. Negative pressure pulmonary edema in the otolaryngology patient.
Otolaryngol Head Neck Surg. 1997;117:62–66.
3. Fremont RD. Post-obstructive pulmonary edema: A case for hydrostatic mechanisms. Chest.
2007;131:1742–1746.
4. Lorch DG. Post-extubation pulmonary edema following anesthesia induced by upper
airway obstruction. Are certain patients at increased risk? Chest. 1986;90:802–805.
5. Majewski J, Górnik-Właszczuk E, Koczy B, et al. Negative pressure pulmonary edema and
hemorrhage. Anestezjol Intens Ter. 2010;42(2):90–93. [in Polish].
ADDITIONAL READING
• www.theasahq.org
• www.uptodate.com
• Non-cardiogenic pulmonary edema
• Laryngospasm
CODES
ICD9
518.4 Acute edema of lung, unspecified
ICD10
J81.0 Acute pulmonary edema
CLINICAL PEARLS
• Pulmonary edema can result from cardiogenic or neurogenic causes, fluid overload, or acute
respiratory distress syndromes, as well as from the generation of negative pressure against
upper airway obstruction. It is possible that many of the cases of postoperative oxygen
desaturation are due to unrecognized NPPE.
• This form of pulmonary edema is typically transient, self-limited, and easily resolved by the
maintenance of a patent upper airway and supplemental oxygen. Mechanical ventilation
may be needed for a very brief period of time.
• The oxygen desaturation following NPPE can be confused with pulmonary aspiration and
pulmonary embolism, which are potentially associated with serious morbidity and
mortality.
NEPHRECTOMY
BASICS
DESCRIPTION
General
• A nephrectomy is the surgical removal of all, or part, of the kidney.
• Nephrectomy procedures include:
– Simple: Removal of the kidney alone. Indications include infection, obstruction, and
hypertension.
– Partial: Removal of a portion of the kidney. Indications include mass or tumor. Has
increased in popularity as a means to preserve nephrons in patients with renal masses that
are <4 cm in size and located in an accessible region of the kidney.
– Radical: Removal of the kidney, surrounding fat, adrenal gland, and ureter. Indications
include renal cell carcinoma.
– Donor: Removal of a healthy kidney, ureter, and as much of the renal vessels as possible.
Indication is for living related renal transplant.
• Procedures: Nephrectomies can be done open, laparoscopically, or with robotic equipment.
The benefits of the laparoscopic approach include less pain, earlier PO intake, and shorter
hospitalization. These must be weighed against the potential for longer operative times, and
are dependent on the surgeon’s level of experience. Additionally, the pneumoperitoneum
significantly decreases renal blood flow.
– Open and laparoscopic nephrectomy involves exposure of the kidney, control and ligation
of the renal vessels at the renal hilum, ligation of the ureter, and removal of the kidney.
– Open and laparoscopic partial nephrectomy involve exposure of the kidney and renal
hilum, delineation of the mass (via direct visualization or ultrasound), submersion of the
kidney in ice (to decrease renal metabolic rate/oxygen consumption), renal artery
clamping, resection of the mass in as brief a period of time as possible (to decrease
ischemia time), and reperfusion. Following reperfusion, bleeding is controlled, the renal
parenchyma is closed to avoid urine leakage, and the wound is closed. In patients at high-
risk for post-resection renal failure, manual compression of the renal artery may be
performed instead of clamping.
Position
• Flexed lateral decubitus: Retroperitoneal approach
• Supine: Transabdominal approach
Incision
• Laparoscopic: 3–4 small incisions in the upper abdomen, one at the umbilicus
• Open nephrectomy: Subcostal, lumbar, retroperitoneal, or flank incision
Approximate Time
• 2–3 hours for either approach
• Laparoscopic times are highly dependent on surgeon experience.
EBL Expected
• 200–500 mL
• Blood loss is significantly higher for partial nephrectomies and nephrectomies performed to
remove large tumors involving renal vessels or the inferior vena cava (IVC).
Hospital Stay
• Laparoscopic: 1–2 days
• Open: 5–7 days
• Laparoscopic: Laparoscopy monitors and equipment
• Partial nephrectomy may require intraoperative ultrasound to localize lesions.
• Nephrectomy for renal cell cancer may require cardiopulmonary bypass if there is
significant tumor extension into the IVC.
• Indications include renal mass, non-functioning kidney, duplex anomalies of the kidney,
vesicoureteric reflux, and multicystic dysplastic kidney.
• Laparoscopic, open, partial, and total nephrectomies are all possible depending on the
pathology.
EPIDEMIOLOGY
Incidence
In the US, approximately 25,000 nephrectomies and 5,000 partial nephrectomies are
performed annually.
Prevalence
• Renal cell carcinoma is most prevalent in males aged 50 years and older.
Morbidity
• Renal failure requiring dialysis
• Cardiovascular events, including perioperative myocardial ischemia
• Hemorrhage
• Respiratory complications, including pneumonia, pulmonary embolus, or respiratory failure
• Injury to surrounding structures, particularly the spleen or pancreas with left nephrectomies
• Urinary leak, if partial nephrectomy undertaken
Mortality
• Dependent on the indication for the procedure and ranges from <1% to 5%
• Simple donor nephrectomies have a perioperative mortality of 0.03%
• Nephrectomies for renal cell cancer have a mortality rate dependent on the stage of their
cancer and medical comorbidities.
• If partial nephrectomy is performed, preparation for blood loss during the resection of the
mass is crucial.
• Avoid further insult to remaining kidney
– Nephrotoxic drugs
– Hypotension
– Hypovolemia
– Sepsis
SYMPTOMS
• May include a sensation of fullness at the site, pain, hematuria, and hypertension
• Donor nephrectomies are typically healthy.
History
• Indication for the procedure
• Obtain a surgical history to assess potential difficulty with the surgical procedure related to
adhesions.
• Obtain a social history, including tobacco abuse, to assess risk of intraoperative and
postoperative complications.
Signs/Physical Exam
No specific physical exam findings; a palpable flank mass may be present in patients with
renal tumors.
MEDICATIONS
• Erythropoietin for patients with renal insufficiency and anemia
• Oral antihypertensive agents to control blood pressure
Labs/Studies
• Type and Screen
• CBC
• BMP
• UA
• EKG, if age >50 years or clinical risk factors present
• Most patients will have a preoperative CT scan that delineates the size and extent of the
mass as well as identifies abnormal anatomy that may prolong surgery or increase blood
loss.
• In patients with renal tumors, a CXR, bone scan, or PET scan may be performed to see if the
cancer has spread.
• Simple nephrectomies performed for secondary hypertension may have significant cardiac
impairment related to long-standing increased left ventricle work.
• Renal cell cancer may be accompanied by para-neoplastic syndromes, including
erythrocytosis, hypercalcemia, and hypertension.
• Donor nephrectomies are carefully screened and generally have limited to no organ
dysfunction.
TREATMENT
Premedications
• No particular preoperative medications indicated
• Consider erythropoietin in patients with renal impairment and significant anemia.
• For all laparoscopic procedures, patients must be counseled that the risk of conversion to
open is approximately 5%.
• If an epidural is planned, consent should be obtained in the preoperative area.
• Blood transfusion may be needed depending on the patient’s comorbidities, extent of
preoperative anemia, and expected duration of surgery.
• A single preoperative dose of a first-generation cephalosporin is adequate for the majority of
nephrectomies.
• If the procedure is performed for chronic infection, coverage for Gram-negative anaerobic
organisms is needed.
INTRAOPERATIVE CARE
• General endotracheal anesthesia is required for either laparoscopic or open approach.
• Combined general and epidural anesthesia may be beneficial for open approach. Assess case
for possible use of cardiopulmonary bypass (tumor involving vena cava) prior to epidural
placement. Anticoagulation needed for pump is a contraindication to CPB.
– Epidural or spinal anesthesia requires a T8 dermatome level.
Monitors
• An arterial line can be used in the setting of concomitant organ dysfunction, partial
nephrectomy, or other renal procedure where large blood loss is anticipated.
• A central line allows for determination of central venous pressure (CVP), which can be used
to guide fluid management and administer vasopressors or fluid resuscitation if indicated.
• Foley catheter to monitor urine output
IV induction is most commonly performed except in pediatric patients.
Maintenance
• Inhalation agent of choice
• Cisatracurium is the neuromuscular blocker of choice in the setting of renal insufficiency as
it is not dependent on renal function for elimination.
Ensure adequate pain control and hemodynamic stability prior to extubation
POSTOPERATIVE CARE
BED ACUITY
• Floor bed is appropriate for the majority of patients.
• A monitored or ICU bed may be necessary in patients with multiple medical comorbidities,
significant intraoperative blood loss, or other intraoperative complications.
ANALGESIA
• Open procedure: Epidural, unless contraindicated
• Laparoscopic procedure: IV analgesics
• Morphine has an active metabolite that is renally cleared. Therefore, it may accumulate in
renal insufficiency and cause respiratory depression.
COMPLICATIONS
• Laparoscopic approach ranges from ~8–17%, compared to an open approach of ~2–4%.
– Renal failure
– Hemorrhage
– Infection
– Nerve injury
– Positioning injury
– Diaphragmatic injury, with subsequent pneumothorax requiring chest tube placement
PROGNOSIS
• Dependent on indication for procedure
• Patients undergoing nephrectomy for a tumor have a prognosis dependent on the type and
stage of cancer as well as medical comorbidities.
• Patients undergoing a simple donor nephrectomy are usually healthy and young with an
excellent postoperative prognosis.
REFERENCES
1. Demyttenaere S, Feldman LS, Fried GM. Effect of pneumoperitoneum on renal perfusion
and function: A systematic review. Surg Endosc. 2007;21(2):152–160.
2. Han KR, Kim HL, Pantuck AJ, et al. Use of American Society of Anesthesiologists physical
status classification to assess perioperative risk in patients undergoing radical nephrectomy
for renal cell carcinoma. Urology. 2004;63(5):841–846.
3. Richstone L, Montag S, Ost MC, et al. Predictors of hemorrhage after laparoscopic partial
nephrectomy. Urology. 2011;77(1):88–91.
4. Richstone L, Seideman C, Baldinger L, et al. Conversion during laparoscopic surgery:
Frequency, indications and risk factors. J Urol. 2008;180(3):855–859.
• Laparoscopy
• Hypertension
• Epidural
CODES
ICD9
V59.4 Kidney donors
ICD10
Z52.4 Kidney donor
CLINICAL PEARLS
• Anesthetic plan is highly dependent on the indication for the procedure and the approach to
nephrectomy.
• For partial nephrectomy, it is important to have adequate IV access since resection of the
lesion may lead to significant blood loss over a short period of time.
NEUROFIBROMATOSIS (NF)
BASICS
DESCRIPTION
• Neurofibromatosis is a genetically inherited or sporadic, progressive phakomatosis; it affects
neuroectodermal tissues (skin, nerves, eye) with a speckled distribution (phakos = speckle,
lens).
• There are 3 main types:
– NF-1 (von Recklinghausen disease): “Peripheral”; most common
– NF-2 (bilateral acoustic or central neurofibromatosis): “Central”
– Schwannomatosis
EPIDEMIOLOGY
Incidence
• NF-1: 1:2,500 to 1:3,000, mean onset 42 years old; most common form, comprising up to
90% of all cases
• NF-2: Birth incidence 1:25,000–50,000, annual incidence; mean onset 24 years old
• Schwannomatosis: Rare, 1:1.7–2.1 million
Prevalence
• Approximately 100,000 Americans
• NF-1: 1:4–5,000
• NF-2: 1:210,000 and higher
Morbidity
NF-1: Varies between no substantial problems other than cutaneous neurofibromas and mild
cognitive impairment to severe neurologic deficits and malignancies. The majority of patients
have a benign disease.
Mortality
• Malignancies limit lifespan
• Arterial hypertension from renal artery stenosis or pheochromocytoma is associated with
premature death.
• Autosomal-dominant with 100% penetrance, but variable expressivity
• New mutations comprise 50% of cases.
PATHOPHYSIOLOGY
• NF-1: Mutation of chromosome 17q11.2 leads to reduced neurofibromin. Neurofibromin acts
as a tumor suppressor, and thus inhibits a cellular proto-oncogene p21 ras and activates
mTOR, a serine/threonine kinase which regulates cell growth. Thus, NF-1 is characterized
by uncontrolled tumor formation that affects the skin and nerves, and is also associated
with a high likelihood of malignancies, macrocephaly, and short stature.
• NF-2: Mutation of chromosome 22q11–q13 leads to a defect in the product merlin, also
known as schwannomin. Merlin acts as a tumor suppressor gene, the function of which is
not fully understood. NF-2 is characterized by bilateral acoustic neurinomas
(schwannomas), leading to hearing loss, often at a young age. Patients are also at an
increased risk for meningiomas and ependymomas.
• Schwannomatosis: Mutation of the INI1 gene. There is no clear pattern of inheritance. It can
skip generations.
• Preoperative assessment is of utmost importance to recognize relevant conditions:
– Respiratory compromise may result from upper airway lesions, cranial and cervical nerve
fibroma, and thoracic deformities. Additionally, obstruction of conducting airways can
result from mediastinal, tracheal, and bronchial fibromas, as well as lung fibrosis and
chest wall deformities.
– Airway obstruction/compromise may occur secondary to macroglossia, macrocephaly,
mandibular abnormalities, and cervical spine involvement.
– Pheochromocytoma: May be undiagnosed and can result in death. Baseline arterial blood
pressure elevation, even in young patients, should alert the anesthetists of this potential.
• If regional anesthesia is considered, assess eligibility clinically and with radiologic
evaluation, preferably through thoracolumbar MRI to rule out neuraxial lesions.
SYMPTOMS
• Varies greatly between individuals and type of neurofibromatosis
• Stridor, difficulty swallowing, throat pain, and changes in voice may suggest airway
involvement.
History
Careful assessment of organ involvement
Signs/Physical Exam
• See “Concomitant Organ Dysfunction”
• NF-2: Bilateral vestibular schwannomas (cranial nerve VIII), leading to deafness;
meningiomas, gliomas, neurofibromas
TREATMENT HISTORY
• No specific medical treatment is available.
• Surgery for corresponding tumors
MEDICATIONS
Depending on organ involvement, patients may be on antiepileptic, cardiac, or pain
medications.
Labs/Studies
• CBC with platelet count
• CXR and possibly thoracic CT in case of respiratory compromise
• Potentially imaging via CT or MRI, if regional anesthesia considered
• Cardiac investigations if required
• Central nervous system:
– Hydrocephalus due to aqueduct stenosis
– Epilepsy
– Syringomyelia
– Cognitive impairment, ADHD
– Cerebral gliomas
• Peripheral nervous system:
– Deafness
– Optic glioma
– Polyneuropathy
• Skin:
– Café-au-lait patches
– Multiple cutaneous or subcutaneous tuberous neurofibromas
– Plexiform neurofibromas (hallmark lesion) in 30% of patients; they are often large and
disfiguring, with malignant progression in 2–16%.
– Lisch nodules (iris hamartomas seen on split lamp examination) are present in 95% of
patients.
– Skin-fold freckling, e.g., axilla, groin, in 70%
• Airway:
– Intraoral lesions (tongue, larynx) may render intubation difficult; it is seen in <5% of
cases. It usually occurs in areas most rich in terminal nerve plexuses.
– Involvement of the cervical region and parapharyngeal space may distort the airway.
• Respiratory system:
– Fibrosing alveolitis
– Intraoral, tracheal, or bronchial neurofibromas
• Skeleton:
– Macrocephaly
– Pathologic fractures, especially of the tibia
– Scoliosis; thoracic curvatures are seen in 10% of patients and kyphoscoliosis in 2%. This
may cause ventilation difficulties and respiratory failure due to reduced lung volume;
increased risk for pneumothorax with insertion of the subclavian CVL; and potential
problems with positioning for intubation and surgery.
– Short stature at 10th–25th percentile
– Bony dysplasia (sphenoid wing dysplasia, bowing of long bone +/– pseudarthrosis of
tibia)
– Compression of the spinal cord with spine deformities, instability of cervical spine
• Vascular:
– Generalized vasculopathy
– Arterial hypertension (seen in 6% of patients) is due to catecholamine-secreting nodular
plexiform neurofibroma, pheochromocytoma, or renal artery stenosis.
– Fibrosing alveolitis in approximately 20%
– Coronary vasospasm
– Aneurysms
• Malignancies with NF-1:
– Pheochromocytoma is seen in approximately 1% of patients.
– Cancerous tumors (e.g., gliomas) are seen in 2% of patients, CML, GI tumors (especially
duodenum, carcinoids).
• Hematologic:
– Benign polycythemia
– NF-1 related coagulopathy has been described in case reports; responds to DDAVP.
• Psychiatric diseases:
– ADHD
– Cognitive impairment, especially learning disabilities
• Other (NF-1):
– Bladder outflow obstruction
– Cardiac hypertrophy and outflow obstruction in 2% of patients, especially pulmonary
stenosis and ventricular failure
• Acute cardiovascular decompensation
• Untreated pheochromocytoma, requiring surgery and/or pretreatment with alpha-blockers
CLASSIFICATIONS
• NF-1: Most common, also known as von Recklinghausen disease; affects the “peripheral”
system
• NF-2: Also known as bilateral acoustic or central neurofibromatosis; affects the “central”
system
• Schwannomatosis
TREATMENT
Premedications
No particular considerations; however, in patients with airway involvement, administer
sedatives with caution and monitoring, or avoid altogether, if appropriate.
If regional anesthesia, risks and benefits need to be discussed at length.
INTRAOPERATIVE CARE
• General anesthesia is typically the preferred method: Inhalational or intravenous techniques
are both feasible.
• Neuraxial anesthesia is not contraindicated, but requires very careful assessment and
consideration, since at least 2/3rd of patients have spinal neuromas and intracranial lesions.
Lumbosacral imaging (e.g., with MRI) may exclude possible spinal tumors. Additionally,
tumors in NF-1 are often highly vascular, thus increasing the risk for epidural hemorrhage
and dural puncture. Kyphoscoliosis may render spinal or epidural anesthesia impossible.
Consider the use of small-bore, atraumatic spinal needles (e.g., 27 G).
• Peripheral nerve blocks possess an increased risk of neural injury; the use of ultrasound may
increase safety.
Monitors
• Careful monitoring of muscle relaxants, since prolonged muscle blockade has been reported.
• Bladder catheterization may be difficult due to ureter obstruction by retroperitoneal
neurofibromas.
• Neurofibromas of the tracheal area are rare, but may be a cause of difficult intubation and
loss of the airway.
• Fiberoptic examination and potentially fiberoptic intubation or awake tracheostomy in
symptomatic patients
Maintenance
• NMBs and suxamethonium may have potentially prolonged action, although only described
in few case reports.
• Kyphoscoliosis may cause difficulties in ventilating the patient.
• Plexiform neurofibromas are associated with severe bleeding. In the event of uncontrolled,
diffuse, and otherwise unexplained intraoperative hemorrhage, the empiric use of DDAVP
should be considered.
Renal impairment and concurrent medication, e.g., antiepileptic drugs, may interfere with
anesthetics or NMBs and delay or fasten emergence.
POSTOPERATIVE CARE
BED ACUITY
Usually PACU, unless surgery or certain medical conditions require ICU
Only in case of unexpected events
COMPLICATIONS
• Respiratory insufficiency due to scoliosis and fibrosing alveolitis
• Bleeding diathesis: Diffuse bleeding is possible despite normal coagulation studies, due to
platelet dysfunction.
• Difficult or impossible intubation due to large neurofibromas affecting tongue, larynx, and
cervical tissues
• Higher risk in regional anesthesia with potential nerve injury and bleeding of plexiform
neurofibromas
• Undiagnosed pheochromocytomas may cause death.
• Cranial herniation in case anesthetic management or condition leads to increased ICP if
intracranial lesions present, such as labor, increased PaCO2, insufficiently blunted
sympathetic response.
REFERENCES
1. Rocco MD, Rosenblatt ML. Ultrasound-guided peripheral nerve block in a patient with
neurofibromatosis. Reg Anesth Pain Med. 2011;36(1):88–89.
2. Sakai T, Vallejo MC, Shannon KT. A parturient with neurofibromatosis type 2: Anesthetic
and obstetric considerations for delivery. Int J Obstet Anesth. 2005;14(4):332–335.
3. Spiegel JE, Hapgood A, Hess PE. Epidural anesthesia in a parturient with neurofibromatosis
type 2 undergoing cesarean section. Int J Obstet Anesth. 2005;14(4):336–339.
4. Richardson MG, Setty GK, Rawoof SA. Responses to nondepolarizing neuromuscular
blockers and succinylcholine in von Recklinghausen neurofibromatosis. Anesth Analg.
1996;82:382–385.
5. Moorthy SS, Radpour S, Weisberger EC. Anesthetic management of a patient with tracheal
neurofibroma. J Clin Anesth. 2005;17:290–292.
6. Lighthall GK, Morgan C, Cohen SE. Correction of intraoperative coagulopathy in a patient
with neurofibromatosis type I with intravenous desmopressin (DDAVP). Int J Obstet
Anesth. 2004;13:174–177.
ADDITIONAL READING
• Ferner RE. Neurofibromatosis 1 and neurofibromatosis 2: A twenty first century perspective.
Lancet Neurol. 2007;6:340–351.
• Hirsch NP, Murphy A, Radcliffe JJ. Neurofibromatosis: Clinical presentations and
anaesthetic implications. Br J Anaesth. 2001;86(4):555–564.
• Jett K, Friedman JM. Clinical and genetic aspects of neurofibromatosis 1. Genet Med.
2010;12(1):1–11.
CODES
ICD9
• 237.70 Neurofibromatosis, unspecified
• 237.71 Neurofibromatosis, type 1 [von recklinghausen’s disease]
• 237.72 Neurofibromatosis, type 2 [acoustic neurofibromatosis]
ICD10
• Q85.00 Neurofibromatosis, unspecified
• Q85.01 Neurofibromatosis, type 1
• Q85.02 Neurofibromatosis, type 2
CLINICAL PEARLS
• Knowledge and careful assessment of relevant concomitant conditions is critical.
• In a rare case of airway obstruction, even elective fiberoptic intubation may fail due to
distorted anatomy.
• If unexpected uncontrolled intraoperative bleeding occurs, DDAVP may rescue the situation.
• In parturients, pre-term labor can occur in up to 30% of cases. Additionally, ICP may
increase if intracranial tumors are present. Neuraxial anesthesia is possible after careful and
thorough assessment and lumbosacral imaging, but should be avoided in NF-1 if imaging
studies are not available.
NEUROGENIC PULMONARY EDEMA
Keren Ziv, MD
BASICS
DESCRIPTION
• Neurogenic pulmonary edema (NPE) is an acute, potentially life-threatening complication of
significant CNS injury, such as subarachnoid hemorrhage (SAH), prolonged seizures, or
traumatic brain injury (TBI).
• NPE consists of a marked increase in pulmonary interstitial and alveolar fluid, with resultant
dyspnea, tachypnea, tachycardia, basilar rales, copious frothy sputum, possible hemoptysis,
and hypoxemia. It usually develops within minutes to hours after injury; however,
immediate and late (days) onset has been described.
• The Starling’s equation describes the effects of hydrostatic and oncotic pressures on fluid
movement between the intravascular and extracellular compartments.
– Capillary hydrostatic pressure: Pressure drives fluid out of the capillary, and is highest at
the arteriolar end of the capillary and lowest at the venular end.
– Capillary oncotic pressure: Plasma proteins keep/draw fluid into the capillary via osmotic
effects. Proteins do not readily cross the endothelial cells and, hence, do not reach
equilibrium within the two compartments. Albumin accounts for 70–80% of the oncotic
pressure of the plasma.
– Transcapillary permeability: Permeability of the vessel wall to water. The capillaries’ semi-
permeable membrane allows water to pass more freely than protein. If the gaps between
the cells of the vessel wall widen, then permeability to proteins increases (results in
edema).
ANATOMY
• NPE “trigger zones” are located in the:
– Hypothalamus
– Cervical spinal cord
– Medulla. Contains several important centers that are believed to contribute to the
pathogenesis of NPE via sympathetic stimulation: Solitary tract, area postrema, medial
reticulated nucleus, and dorsal motor nucleus. Perioperative bilateral lesions in the
medulla at the solitary tract and at the A1 group of neuroadrenergic neurons can cause
hypertension and NPE.
The exact mechanism is unknown. Increased intracranial pressure (ICP), brain injury, or
hemorrhage is believed to cause ischemia or compression of medullary centers; this is
believed to begin a cascade of events that alter Starling’s forces:
• Increased pulmonary capillary hydrostatic pressure results in an outward driving force of
fluids from the pulmonary capillaries.
– The inciting CNS injury sets off a massive sympathetic discharge. This results in systemic
arterial hypertension, peripheral vasoconstriction, increased pulmonary artery pressure,
and pulmonary vasoconstriction.
– The increased myocardial workload (oxygen consumption) can cause deterioration of
cardiac function. Decreases in left ventricular function can lead to increased left atrial
pressures with resultant pulmonary edema.
• Increased pulmonary artery permeability is a key step preceding NPE.
– Hemodynamic-independent: Some studies suggest that adrenergic activation increases
pulmonary vessel permeability. Epinephrine and norepinephrine can have:
Direct effects that increase vascular permeability
Indirect effects by stimulating secondary mediators which increase the vascular
permeability, such as histamine or bradykinin
– Hemodynamic-dependent: The “Blast theory” proposed by Theodore and Robin in 1975
states that a severe rise of pulmonary capillary pressure causes increased pulmonary
vascular permeability, causing a shift of intravascular volume from the high-resistance
systemic circulation to the low-resistance pulmonary circulation. Microvascular injury
may be caused by excessive pulmonary vasoconstriction; the consequent increase in
vascular permeability results in edema.
• Capillary oncotic pressure: The increased permeability allows for passage of proteins
through the capillaries, which then exert oncotic pressure and draw fluid out of the
capillaries. Studies have shown that the alveolar fluid of patients who have developed NPE
has a similar protein concentration to plasma.
• Patients who develop NPE have a very poor prognosis.
– Associated with a 60–100% mortality
– Reflects the severity of the underlying etiology; thus, an ominous sign
– One retrospective study of 680 postmortem deaths from non-traumatic intracranial
hemorrhage showed that pulmonary edema was seen in approximately 75% of cases.
• NPE may result from several types of cerebral lesions; the most common are:
– Fatal subarachnoid hemorrhage: seen in 70% of patients
– Status epilepticus: seen in 30% of patients
– Traumatic brain injury: seen in 50% of patients
• Presentation:
– Immediately (minutes to hours); most common
– Delayed (days) is also seen; less common
• Associated with hemodynamic and cardiac abnormalities:
– Neurogenic shock
– Left ventricular failure; usually transient and reversible
– Elevated troponin level; does not necessarily indicate permanent myocardial injury
• Chest radiography:
– Pulmonary infiltrates; maybe in a “butterfly” pattern
– Cardiac silhouette is usually normal.
• Differential diagnosis includes:
– Aspiration pneumonia
– Cardiac dysfunction: Often NPE with cardiac changes is erroneously attributed to coronary
disease. ECG and enzyme levels are not useful in distinguishing between myocardial
infarction and neurologic etiology of cardiopulmonary dysfunction, as they may be
abnormal in both entities. The transient nature of NPE helps distinguish between
neurologic and cardiac origins.
– Acute respiratory distress syndrome (ARDS)
• Treatment
– Underlying neurologic injury. Because overall outcome is dependent upon the inciting
cause, efforts should focus on this. There should be an emphasis on decreasing the ICP.
– Supportive treatment consists of supplemental oxygen with or without mechanical
ventilation, depending on the severity of hypoxemia.
Maintain an oxygen saturation >94%.
Implementation of PEEP should be optimized to balance against decreased cerebral
venous drainage and worsening of ICP.
– Medications: There are few studies that evaluate the efficacy of medications to treat NPE
in humans; however, the following may be useful:
Beta-adrenergic antagonists may decrease pulmonary capillary permeability but are
usually contraindicated in the setting of cardiopulmonary and hemodynamic
compromise.
Dobutamine may increase cardiac output, counter alpha agonism, and promote diuresis
(improved renal perfusion).
Steroids have not been tested in humans and may be detrimental.
Diuretics should be avoided in the absence of hypervolemia due to the risk of
hypotension (can worsen cerebral perfusion pressure). However, mannitol is commonly
administered to reduce brain edema, but it has unproven benefits for pulmonary edema.
Chlorpromazine, via alpha-adrenergic blockade, has been used in case reports.
EQUATIONS
ADDITIONAL READING
• Ahrens J, Capelle H, Przemeck M. Neurogenic pulmonary edema in a fatal case of
subarachnoid hemorrhage. J Clin Anesth. 2008;20:129–132.
• Muroi C, Keller M, Pangalu A, et al. Neurogenic pulmonary edema in patients with
subarachnoid hemorrhage. J Neurosurg Anesthesiol. 2008;20(3):188–192.
• Pender ES, Pollack CV. Neurogenic pulmonary edema: Case reports and review. J Emerg
Med. 1992;10:45–51.
• Sedy J, Zicha J, Kunes J, et al. Mechanisms of neurogenic pulmonary edema development.
Physiol Res. 2008;57:499–506.
CODES
ICD9
514 Pulmonary congestion and hypostasis
ICD10
J81.1 Chronic pulmonary edema
CLINICAL PEARLS
• Neurogenic pulmonary edema is an acute complication of severe neurologic perturbation. It
is usually self-limited, and mortality is mainly conferred by the underlying neurologic
insult.
• Treatment is mainly supportive with an emphasis on reducing the intracranial pressure.
• Many cases of NPE resolve within days.
• There have been recent reports of successful treatment regimens in patients with NPE after
SAH:
– Immediate treatment of ICP with intubation, sedation, mannitol/hypertonic saline, and, if
needed, bolus thiopental
– Countering alpha-adrenergic overstimulation with dobutamine
NEUROGENIC SHOCK
Keren Ziv, MD
BASICS
DESCRIPTION
• Neurogenic shock is a type of distributive shock resulting from the loss of sympathetic
outflow and unopposed parasympathetic (vagal) nerve activity.
• Usually due to a relatively high spinal cord injury (SCI), such as the cervical spine or high
thoracic (usually above level T6) vertebrae. It may also result from regional anesthesia
(high block).
• There is no universally accepted definition of neurogenic shock. Some define it as an SBP
<100 mm Hg with an HR <60 bpm, whereas others define it as an SBP <90 mm Hg (1,2).
Overall, it is a significantly decreased MAP from baseline value, and is usually symptomatic.
• Neurogenic shock differs from spinal shock in that spinal shock is defined as the temporary
loss of spinal reflex activity occurring below a total or near-total SCI. The term “shock” is
not a description of the circulatory system, but of reflex activity.
EPIDEMIOLOGY
Prevalence
• 15–52.5 cases per million in the population. 80% males between 15 and 35 years, 5%
children (3)
• In a recent study of 490 patients presenting with isolated SCI, neurogenic shock occurred
with:
– Cervical cord injuries: 19.3% (4)
– Thoracic injuries: 7%
– Lumbar injuries: 3%
Morbidity
• Severe hypotension may result in significant end organ damage to the brain, kidneys, and
heart.
• Further nerve injury can result from an unstable spine, particularly during intubation.
Mortality
Untreated neurogenic shock may result in death due to organ hypoperfusion.
• Severe injury to the CNS:
– Brain
– Cervical spinal cord
– High thoracic spinal cord
• Other causes include:
– Spinal anesthesia
– Drugs
– Emotional stress
– Pain
– CNS dysfunction
– Parasympathetic nerves have a craniosacral outflow and their preganglionic and
postganglionic connections are close to the target organs.
Cranial nerves: CN 3, 7, 9, 10
Sacral nerves: S2, S3, S4
– Sympathetic preganglionic neurons have a thoracolumbar outflow. T2-L2 nerves exit the
cord via ventral roots and synapse with postganglionic neurons in the paravertebral chain.
Cardiac sympathetic neurons are carried from T1 to T4.
• Neurogenic shock occurs due to interruption of spinal sympathetic outflow causing loss of
vasomotor tone to peripheral arterial beds as well as the loss of compensatory reflex
tachycardia. This results in:
– Increased venous capacitance
– Decreased venous return
– Decreased cardiac output
– Hypothermia
– Warm/dry skin due to the loss of the ability to sweat
– Bradycardia (unopposed parasympathetic tone results via the vagal nerve).
Prevention of primary injury
• Neurogenic shock is a diagnosis of exclusion.
• Classic findings are:
– Hypotension
– Bradycardia
– Motor and sensory deficits (corresponding to the level of cord injury)
– Warm extremities
– Radiologic evidence of vertebral injury
– However, only 20% of patients present with classic neurogenic shock symptoms (4).
• Diagnosis may be difficult due to associated injuries. A head injury may make
motor/sensory assessment impossible, or hypotension may be due to concomitant injury
such as bleeding. Thus, prior to making the diagnosis of neurogenic shock, other causes
must be sought out.
• Concomitant hypovolemic shock from occult bleeding origin in the abdomen, chest, etc.
• Isolated head injury causes Cushing’s triad (hypertension, bradycardia, abnormal
respiration) as opposed to shock.
• Spinal shock is due to the loss of spinal reflex activity below the level of SCI and is not of a
circulatory etiology; typically resolves in 3–6 weeks. The term “shock” is a misnomer.
TREATMENT
• Adequate IV access and a secure airway are mandatory. Techniques to maintain cervical
immobility will likely be necessary if intubation is required.
• Monitors. In addition to standard monitors, invasive monitors are usually necessary to aid
with management and assess response to therapy (arterial line, central line, pulmonary
artery catheter, transesophageal echocardiogram).
• Fluid resuscitation is performed to increase the effective circulating blood volume.
Transfusion with blood products may be required depending on blood loss. A Foley catheter
is placed for loss of bladder function and assessment of volume resuscitation.
• Vasopressor support is often required if volume fails to treat hypotension.
– Inotropic agents, such as dopamine, dobutamine, and epinephrine, may be added to
improve cardiac output and perfusion pressure.
– Infusion of an alpha-adrenergic agent (phenylephrine or norepinephrine) or vasopressin
may be indicated to provide direct vasoconstriction and thus increase blood pressure.
Isolated vasoconstrictive activity has the potential for worsening bradycardia.
– In the presence of severe bradycardia, atropine or a temporary pacemaker may be
required.
• Surgery may be needed to stabilize the spinal cord especially in cases of complete
transection or removal of a foreign body.
• High-dose steroid administration for SCI is usually center-dependent and discussed with
emergency, neurosurgery, or orthopedic personnel.
FOLLOW-UP
• Duration is variable and may last hours to weeks.

• Recovery is usually incomplete and postural hypotension may persist.
REFERENCES
1. Zipnick RI, Scalea TM, Trooskin SZ, et al. Hemodynamic responses to penetrating spinal
cord injuries. J Trauma. 1993;35:578–583.
2. Levi L, Wolf A, Belzberg H. Hemodynamic parameters in patients with acute cervical cord
trauma: Description, intervention, and prediction of outcome. Neurosurgery.
1993;33:1007–1017.
3. Grigorean VT, Sandu AM, Popescu M, et al. Cardiac dysfunction following spinal cord
injury. J Med Life. 2009;2(2):133–145.
4. Guly HR, Bouamra O, Lecky FE. The incidence of neurogenic shock in patients with
isolated spinal cord injury in the emergency department. Resuscitation. 2008;76:57–62.
5. Piepmeyer JM, Lehmann KB, Lane JG. Cardiovascular instability following acute cervical
spine trauma. Cent Nerv Syst Trauma. 1985;2:153–159.
• Total spinal anesthesia
CODES
ICD9
958.4 Traumatic shock
ICD10
T79.4XXA Traumatic shock, initial encounter
CLINICAL PEARLS
• Type of distributive shock resulting in decreased sympathetic tone and unopposed vagal
tone causing hypotension and bradycardia
• The most common etiology is a high SCI.
• May lead to organ hypoperfusion and death
• Fluids are the initial treatment; vasopressors may be necessary to maintain hemodynamic
stability.
NEUROMUSCULAR JUNCTION
Sukhdip Singh, MD
Patricia Dalby, MD
BASICS
DESCRIPTION
• Neuromuscular junction (NMJ) describes the synapse of the nerve terminal with the muscle
membrane.
• NMJ is an important site for the action of various drugs. Additionally, it is affected by
various diseases, disorders, and pathologic processes.
• Acetylcholine (ACh) is synthesized in the neuron from acetyl coenzyme A and choline by the
enzyme choline acetyltransferase and is then packaged into vesicles.
• Release of ACh from the nerve terminal:
– During a nerve action potential, Na+ channels open and allow for an influx of Na+ with
subsequent depolarization of the nerve terminal.
– Depolarization of the nerve terminal causes the opening of calcium channels, allowing
calcium to enter the nerve.
– The influx of Ca2+ mobilizes ACh-containing vesicles to attach to release sites (active
zones) on the presynaptic neuronal membrane.
– Docking is followed by the release of vesicle content (ACh) into the synaptic cleft.
• Generation of a muscle fiber action potential:
– ACh diffuses across the synaptic cleft and binds to the acetylcholine receptor (AChR) on
muscle cells.
– AChR binding opens anion channels, which results in influx of Na+ and Ca2+.
– This ion entry generates an end plate potential (EPP). If the EPP is greater than the
threshold potential, a muscle fiber action potential is generated leading to muscle cell
contraction.
• ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase to terminate the
process.
ANATOMY
• A motor neuron divides into multiple branches that lose their myelin sheath before
synapsing with the muscle cells.
• All of the muscle cells supplied by a single motor neuron form a motor unit.
• There is a gap between the nerve terminal and muscle membrane called the synaptic cleft.
The postsynaptic membrane has folds or invaginations forming primary and secondary
clefts. AChRs are concentrated on the crests of the folds.
• The presynaptic nerve ending has membrane thickenings called active zones around which
the Ach-containing vesicles are clustered.
• The area of the muscle immediately around the NMJ is the perijunctional zone.
• Postjunctional AChRs are of 3 types—mature or junctional type, extrajunctional or
immature fetal type, and the neuronal α7 type (1,2).
• The physiologic process of normal neuromuscular transmission is affected by various
disorders and pathophysiologic states.
• Upregulation of AChRs: Increase in fetal immature type of AChRs occurs within 48 hours of
an insult.
– Associated conditions include stroke, spinal cord injury, burns, prolonged immobilization,
prolonged exposure to neuromuscular blocking drugs, multiple sclerosis, and Guillain–
Barré Syndrome.
– Immature fetal AChRs are very sensitive to succinylcholine (SCh) and are resistant to
nondepolarizing muscle relaxants (NDMRs).
Clinical implication: SCh should not be used after 24 hours of an insult. Exposure to SCh
causes an increased K+ efflux and hyperkalemia.
• Myasthenia gravis (MG): Autoantibodies directed against the postsynaptic AChRs leading to
a decreased number of receptors.
– Clinical implication: Patients with MG are resistant to SCh, but the response can be
unpredictable; patients treated with plasmapheresis or pyridostigmine can have a
decreased activity of pseudocholinesterase resulting in potentiation of SCh action. These
patients are very sensitive to NDMRs.
• Lambert Eaton Myasthenic Syndrome (LEMS): Autoantibodies directed against presynaptic
voltage-gated Ca2+ channels resulting in decreased release of ACh at the motor endplate.
– Clinical implication: Patients with LEMS are very sensitive to both depolarizing and
nondepolarizing muscle relaxants.
• Muscular dystrophy: In both Duchenne and Becker muscular dystrophy, there is a defect in
dystrophin production leading to absent or abnormal dystrophin. The NMJ has an
upregulation of extrajunctional receptors.
– Clinical implication: These patients are very sensitive to SCh, which can lead to
hyperkalemia and cardiac arrest. Response to NDMRs is variable from normal to increased
sensitivity. Although unproven, increased association with malignant hyperthermia and
rhabdomyolysis has been suggested.
• Myotonic dystrophy: Disorder characterized by delayed or slowing of muscle relaxation
following voluntary contraction. This manifests as generalized myotonias and later
progresses to muscle weakness and atrophy.
– Clinical implication: SCh is contraindicated as it can precipitate myotonic contractions and
trismus making endotracheal intubation difficult. Although the response to NDMRs is
normal, a reduced dose is required due to underlying muscle wasting. Anticholinesterase
medications, such as reversal agents, can precipitate myotonias.
• Neuromuscular monitoring: Assess neuromuscular blockade (NMB) during general
anesthesia.
– Single twitch: Usually given at 0.1 Hz amplitude every 10 seconds and increased until the
current is slightly greater than that needed for a maximal stimulation. Comparison of
twitch height after NMB is then done relative to the maximal twitch height.
Useful for establishing the pharmacodynamic properties of an agent but requires a
baseline determination of twitch height per individual patient.
– Train of four (TO4): 4 stimuli are given at 2 Hz and repeated every 10–12 seconds. The
strength of each twitch is equal without NMB, but following NMB administration, there is
a decrease relative to the strength of the blockade. The phenomenon occurs because after
onset of NMB there is enough ACh available to mount the first twitch but with each
stimulus the amount of ACh diminishes.
Fade is the phenomenon of the relative decrease of first twitch (T1) to the fourth twitch
(T4). A common clinical practice is to compare the strength of the first twitch to the
remaining 3.
When there is 90% suppression of the first twitch (T1), only 1 twitch is perceived; at 75%
suppression, 3 twitches are perceived.
A commonly used clinical correlate is if T4/T1 is approximately 0.75, then an awake
patient can generate a 15 mL/kg vital capacity with an effective cough and sustained
head lift.
– Double burst stimulation (DBS): 2 short bursts of stimulation that are delivered as 3
stimuli at 50 Hz separated by 750 ms
May increase the manual perception of fade because the response to the 3 intense stimuli
is felt as one muscle contraction.
When fade is present, there is a 75% chance that the TO4 is <0.6, but if there is no fade
with DBS then there is a 90% chance that TO4 is ≥0.6.
– Tetanic stimulation: 50 Hz for 5 seconds
Used clinically with the TO4 to measure the degree of profound muscle relaxation
– Post-tetanic count (PTC): Measured with a 1 Hz simulation 3 seconds after tetanic
stimulation (50 Hz for 5 seconds)
If the PTC is 10, then that is similar to the appearance of T1 or 90% suppression. If there
is no PTC at all, then the NMB is so prolonged that it cannot be reversed reliably.
Post-tetanic facilitation occurs because the potent tetanic stimulation causes the
increased release of ACh quanta into the synaptic cleft.
• Drugs acting on the NMJ:
– Depolarizing muscle relaxants: Imitate the action of ACh. Cause sustained depolarization
of the motor end plate leading to initial contraction followed by prolonged muscle
relaxation.
Prolonged administration of SCh can lead to phase II block which has characteristics of
NDMR block.
– NDMRs: Compete with ACh by preventing ACh from binding to AChRs.
Anticholinesterases inhibit the degradation of ACh. The increased concentration of ACh
facilitates interaction with AChRs and “reverses" the NDMR block (increases the ratio of
Ach to NDMR).
– Other medications affecting the neuromuscular transmission include volatile anesthetics,
barbiturates, alcohol, cocaine, local anesthetics, aminoglycoside antibiotics,
phenothiazines, and calcium channel blockers.
• Neuromuscular disorders: Clinical implications of specific disorders are discussed in
“Pathophysiology” section.
– These patients are prone to increased cardiac and respiratory depression with anesthetic
drugs.
– Oropharyngeal muscle weakness, decreased laryngeal reflexes, and prolonged gastric
emptying time predispose these patients to increased risk for intraoperative aspiration and
postoperative respiratory compromise.
– Regional and local anesthesia is preferred. If required, general anesthesia may be
maintained with short-acting agents.
– SCh should be avoided due to risk of hyperkalemia and malignant hyperthermia.
– NDMRs should also be avoided. If muscle relaxation is necessary, short-acting agents, such
as mivacurium, should be used.
GRAPHS/FIGURES
REFERENCES
1. Martyn JAJ, Fukushima Y, Chon JY, et al. Up-and-down regulation of skeletal muscle
acetylcholine receptors. Intl Anesthesiol Clin. 2006;44:123.
2. Martyn JAJ, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic
states: Etiologic factors and molecular mechanisms. Anesthesiology. 2006;104:158–169.
3. Fagerlund MJ, Eriksson LI. Current concepts in neuromuscular transmission. Br J Anaesth.
2009;3:108–114.
4. Naguib M, Flood P, McArdle JJ, et al. Advances in neurobiology of the neuromuscular
junction: Implications for the anesthesiologist. Anesthesiology. 2002;96:202–231.
5. Shear TD, Martyn JA. Physiology and biology of neuromuscular transmission in health and
disease. J Crit Care. 2009;24:5–10.
• Duchenne muscular dystrophy
• Myasthenia gravis
• Myasthenic syndrome
CLINICAL PEARLS
• The most common sites for monitoring of the NMJ during general anesthesia are the ulnar
and facial nerves, but other peripheral nerves, such as the median, posterior tibial, and
common peroneal, can also be used.
• Avoid SCh in patients with neuromuscular disorders and burns status post 24 hours due to
the risk of hyperkalemia.
• Avoid reversing a phase II block with anticholinesterases as the reversal response can be
unpredictable.
• Patients taking certain antibiotics, such as aminoglycosides and polymyxin B, may be more
sensitive to NDMRs.
NONCARDIOGENIC PULMONARY EDEMA
BASICS
DESCRIPTION
Noncardiogenic pulmonary edema (NCPE) is caused by one of 2 basic mechanisms:
• An imbalance of Starling forces
• Lymphatic insufficiency
• Starling forces: NCPE can result from increased negative interstitial pressure, increased
alveolar–capillary membrane permeability, or decreased plasma oncotic pressure.
– Increased negative interstitial pressure (Ppmv): Imbalances between intra-alveolar
pressure and interstitial or intrapleural pressure can lead to an increased transcapillary
pressure gradient causing fluid shift from the microvessels (Pmv) to the perimicrovascular
interstitium (Ppmv) with resultant pulmonary edema.
– Increased alveolar–capillary membrane permeability (K): Endothelial injury is believed to
result from inflammatory processes or sympathetic discharge. It can result in an influx of
water, solutes, and macromolecules into the alveoli.
– Decreased plasma oncotic pressure (πmv): Occurs in low-protein states such as with
hypoalbuminemia in liver disease or critical illness, nephrotic syndrome, or protein-losing
enteropathy. Pulmonary edema from decreased oncotic pressure usually involves other
exacerbating factors since low-oncotic states alone are typically not sufficient to cause
clinically significant presentations.
– Increased hydrostatic pressures (Pmv): Involved in the pathogenesis of cardiogenic
pulmonary edema. Not commonly a cause of NCPE states. Involved in the pathogenesis of
cardiogenic pulmonary edema. However, it may possibly play a role in neurogenic
pulmonary edema (NPE) and negative pressure pulmonary edema (NPPE).
• Lymphatic insufficiency: NCPE can occur from blockage of lymphatic drainage, which is
usually related to either fibrotic disease or inflammatory disease but can also be seen after
lung transplantation.
• NCPE results in:
– Increased interstitial hydrostatic pressure
– Increased interstitial oncotic pressure
– Atelectasis with decreased functional residual capacity
– Decreased PaO2, with an increased A-a gradient and a/A ratio
– Increased work of breathing (in the spontaneously ventilating patient)
• NPPE or postobstructive pulmonary edema has been shown to occur in up to 1/1,000
patients receiving general anesthesia. It requires 2 entities: A negative intrathoracic pressure
and a pathological state that prevents the intra-alveolar pressure to accommodate the
gradient (obstruction). The increased intrapleural pressure transmits to the alveoli which
draw fluid from the pulmonary capillaries into the interstitial space and ultimately the
alveoli. On a more global scale, this acute derangement increases venous return and left
ventricular afterload, which can potentially favor edema secondary to hydrostatic forces. It
can occur:
– Post-extubation: Accounts for approximately 74% of all perioperative NPPE. It can result
from either laryngospasm or occlusion of the endotracheal tube (e.g., biting the airway
conduit), as well as bronchospastic disease.
– Initial airway management: Usually seen in patients with head and neck tumors, but also
with laryngospasm and epiglottis-induced obstruction.
– Airway collapse: Seen with obesity and obstructive sleep apnea; can cause ongoing airway
obstruction and subacute or chronic NPPE.
– Surgical procedures: An airway procedure such as tracheal dilation can result in complete
airway obstruction while the patient remains spontaneously breathing.
– Pneumothorax: A sudden release can generate sufficient negative interstitial pressure to
generate pulmonary edema (usually unilaterally).
• Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS): These entities are
the end-result of a multitude of disease processes that result in alveolar–capillary membrane
injury from inflammatory processes. They are often classified as direct or indirect.
– ALI is determined by a chest radiograph with bilateral infiltrates, a normal capillary
wedge pressure or lack of evidence for cardiogenic failure, and a PaO2/FiO2 (P/F) ratio
<300. ARDS is a more severe form of ALI with a P/F <200.
– Direct lung injury can result from pneumonia/pneumonitis, inhaled toxins, and aspiration.
Ventilator-induced lung injury (VILI) must also be considered.
– Indirect lung injury can result from shock, sepsis, trauma, and transfusion-related ALI.
Although a component of pulmonary edema seen after cardiopulmonary bypass may be
due to alveolar–capillary membrane injury, the mechanism and etiology are not
completely understood.
• Lymphatic insufficiency: In the perioperative period, NCPE may be seen in patients after
lung transplant.
• Neurogenic pulmonary edema: The pathogenesis is not completely understood. Theories
include:
– Massive sympathetic discharge that increases hydrostatic pressures secondary to systemic
hypertension, peripheral vasoconstriction, increased pulmonary artery pressure, and
pulmonary vasoconstriction.
– Increased pulmonary artery permeability from direct or indirect effects of epinephrine and
norepinephrine: Indirect effects may involve the secondary release of histamine or
bradykinin.
• Drug-induced: Pathogenesis is not completely understood.
– Narcotic overdose with heroin is the most frequent offending agent; however, parenteral
and intravenous forms of other legal preparations have also been associated with NCPE.
– Cocaine
– Chemotherapeutic agents including cytarabine, recombinant IL-2, all-trans-retinoic acid,
arsenic trioxide, mitomycin plus vinblastine, and intrathecal methotrexate (1)
• Anaphylaxis can result in increased alveolar–capillary membrane injury. Common
perioperative offenders include neuromuscular blocking agents, antibiotics, latex, and
anesthetics.
• Pulmonary edema can result from:
– Severe preeclampsia: It is a defining criterion to separate severe preeclampsia from mild
disease.
– Noncardiogenic causes (decreased oncotic pressure, increased pulmonary capillary
permeability) combined with increased intravascular hydrostatic pressure. Usually
develops 2–3 days postpartum. Treatment is mostly supportive, including supplemental
oxygen, fluid restriction, and diuretic therapy, but may also require mechanical
ventilation with tracheal intubation. Pulmonary artery catheterization may optimize
therapy.
– Cardiogenic etiologies: An echocardiogram may aid with diagnosis.
– Amniotic fluid embolus; usually accompanied with hemodynamic collapse (2).
• Pulmonary edema in the perioperative period can present with hypoxia, rales, frothy
sputum, and increased peak and plateau airway pressures. The clinical scenario must always
be taken into account, and cardiogenic pulmonary edema should be excluded (acute left
heart dysfunction, arrhythmias).
• NPPE: The clinical scenario is usually airway obstruction (stridor, wheezing, and inability to
ventilate) in a patient who is able to generate high-negative intrathoracic pressure (e.g.,
young, healthy, athletes who are American Society of Anesthesiologists physical status
categories I and II).
– Obstruction can also occur in patients with foreign body aspiration, oropharyngeal
tumors, and postoperative residual curarization leading to upper airway obstruction.
– Intubation may be required but simple measures, such as the application of positive
pressure in laryngospasm and bronchodilator therapy in patients with acute asthma
exacerbations, may alleviate the underlying process.
– After establishing a patent airway, treatment is largely supportive as symptoms usually
resolve within 24 hours.
– Diuretic therapy is controversial since the primary offense is not intravascular
hypervolemia. Additionally, these patients may be intravascularly euvolemic or
hypovolemic, and diuretic therapy could lead to further deterioration via hypovolemic
shock.
• Anaphylaxis may present as wheezing, hypotension, and shock.
– Treatment is supportive and aimed at removing the offending agent.
– Epinephrine is the primary pharmacologic agent for anaphylactic shock (0.2–0.5 mg every
5 minutes as needed). Histamine blockers (diphenhydramine, famotidine, ranitidine) are
also beneficial.
– Measurement of tryptase and histamine levels can help in the diagnosis of an anaphylactic
process; however, its clinical effects are not immediate.
• ALI/ARDS: Compared with NPPE and anaphylaxis, ALI tends to develop over hours to days
but progresses rapidly.
– Of all treatment options studied, the only modality that has been demonstrated to reduce
mortality is ventilation with low-tidal volumes of 6 mL/kg predicted body weight (3).
Other lung protective ventilation strategies include low inspiratory pressures (goal plateau
pressure <30 cmH2O), moderate positive end-expiratory pressure, and permissive
hypercapnia in addition to lower tidal volumes (5).
– In the absence of shock, a fluid-conservative strategy is favored (5).
– Perioperatively, inhaled nitric oxide, inhaled epoprostenol, glucocorticoids, high-
frequency oscillatory ventilation, and extracorporeal life support offer strategies to
improve oxygenation (5).
• Neurogenic pulmonary edema treatment is aimed at decreasing intracranial pressure in
addition to supportive therapy. Diuretic therapy could be deleterious if it results in
hypotension and impaired cerebral perfusion pressures.
• Opioid overdose: Naloxone has not been shown to hasten recovery, and supportive therapy
remains the mainstay of treatment.
EQUATIONS
Starling equation: Q = K [(Pmv – Ppmv) – (πmv – πpmv)], where
• Q = Net transcapillary flow of fluid
• K = Transcapillary permeability
• Pmv = Hydrostatic pressure in microvessels
• Ppmv = Perimicrovascular interstitium
• πmv = Plasma protein oncotic pressure in the peripheral vessels
• πpmv = Protein oncotic pressure in the perimicrovascular interstitium
REFERENCES
1. riasoulis E, Pavlidis N. Noncardiogenic pulmonary edema: An unusual and serious
complication of anticancer therapy. Oncologist. 2001;6:153–161.
2. Gist RS, Stafford IP, Leibowitz AB, et al. Amniotic fluid embolism. Anesth Analg.
2009;108:1599–1602.
3. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as
compared with traditional tidal volumes for acute lung injury and the acute respiratory
distress syndrome. New Engl J Med. 2000;342:1301–1308.
4. Schultz MJ, Haitsma JJ, Slutsky AS, et al. What tidal volumes should be used in patients
without acute lung injury? Anesthesiology. 2007;106:1226–1231.
5. Diaz JV, Brower R, Calfee CS, et al. Therapeutic strategies for severe acute lung injury. Crit
Care Med. 2010;38:1644–1650.
ADDITIONAL READING
• Krodel DJ, Bittner EA, Abdulnour R, et al. Case scenario: Acute postoperative negative
pressure pulmonary edema. Anesthesiology. 2010;113:200–207.
• Alveoli
• Anaphylaxis
CODES
ICD9
514 Pulmonary congestion and hypostasis
ICD10
J81.1 Chronic pulmonary edema
CLINICAL PEARLS
• Noncardiogenic pulmonary edema (NCPE) arises from a number of etiologies, and prompt
attention should be given to identifying the underlying causes with a focus on diagnosing
life-threatening sources rapidly.
• Once a diagnosis is made, appropriate therapy can be instituted; most treatments for NCPE
include airway management, supportive care, and removal of the offending agent.
• In patients with acute lung injury and acute respiratory distress syndrome, adapting lung
protective ventilation is important to decrease mortality and morbidity.
NON-INVASIVE BLOOD PRESSURE (NIBP) CUFF
BASICS
DESCRIPTION
• The non-invasive blood pressure (NIBP) cuff provides an indirect estimation of systolic
blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and
pulse pressure (PP).
• Readings are based on the pulsatile phenomena of blood ejection into the systemic arteries
and generation of changing pressure (pulse wave) within the arterial tree during the cardiac
cycle.
• Auscultatory technique: Based on the auscultation of Korotkoff sounds; normally, blood flow
in arteries is laminar and does not produce sound, whereas turbulent flow does.
– The inflated cuff causes mechanical constriction and deformation of the artery.
– When the cuff pressure is >SBP, the artery is completely occluded during the whole
cardiac cycle and no sound is produced.
– When the cuff pressure is <SBP and >DBP, turbulent flow occurs. Appearance of the first
sound during cuff deflation indicates SBP.
– When the cuff pressure is <DBP, the artery is fully open, and arterial flow is laminar with
no sound production. Disappearance of the sound or a muffled tone after further deflation
indicates DBP.
• Oscillometric technique utilizes a pressure transducer to measure cuff pressure oscillation.
– The amplitude of pressure changes in the occluding cuff is measured once the cuff
pressure is <SBP; blood will pass over the occluded portion of the artery and arterial PP
waves will be transmitted to the air in the cuff (resulting in cuff pressure fluctuations or
oscillations).
– The oscillations with maximal amplitude indicate MAP. Different devices utilize different
algorithms and coefficients to derive the readings (e.g., measure MAP and extrapolate SPB
and DBP, measure MAP and SBP and extrapolate DBP, etc).
– Oscillatory measurements are made over several cardiac cycles at each increment of
deflation to smooth out pronounced respiratory variations or motion artifacts.
• Blood pressure is mainly the product of cardiac output (CO) and peripheral vascular
resistance (PVR): MAP = (CO × SVR), where SVR is the systemic vascular resistance.
– Compliance of the arterial vasculature has a significant effect on BP. Contraction of
smooth muscle (vasoconstriction) and stiff arteries (atherosclerosis) result in poor
compliance (increased resistance) and decrease the ability to accommodate the incoming
stroke volume. (increased SBP, decreased DBP, unchanged MAP).
– Increases in cardiac output (increased amount of blood pumped into the arterial
circulation) can increase the BP.
– Rheology: Viscosity affects the SVR; thus increases in viscosity also increase the SVR and
BP.
– Because BP is dependent on both CO and SVR, MAP can serve as a surrogate to assess
these factors and what comprises them (volume status, contractility, heart rate, presence
of perfusing rhythms). MAP is of special importance since it is the perfusion pressure.
MAP can be estimated using the following formula: MAP = 1/3 SBP + 2/3 DBP.
ANATOMY
• Position: The NIBP cuff is placed over the upper or lower extremity; the readings record
pressures in the brachial or femoral artery, respectively. The “bladder” should be over the
artery (so that excessive external pressure is not needed to compress the artery), and ideally
the lower edge of the cuff should be approximately 2 cm above the antecubital fossa (to
avoid artifacts from bending at the elbow).
• Level in relation to the heart: The extremity should be at the heart level for accurate
measurements. If the extremity is below the heart level, it will falsely elevate the BP. If the
extremity is above the heart level, it will falsely decrease the BP. To correct for this, add or
subtract 0.7 mm Hg for each cm that the cuff is above or below the level of right atrium.
• Size: Should match the extremity size to measure the BP accurately.
– The cuff’s bladder width should be ~40% of the circumference of the extremity to provide
adequate occlusion of flow.
– The cuff’s bladder length should be ~60% of the extremity (e.g., upper extremity:
shoulder to the elbow; lower extremity: knee to the ankle) to provide adequate occlusion
of flow.
– BP will be falsely high if the cuff is too small for the size of the extremity or when the cuff
is applied too tightly. It does not adequately disperse the pressure over the arterial
surface.
– BP will be falsely low if the cuff is too large for the size of the extremity or when cuff
deflations are too quick. Pressure is spread over too large an area and produces a damping
effect on the oscillometric pulses.
• Because BP is dependent on both CO and PVR, MAP can also serve as a surrogate to assess
PVR and factors that constitute CO (volume status, contractility, heart rate, presence of
perfusing rhythm).
• Low BP states
– Decreases in SVR
Anesthetic agents (vasodilation)
Sepsis
Neurogenic shock
Anemia
Allergic reactions
Severe hypoxia and acidosis
Hypocalcemia
Arteriovenous malformation with shunt
– Reduced CO
Negative inotropes
Ischemia
Infarction
Aortic stenosis
Reduced preload (hypovolemia, increased venous capacitance, decreased LV compliance,
obstruction such as tamponade)
Tamponade
Arrhythmias
• High BP states
– Increases in SVR
Sympathetic stimulation
Vasopressor administration
Pain
Hypothermia
Coarctation of the aorta
Application of a cross-clamp over major central arteries
– Increased CO
Sympathetic stimulation
Pain
Positive inotropes
Increased preload from hypervolemia
Increased heart rate
• Decreases in either SVR or CO can be compensated by increases in the other, thus
maintaining the same MAP. For example, in patients with cardiomyopathy and low CO, PVR
is increased to maintain MAP. In septic patients with low PVR, CO increases to normalize
MAP.
• Cuff-based NIBP continues to be the standard method used in the perioperative settings. It
has the benefit of being non-invasive, as its name suggests, as well as provides an estimate
of overall hemodynamic function. Limitations:
– “Snapshot” of the dynamic and pulsatile circulation. Does not provide beat-to-beat
readings.
– Obesity: The conical shape of an extremity can result in uneven dispersion over the
arterial surface.
– Shivering can interfere with oscillatory measurements.
– Hypotension: At low BP, oscillatory measurements may not be easily detectable by the
cuff and transducer.
– Arrhythmias can prevent oscillatory measurements.
• Under resting conditions in adults, the normal SBP is 90–120 mm Hg and the DBP is 60–80
mm Hg. An adequate MAP is needed for optimal perfusion of vital organs (brain, heart,
kidney); however, normal BP values, by itself, cannot assure adequate perfusion. Example:
Low CO and tissue perfusion in the face of a high SVR and normal MAP.
• High BP exerts additional afterload on the LV, leads to increased LV O2 consumption, and
may precipitate an ischemic episode. Additionally, it can increase perioperative bleeding
and may result in hemorrhagic stroke or rupture of an aortic aneurysm. Even mild
elevations in BP may be lethal in patients with aortic dissections.
EQUATIONS
• MAP = 1/3 SBP + 2/3 DBP; where MAP is the mean arterial pressure, SBP is the systolic
blood pressure, and DBP is the diastolic blood pressure
• MAP = CO × SVR; where CO is the cardiac output and SVR is the systemic vascular
resistance
REFERENCES
1. Ramsey M. Blood pressure monitoring: Automated oscillometric devices. J Clin Monit.
1991;7(1):56–67.
2. Stokes DN, Clutton-Brock T, Patil C, et al. Comparison of invasive and non-invasive
measurements of continuous arterial pressuring using the Finapres. Br J Anaesth.
1991;67(1):26–35.
• Cardiac output
• Afterload
• Vascular compliance
CLINICAL PEARLS
• The NIBP cuff is a standard ASA monitor; it provides an assessment of overall hemodynamic
function.
• Limitations of the NIBP include:
– Inability to detect beat-to-beat pressures
– Inaccuracy at low pressures
– Requires appropriate cuff/bladder size selection
– Decreased accuracy or inability to measure pressures during arrhythmias, movement,
shivering
OBESITY HYPOVENTILATION SYNDROME
(OHS)/PICKWICKIAN SYNDROME
BASICS
DESCRIPTION
• Pickwickian syndrome, also known as obesity–hypoventilation syndrome (OHS) most
commonly occurs in patients with obstructive sleep apnea (OSA). However, in 10% of cases,
it can occur alone. OHS is characterized by:
– Daytime chronic hypercapnia (arterial CO2 tension >45 mm Hg)
– Obesity (BMI >30)
– Increase in PaCO2 >10 mm Hg from awake supine values and/or oxygen desaturation
(secondary to hypercapnea) during sleep that cannot be explained by apneic or hypopneic
events.
• Symptoms often overlap those of OSA: Dyspnea, daytime somnolence, and possibly right
heart failure (1).
• OHS patients have abnormal medullary respiratory center control; specifically, they lack a
compensatory increased ventilatory drive to offset the effects of the mechanical restrictions
of obesity.
• The name “Pickwickian” comes from a character (a “fat boy” who is constantly falling
asleep) in “The Posthumous Papers of the Pickwick Club” by Charles Dickens.
EPIDEMIOLOGY
Prevalence
Associated with obesity; therefore, the incidence and prevalence of OHS are expected to rise
as the prevalence of obesity increases (2)[B].
Prevalence
• 10–15% of patients with obstructive sleep apnea (OSA) develop OHS.
• Between 1986 and 2000, the number of individuals with BMI >40 increased 4-fold in the
US.
Morbidity
Increased risk for hypoxemia, pulmonary hypertension, cor pulmonale, systemic
hypertension, and coronary artery disease
Mortality
The 18-month mortality among hospitalized patients with OHS is significantly higher (23%)
compared to obese patients without OHS (9%) (3)[B].
• Obesity
• Gender is not a risk factor.
• Obstructive sleep apnea results from excessive/redundant airway tissue that causes a
variable, extrathoracic obstruction to air flow. During sleep and in the supine position, the
negative inspiratory pressures are more likely to cause these tissues to collapse, whereas
during exhalation, the positive pressures “push aside" the tissue. This results in hypoxic
events (chronic hypoxia can increase pulmonary artery pressures, polycythemia), increased
catecholamines (hypertension, arrhythmias), and poor sleep quality (daytime somnolence,
fatigue). It has a significant association with obesity, but may occur in other circumstances
such as enlarged tonsils. Although the majority of OHS patients have concurrent OSA
(90%), it can occur in isolation; thus although they commonly overlap, they are clinically
distinct.
• The precise mechanism of OHS is unknown, but is believed to result from a combination of:
– Impaired respiratory mechanics (manifests as a restrictive ventilatory defect). Total lung
capacity, vital capacity, and compliance are decreased, whereas residual volume, work of
breathing (O2 consumption, CO2 production), and airway resistance are increased (1).
– Abnormal medullary respiratory center control. OHS patients appear to lack a
compensatory increased ventilatory drive to offset the effects of the mechanical
restrictions of obesity. On the other hand, obese patients (without OHS) demonstrate an
increased ventilatory response. Studies have suggested that OHS patients have a leptin
deficiency or resistance. Leptin is normally produced by adipose tissue and acts on the
central respiratory center to stimulate ventilation (4)[A].
Anesthetic GOALS/GUIDING Principles
• Perioperative care of patients should focus on maintaining appropriate CO2 levels to avoid a
“relative" respiratory alkalosis. Concurrent management also requires addressing and
managing comorbid issues of obesity (BMI >30) and typically obstructive sleep apnea
(present in 90% of patients with OHS).
• During induction and emergence, position the patient in an upright position (reverse
Trendelenburg) to improve respiratory mechanics and facilitate endotracheal intubation.
• Use short-acting anesthetic drugs. Benzodiazepines, opioids, and intravenous and
inhalational agents that affect the hypoxic and hypercarbic drive may have more profound
effects on patients with OHS.
• Opioid-sparing techniques for analgesia should be considered (local infiltration, regional or
neuraxial blockade).
• Postoperative rehabilitation, mobilization, and physical therapy. Postoperatively, consider
prolonged observation in the recovery room, or admission to the hospital and continuous
pulse oximetry.
SYMPTOMS
• Due to reduced mobility, cardiac disease may remain asymptomatic for years.
• Edema and dyspnea on exertion are common and nonspecific.
History
• OHS is under-diagnosed and undertreated. Therefore, morbidly obese patients should be
asked about snoring, fatigue, somnolence, or morning headaches that are suggestive of OSA.
• Previous anesthesia and hospitalization records
• Tobacco, alcohol, and drug abuse can aggravate chronic hypoventilation.
• Duration: The risk of cardiomyopathy increases steeply after 10 years of symptoms.
Signs/Physical Exam
• Signs of heart failure (increased jugular venous pressure, hepatomegaly, edema) may be
difficult to detect due to excess fat.
• Neck circumference >40 cm is associated with OSA.
• Pulse oximeter readings can be normal in the presence of hypercapnia.
TREATMENT HISTORY
• Bariatric surgery (malabsorptive, restrictive, or combined)
• Home CPAP or BiPAP. Inquire about settings and supplemental oxygen.
MEDICATIONS
• Insulin or oral hypoglycemic for diabetes
• Medications for associated cardiovascular conditions
• Diuretics for hypertension or edema
• Antidepressants
• Medications for obesity: Lipase inhibitors (orlistat) or appetite suppressants (rimonabant,
sibutramine, phentermine)
• Dietary or herbal medications for weight loss
Labs/Studies
• Serum electrolytes including serum creatinine
• Arterial blood gases: Hypercarbia, A-a gradient
• EKG to detect ischemia, arrhythmias, atrial or ventricular enlargement
• Echocardiography to evaluate myocardial contractility, diastolic dysfunction, right
ventricular hypertrophy, pulmonary artery pressures (derived), and valve function;
significant tricuspid regurgitation is evidence of pulmonary hypertension.
• Routine pulmonary function testing is NOT recommended for preoperative testing.
• Formal sleep studies may be needed if the patient’s history is consistent with OHS and there
is no established diagnosis.
• Pulmonary system
• Musculoskeletal system (arthritis)
Epidural analgesia is feasible but technically more demanding. Opioids, (particularly long-
acting opioids, such as morphine) may have more profound effects on ventilation and
oxygenation.
Rare, but includes congestive heart failure exacerbation from cor pulmonale
TREATMENT
Premedications
• Benzodiazepines and opioids should be cautiously administered with continuous pulse
oximetry, even in the holding suite.
• Consider H2 blockers, non-particulate antacids, or proton pump inhibitors to reduce the risk
of aspiration
• DVT prophylaxis
• Increased risk for perioperative cardiovascular (myocardial infarction, congestive heart
failure, arrhythmias), and pulmonary (aspiration, pneumonia, respiratory failure,
respiratory depression) complications.
• Regional analgesic techniques, if appropriate
INTRAOPERATIVE CARE
• Spinal, epidural, and regional anesthesia have been safely performed, but may be
technically more difficult. Benefits include avoidance of airway management (bag-mask
ventilation and laryngoscopy) and controlled ventilation, as well as a decreased need for
opioid analgesics. Drawbacks include inability for an obese patient to tolerate surgical
positioning, and failed block or complication that necessitates induction of general
anesthesia under suboptimal circumstances.
• If general anesthesia is needed, endotracheal intubation with positive pressure ventilation is
preferred. Patients have altered chest wall mechanics and response to hypercarbia and
hypoxia, as well as decreased functional residual capacity (FRC).
Monitors
• Arterial line may be indicated for monitoring arterial blood gases.
• Attention to adequate preoxygenation: Morbidly obese patients desaturate quickly due to
decreased FRC and increased oxygen consumption. Administering CPAP (6 cm H2O) for 5
minutes while preoxygenating (followed by PEEP after intubation) may be useful in
decreasing the level of atelectasis (compared to PEEP alone).
• Appropriate positioning: The head and shoulders generally need to be elevated using
additional pillows, blankets, or other support material. The head-elevated laryngoscopy
position (5)[B] can improve laryngeal exposure during laryngoscopy.
• Other general obesity considerations: Consider a rapid-sequence induction due to concerns
about aspiration and difficulty with mask ventilation. Prepare for a difficult airway, and
consider the use of an indirect video laryngoscopy (6)[B].
Maintenance
• PEEP can decrease atelectasis and increase FRC (decreases V/Q mismatch and increases
oxygen storage capacity).
• Avoid over-correction of ETCO2 to normal levels. Patients are chronically hypercarbic and
have metabolic compensation (increased HCO3-). Acute decreases can result in an acute
alkalosis.
• Inhaled anesthetic agents with low fat solubility (desflurane or sevoflurane) and intravenous
propofol infusion are reasonable choices.
• Dexmedetomidine can decrease postoperative opioid requirements without causing
• Remifentanil, combined with inhaled anesthetics or propofol, allows for intraoperative
analgesia without residual respiratory depression postoperatively. Particularly useful in
cases with brief, profound stimulation (e.g., micro direct laryngoscopy).
• Extubation should be performed in a semi-recumbent position, when the patient is fully
reversed and awake.
• Consider placing a nasal airway preemptively, to avoid post-extubation airway obstruction,
if appropriate.
FOLLOW-UP
BED ACUITY
• Resume CPAP or noninvasive positive pressure ventilation
• Continuous pulse oximetry
• Consider an observation unit or ICU for monitoring
• Consider postoperative arterial blood gas
• Sleep medicine evaluation if OHS diagnosis suspected but not established
COMPLICATIONS
• Cardiovascular: Arrhythmias from respiratory acidosis, myocardial ischemia from hypoxia
• Respiratory: Aspiration, atelectasis, pneumonia, respiratory failure
REFERENCES
1. Piper AJ, Grunstein RR. Current perspectives on the obesity hypoventilation syndrome.
Curr Opin Pulm Med. 2007;13:490–496.
2. Flegal KM, Carroll MD, Ogden CL, et al. Prevalence and trends in obesity among US adults
1999–2008.
3. JAMA. 2010;303:235–241.
4. Nowbar S, Burkart KM, Gonzales R, et al. Obesity associated hypoventilation in
hospitalized patients: Prevalence, impact, and outcome. Am J Med. 2004;116(1):1–7.
5. Olson AL, Zwillich C. The obesity hypoventilation syndrome. Am J Med. 2005;118:948–
956.
6. Levitan RM, Mechem CC, Ochroch EA, et al. Head-elevated laryngoscopy position:
Improving laryngeal exposure during laryngoscopy by increasing head elevation. Ann
Emerg Med. 2003;41:322–330.
7. Marrel J, Blanc C, Frascarolo P, et al. Video laryngoscopy improves intubation condition in
morbidly obese patients. Eur J Anaesthesiol. 2007;24:1045–1049.
ADDITIONAL READING
• Paurier P, Alpert MA, Fleisher LA, et al. Cardiovascular evaluation and management of
severely obese patients undergoing surgery: A science advisory from the American Heart
Association. Circulation. 2009;120:86–95.
• Cor pulmonale
• Minute ventilation
• Continuous positive airway pressure
• Atelectasis
CODES
ICD9
278.03 Obesity hypoventilation syndrome
ICD10
E66.2 Morbid (severe) obesity with alveolar hypoventilation
CLINICAL PEARLS
• OHS is often unrecognized, but should be considered and suspected in morbidly obese
patients, particularly with a diagnosis of OSA.
• Minimize the use of opioid analgesics, if possible, and consider regional analgesia whenever
feasible. Have a low threshold for postoperative continuous pulse oximetry.
• Postoperative monitoring for apnea
OCULOCARDIAC REFLEX
Radha Arunkumar, MD
BASICS
DESCRIPTION
• The oculocardiac reflex (OCR) is a trigeminovagal reflex. It was first described in 1908 by
Dr. Aschner who observed that the application of pressure on the eyeball resulted in slowing
of the heart (1).
– The afferent pathway is the ophthalmic division of the trigeminal nerve (CN V), through
the Gasserian ganglion, and ending in the trigeminal sensory nucleus in the floor of the
fourth ventricle.
– The efferent pathway is through the vagus nerve (CN X) to the heart.
• Perioperatively, it is most commonly encountered with ophthalmic cases (e.g., pediatric
strabismus surgery) due to pressure on the globe or traction of the extraocular muscles. It
can also occur:
– From orbital floor fractures and neurosurgical procedures involving the trigeminal nerve
– After enucleation by stimulation of cranial nerve V in the presence of a tense orbital
hematoma
– During the performance of a retrobulbar block. Interestingly, retrobulbar blocks may
abolish subsequent occurrence.
EPIDEMIOLOGY
Incidence
Strabismus surgery: 14–90% depending on the premedication, anesthetic agent, and
definition of OCR chosen (2)
Prevalence
Can occur in any age group but is more frequent in children and young adults due to their
inherent vagal tone
Morbidity
There are several case reports of asystole and cardiac arrest in the literature that resulted in
successful resuscitation.
Mortality
Even though death is very rare, a handful of case reports of deaths with unsuccessful
resuscitation have been reported, both directly attributable to OCR and to underlying cardiac
disorders such as occult myocarditis.
• Light general anesthesia
• Stimulus strength and duration
• Age (pronounced in children)
• Augmented vagal tone
• Potent narcotics
• Beta-blockers
• Calcium channel blockers
• Hypoxia
• Hypercarbia
• Acidosis
• A reflex is an involuntary reaction or spontaneous movement to a stimulus; it is mediated
via a reflex arch that is comprised of afferent and an efferent limb. The afferent pathway is
usually sensory, and the efferent pathway is either motor or autonomic (sympathetic or
parasympathetic).
• Trigeminal nerve afferent: Pressure on the eye globe or traction of the extraocular muscles
returns sensation via trigeminal nerve afferents.
– The afferent pathway is through the ophthalmic division of the trigeminal nerve (CN V)
ending in the trigeminal sensory nucleus in the floor of the fourth ventricle.
• Vagal efferent: The right vagus nerve primarily innervates the SA node while the left vagus
nerve primarily innervates the AV node; however, there is a significant overlap in the
anatomic distribution. The vagus nerve provides the parasympathetic innervation to the
heart, and its actions are mediated by the release of acetylcholine neurotransmitter (binds
to cardiac muscarinic receptors)
– The most common vagal efferent response is sinus bradycardia. However, junctional
rhythm, atrioventricular block, bigeminy, and even cardiac arrest have been reported.
– OCR has a very quick onset along with a quick offset when the stimulus is stopped.
• OCR is exaggerated by:
– Hypoxia, hypercarbia, and acidosis alter the cardiac resting membrane potential and make
the heart more susceptible to bradycardia
– Augmented vagal tone, especially in children
– Potent narcotics: Through their inhibitory action on the sympathetic nervous system
– Beta-blockers: Reduce the sympathetic response of the heart thereby augmenting the vagal
cardiac response
– Calcium channel blockers: Cause peripheral vasodilatation which exaggerates the
bradycardia and hypotension
• Gentle surgical manipulation and minimizing mechanical stimulation are believed to be
more effective in preventing OCR than other techniques.
• Avoid hypoxia, hypercarbia, acidosis, and light general anesthesia.
• Pretreatment with atropine or retrobulbar block has not been shown to be effective
prophylaxis.
• Effects of different anesthetic regimens on the incidence of OCR have been studied during
pediatric strabismus surgery.
– Ketamine infusion without volatiles has been found to have the most hemodynamic
stability compared to propofol infusion and volatile agents (2,3)[A].
– Propofol or remifentanil anesthesia has been associated with a higher incidence of OCR
during strabismus surgery compared to sevoflurane or desflurane anesthesia (4)[A].
– No difference has been found between desflurane and sevoflurane (5)[B].
DIAGNOSIS
• ECG: Sudden onset of sinus bradycardia that is defined as a 10–20% decrease in resting
heart rate that is sustained for 5 seconds or longer
• Pulse oximetry: Correlating pulse will decrease or be dampened.
• Blood pressure: Hypotension
Inadvertent anticholinergic administration
TREATMENT
• Vigilant intraoperative monitoring is important because the reflex ceases when stimulation
stops.
• Inform the surgeon; discontinuing stimulation is the first step in treating OCR.
• Sustained and repeated stimulation may cause the OCR to fatigue.
• Persistent bradycardia is treated with IV atropine or glycopyrrolate; if the patient remains
unresponsive, epinephrine administration may be necessary.
• Local injection of lidocaine near the eye muscle or peribulbar/retrobulbar block with local
anesthetic may be needed. Local anesthetics interfere with excitation and conduction of
action potential in the nerves by blocking the voltage-gated sodium channel; this blocks the
afferent limb of the reflex arc.
REFERENCES
1. Dewar KM, Wishart HY. The oculocardiac reflex. Proc R Soc Med. 1976;69(5):373–374.
2. Hahnenkamp K, Honemann CW, Fischer LG, et al. Effect of different anaesthetic regimes on
the oculocardiac reflex during paediatric strabismus surgery. Paediatr Anaesth.
2000;10(6):601–608.
3. Mizrak A, Erbagci I, Arici T, et al. Ketamine versus propofol for strabismus surgery in
children. Clin Ophthalmol. 2010;4:673–679.
4. Choi SR, Park SW, Lee JH, et al. Effect of different anesthetic agents on oculocardiac reflex
in pediatric strabismus surgery. J Anesth. 2009;23(4):489–493.
5. Oh AY, Yun MJ, Kim HJ, et al. Comparison of desflurane with sevoflurane for the incidence
of oculocardiac reflex in children undergoing strabismus surgery. Br J Anaesth.
2007;99(2):262–265.
ADDITIONAL READING
• Arasho B, Sandu N, Spiriev T, et al. Management of the trigeminocardiac reflex: Facts and
own experience. Neurol India. 2009;57:375–380.
• Bradycardia
• Retinal detachment
CLINICAL PEARLS
• OCR is iatrogenic and most commonly occurs during pediatric strabismus surgery due to
traction of extraocular muscles.
• The afferent pathway is the ophthalmic division of the trigeminal nerve; the efferent
pathway stems from the vagus nerve.
• Sinus bradycardia is most common, but other dysrhythmias including cardiac arrest can
occur.
• Discontinuing surgical stimulation is key to management of OCR.
• Premedication is not helpful, but IV treatment with atropine or glycopyrrolate should be
administered if bradycardia is persistent.
OMPHALOCELE
John T. Chalabi, MD
Swati Patel, MD
BASICS
DESCRIPTION
• Omphalocele is a midline abdominal wall defect. The herniated viscera is covered by a
membrane that consists of:
– Peritoneum on the inner surface
– Amnion on the outer surface
– Wharton’s jelly between the layers (1)
• It results due to the failure of the bowel to return to the abdominal cavity after physiologic
midgut herniation (PMH) that occurs during the 6th–10th week of gestation.
• The defect is typically identified on prenatal ultrasound (after the 12th week of gestation).
• Omphalocele commonly contains small intestine and liver; however, large intestine, bladder,
spleen, stomach, uterus, and ovaries can also be present in the defect (2).
• The physiologic impact is based on the size of the defect and associated anomalies. Bowel
function is usually preserved. However, there is a high incidence of associated congenital
anomalies (see Concomitant Organ Dysfunction).
• Surgical management:
– Staged silo repair: Spring-loaded versus stitched (with gradual reduction of abdominal
contents over 7–10 days)
– Primary closure is performed for smaller defects.
– Delayed closure (months later) is performed for giant omphaloceles.
EPIDEMIOLOGY
Prevalence
Ranges between 1.5 and 3 per 10,000 births (1)
Prevalence
• The Office of Rare Diseases (ORD) of the National Institutes of Health (NIH) lists the
omphalocele as a “rare” disease, affecting <200,000 people in the US.
• Male-to-female ratio is 1:1.
Morbidity
• In the absence of other major anomalies, the rate of long-term morbidity is about 20%.
• Major complications include:
– Respiratory failure
– Failure to thrive
– Intestinal ischemia/obstruction, short gut syndrome
– Wound infection and dehiscence
Mortality
In the literature, a 61% mortality is reported for omphalocele with associated anomalies, in
contrast to <15.5% in those without (3).
• Maintain adequate ventilation
• Maintain hemodynamics and avoid hypovolemia
• Prevent trauma to the herniated viscera
• Maintain normothermia
• Correct hypoglycemia
SYMPTOMS
• Range from none to severe respiratory and/or hemodynamic shock; depends on the size of
the hernia, concomitant diseases, and neonatal reserve.
• Gastroesophageal reflux (GERD) is not uncommon.
History
• Size of the omphalocele
• Mode of the delivery (vaginal, cesarean, etc.)
• Any concomitant disease/syndromes
• Hemodynamic stability and volume status
• Acid–base status and potential lung disease associated with prematurity or hypoplasia
Signs/Physical Exam
• Membrane-covered defect ranging in size from 2 to 15 cm.
• Respiratory: Look for signs of respiratory distress (patients with large defects are often
intubated in the delivery room).
• Cardiovascular: Look for signs of hemodynamic instability secondary to hypovolemia (weak
pulses, poor distal extremity perfusion) or loud murmurs and decreased oxygen saturation
suggesting the presence of congenital heart disease
MEDICATIONS
• Broad spectrum antibiotics
• Total peripheral nutrition (TPN)
• H2 receptor blockers

Labs/Studies
• CBC, electrolytes, blood glucose, coagulation studies, type and cross, and blood gas
• Chest radiograph and echocardiogram
• Chromosome anomalies, notably trisomy 13, 14, 15, 18, and 21, are present in up to 30% of
cases.
• Cardiac defects are common; they are seen in 30–50% of cases.
• Neural tube defects are present in up to 40% of patients with omphalocele.
• Beckwith–Wiedemann syndrome is seen in 10% of patients. It presents as macroglossia,
organomegaly, early hypoglycemia (from pancreatic hyperplasia and excess insulin), and an
increased risk of Wilms’ tumor, hepatoblastoma, and neuroblastoma developing later in
childhood.
• Pentalogy of Cantrell presents with omphalocele associated with ectopia cordis, anterior
diaphragmatic hernia, defect of the pericardium and various congenital intracardiac
anomalies, and defects of the lower sternum.
• Organ dysfunction associated with prematurity, if present
• Unlike gastroschisis defects, the bowel is completely covered by a sac that protects it from
infection and large insensible fluid losses. This allows time for:
– Thorough assessment of comorbidities prior to surgical repair
– Correction of hemodynamic instability
• Large defects (giant omphalocele), if reduced quickly, may lead to ventilatory compromise,
impede venous return, and cause aortocaval compression from direct compression
(abdominal compartment syndrome). These defects may take several months to
reduce/repair.
CLASSIFICATIONS
Omphaloceles are categorized as:
• Small (<2 cm)
• Medium (2–5 cm)
• Giant (6 cm and bigger)
TREATMENT
Premedications
Not anticipated
• Risks particular to associated anomalies, if present.
• Need for continued postoperative intubation
INTRAOPERATIVE CARE
General anesthesia with endotracheal tube is the anesthetic technique of choice.
Monitors
• Standard ASA monitors: A pulse oximeter above and below the diaphragm should be placed.
• Monitor for significant increases in peak inspiratory pressure (PIP), reductions in tidal
volume (TV), or oxygen desaturation throughout the abdominal closure. These
abnormalities may indicate that the primary closure will not be tolerated.
• Consider invasive monitoring as necessary:
– Arterial catheter for hemodynamic and blood gas monitoring if respiratory problems are
anticipated (large defect, pulmonary hypoplasia, etc.) or if the patient has congenital
heart disease or cardiovascular instability.
– +/– CVP
– Foley catheter
• Decompress the stomach prior to performing a rapid-sequence induction
• Choice of induction agents should be based on hemodynamic status and any coexisting
cardiac conditions.
• Care with (or avoidance of) bag-mask ventilation to avoid bowel distention
• The endotracheal tube size should be chosen to allow high-pressure ventilation if necessary.
Maintenance
• Typically opioid and volatile agents are utilized. However, the choice of agents should be
tailored to comorbid conditions, as appropriate.
• Muscle relaxation to facilitate abdominal relaxation
• Nitrous should be avoided as it may cause bowel distention and difficulty with reduction of
the hernia.
• Avoid hypothermia: Warm fluids, place a full body warmer, warm the room
• If on TPN, decrease to 1/2 maintenance and monitor for hypoglycemia
• Fluid requirements can be up to 50–200 mL/kg/hr depending on the extent of bowel
involvement and exposure. Large fluid requirements must be balanced with any coexisting
heart disease.
• Most patients will remain ventilated postoperatively.
• May consider extubation postoperatively in patients with small defects.
– Consider size of patient, comorbidities, hemodynamic stability
FOLLOW-UP
BED ACUITY
NICU
As indicated
COMPLICATIONS
• Respiratory failure/compromise
• Pulmonary edema
• Hemodynamic collapse
• Electrolyte imbalance
• Infection: GI (necrotizing enterocolitis), peritonitis wound, pulmonary, etc.
• Abdominal compartment syndrome
• Hypertension secondary to decreased renal perfusion
• Postoperative ileus requiring prolonged TPN (less common than with gastroschisis)
REFERENCES
1. Ledbetter DJ. Gastroschisis and omphalocele. Surg Clin North Am. 2006;86(2):249–260.
2. Frolov P, Alali J, Klein MD. Clinical risk factors for gastroschisis and omphalocele in
humans: A review of the literature. Pediatr Surg Int. 2010;26(12):1135–1148.
3. Henrich K, Huemmer HP, Reingruber B, et al. Gastroschisis and omphalocele: Treatments
and long-term outcomes. Pediatr Surg Int. 2008;24(2):167–173.
ADDITIONAL READING
• Brusseau R, McCann ME. Anaesthesia for urgent and emergent surgery. Early Hum Dev.
2010;86(11):703–714.
• Gastroschisis
• Hypothermia
CODES
ICD9
756.72 Omphalocele
ICD10
Q79.2 Exomphalos
CLINICAL PEARLS
• Assess for associated anomalies (chromosomal, congenital heart disease, neural tube defects)
• Adequate volume resuscitation should take place prior to surgical repair
ONE LUNG VENTILATION
Daniel Castillo, MD
BASICS
DESCRIPTION
• One lung ventilation (OLV) is achieved by isolating either the right or left lung in order to:
– Isolate ventilation in the case of a bronchopleural fistula or to protect the healthy lung
from pus, blood, other fluids, or protein in the affected lung
– Facilitate surgery/exposure by collapsing one lung while the other lung sustains
ventilation and gas exchange during the procedure
• Lung isolation can be achieved by 3 basic methods (1,2,3)[B].
– Placing a right or left endobronchial double lumen tube (DLT)
– Placing a single lumen endotracheal tube in conjunction with a bronchial blocker (Arndt,
Cohen, balloon-tipped luminal catheters) or utilizing a commercially available
endotracheal tube with a built-in blocker (Univent) (4,5,6)[B]
– Placing a single lumen tube in the right or left main bronchus
• Lung isolation can also be done through a tracheostomy tube and is most commonly done
with a bronchial blocker (3)[B].
• Ventilation (V) and perfusion (Q): The relationship between V and Q determines gas
exchange, with the ideal V/Q ratio being 1; however, there are physiologic regional
differences.
– Alveolar lung units are said to “shunt” when V < Q, whereas “dead space” results when V
> Q.
– Lung base: V and Q are highest in this “dependent area” when standing up. However,
perfusion is proportionally greater than ventilation (V < Q), creating a shunt.
– Mid-lung (Zone 2): V and Q decrease at different proportions, resulting in ventilation and
perfusion matching (V = Q).
– Apices: V and Q continue to decrease at different proportions, resulting in ventilation
exceeding perfusion (V > Q) and creating dead space.
– At any given time, shunting and dead space occur in different areas without derangements
in oxygenation or CO2 removal. Thus, V/Q matching must be understood on a spectrum
based upon the number of units with mismatch, as well as the lung’s ability to compensate
(distal units able to upload O2 and dispose of CO2, hypoxic pulmonary vasoconstriction
[HPV], and supplement O2).
• Bilateral ventilation with general anesthesia, different ventilatory modes, lateral position,
and an open chest
– Spontaneous ventilation: Anesthetic agents (volatile and intravenous) decrease the
functional residual capacity by impairing diaphragmatic and intercostal muscle function.
This results in cephalad movement of the abdominal contents and decreased chest wall
expansion. This increases the number of atelectatic alveolar units (V = 0).
– Lateral position: The upper lung (non-dependent) has increased compliance since the
abdominal pressure is mostly exerted over the lower lung (dependent and lower
compliance). Perfusion remains gravity-dependent and preferentially flows to the
dependent lung.
– Positive pressure ventilation (PPV) and muscle paralysis: Although PPV can improve V/Q
matching by overcoming the abdominal pressure on the diaphragm, the non-dependent
areas are preferentially ventilated while the dependent areas are preferentially perfused.
– Open chest: Exposing the non-dependent lung to atmospheric pressure increases its
compliance and PPV is preferentially diverted. However, perfusion remains gravity-
dependent and preferentially flows to the dependent lung.
• OLV: When ventilation only occurs to one side, any blood flow to the non-ventilated lung
becomes shunt flow (V < Q). This results in a large alveolar–arterial oxygen gradient and
decreased PaO2. Factors that aid with redistribution of pulmonary blood flow to the
dependent lung help to maintain PaO2 in an acceptable range during surgery. Despite the
effect on PaO2, it has much less effect on PaCO2. The ventilated lung is able to compensate
by eliminating a higher amount of CO2 to compensate for OLV (provided that minute
ventilation is maintained).
– Spontaneous ventilation: In addition to the non-dependent lung being shunted, cephalad
movement of abdominal contents will also increase the number of atelectatic units in the
dependent lung.
– PPV aids with offsetting the effect of the abdominal contents to the dependent, ventilated
lung.
– Lateral position: Blood that flows to the non-dependent lung is shunted (there is no
ventilation). Gravity shifts the blood flow towards the dependent and ventilated lung.
Maneuvers that “shift" blood flow to the non-dependent lung will therefore worsen
shunting.
– Open chest: Exposure of the pleural cavity to atmospheric pressure on the surgical side
will help initiate collapse of the non-ventilated lung, as well as further shift/defer
perfusion to the dependent lung.
• HPV: A physiologic response by pulmonary capillary vessels to low oxygen tension in the
alveoli. Vasoconstriction occurs, decreasing blood flow to the alveoli and diverting blood to
ventilated alveoli. By optimizing blood flow, the end result is a decrease in shunting.
ANATOMY
• The lungs are contained in the chest cavity, which is formed by the rib cage, the diaphragm,
and chest muscles. Parietal pleura lines the inside of the rib cage.
• Each lung is surrounded by its own visceral pleura. The intrapleural space is a potential
space that lies between the parietal and visceral pleura has a negative pressure that “brings"
together or “sucks" the two surfaces towards each other.
• The tracheobronchial tree starts with the trachea and divides in a dichotomous fashion,
ending in alveolar sacs.
• The trachea is about 11–13 cm long in an adult, starts at the cricoid cartilage, and first
divides/bifurcates at the level of T5 (carina) to form the right and left main stem bronchus.
• The right bronchus is wider, diverges from the trachea at a 25° angle and branches into the
upper, middle, and lower lobes. The right upper lobe branches at approximately 1–2.5 cm
distal to the carina.
• The left bronchus diverges from the trachea at a 45° angle and branches into an upper and
lower lobe. The left upper lobe diverges approximately 5 cm distal to the carina.
• Because of these differences, right and left DLTs are slightly different in their endobronchial
lumen design. Right DLTs have a side opening (Murphy’s eye) close to the tip and
surrounded by the cuff so that it can be positioned at the right upper lobe origin to assure
its ventilation; the cuff of a left DLT may inadvertently block the right main bronchus (2,7)
[B].
• OLV is indicated:
– In massive hemorrhage or infection to isolate the lungs and avoid spillage and
dissemination of infection
– To control distribution of ventilation; bronchopleural fistulas, surgical opening of
conductive airway, tracheobronchial tree disruption, severe hypoxemia due to unilateral
lung disease
– Exposure for surgical procedures: Aortic surgery, spine surgery, lung resection, esophageal
surgery, single lung transplantation, and thoracoscopy among others
• Pulmonary circulation has much less smooth muscle to control tone than systemic
circulation; therefore, any increase in pulmonary arterial pressure (mitral stenosis,
congestive heart failure, thromboembolism) can recruit and dilate pulmonary vessels and
potentially interfere with HPV. Other mechanisms that have been traditionally attributed to
interfere with HPV are direct vasodilating drugs (nitroglycerin, nitroprusside, etc.) and
volatile anesthetics.
• Prior to the initiation of OLV for surgical procedures, the patient’s comorbidities should be
assessed and optimized to decrease morbidity (cardiac function, pulmonary hypertension,
chronic obstructive pulmonary disease, coagulopathy).
• Initiation of OLV. Ventilation should be adjusted properly to minimize hypoxia.
– Start by ventilating both lungs with tidal volumes of 6–8 mL/breath, a normal I:E ratio, a
rate of 8–10/min, and 100% FIO2. The goal is to observe the peak and plateau airway
pressures.
– Upon instituting OLV, adjust the respiratory rate according to the PaCO2 without changing
the tidal volume.
– If the peak and plateau pressures do not increase by >5–8 mm▒Hg, maintain the same
tidal volume; otherwise, decrease tidal volume so that the airway pressure is maintained
within the above-mentioned range.
– Increase the respiratory rate as needed to maintain normocarbia; keep in mind that this
can indirectly increase airway pressures.
• Collapsing the non-dependent lung: Exposure of the pleural cavity to atmospheric pressure
on the surgical side will initiate collapse of the lung.
– Accelerated by a higher FIO2 before lung isolation, clearing the airway of secretions, and
applying gentle suction to the non-ventilated lung
– Slowed or hampered by small airway diseases, secretions in the airway, tumor pressure on
the airway, malpositioning of the DLT, and pleural adhesion and fibrosis
• Factors that aid with diverting blood flow and maintaining a PaCO2 in an acceptable range
during surgery:
– Passive: Gravity (lateral decubitus), pre-existing lung disease (mass), surgical
manipulation and interventions (ligation of vessels)
– Active (more effective): HPV
• Hypoxia:
– DLT malposition (major cause): Fiberoptic examination of the tube position is necessary in
any patient with OLV and hypoxia; confirm that the tube is not too deep (endolobar) or
that the cuff is not herniating upwards into the carina (8)[B].
– Shunting: Interventions to decrease shunting depend upon the severity of hypoxia. If mild,
consider starting with continuous positive airway pressure (CPAP) to the non-dependent
lung followed by positive end expiratory pressure (PEEP) to the dependent lung (may
“shunt” blood to the non-dependent lung and worsen hypoxia). When acute or severe,
temporary re-expansion of the non-dependent lung and/or clamping of the pulmonary
artery to the non-dependent lung (if surgical conditions permit).
– Secretions: Can cause localized hypoventilation, which can be improved by suctioning
– Decreased cardiac output: Can impair oxygen delivery to tissues. Increasing the CO may
improve hypoxia by improving mixed venous O2.
GRAPHS/FIGURES
FIGURE 1. Left-sided double lumen tube. The endobronchial lumen sits in between the carina and left upper lobe. There is
an increased margin for error while positioning, and even for right sided lung surgeries and procedures, a left DLT is
commonly placed (with ventilation to the left lung/dependent lung through the endobronchial lumen).
FIGURE 2. Right-sided double lumen tube. The endobronchial lumen sits below the carina. However, because of the
shorter distance between the carina and right upper lobe takeoff, there is little margin for error while positioning. In order
to avoid occlusion and shunting of the right upper lobe, a Murphy’s eye is embedded into the endobronchial cuff to allow
ventilation. Ventilation also occurs through the endobronchial lumen.
FIGURE 3. Fiberoptic view of a properly positioned left double lumen tube via the tracheal lumen. The carina should be
visualized along with the endobronchial cuff slightly above the bronchial lumen. The posterior tracheal rings can aid with
identifying that the view is of the trachea, and not endobronchial.
REFERENCES
1. Koshy T, Nair SG. Positioning of double-lumen endobronchial tubes: Correlation between
clinical and bronchoscopic findings. Indian J Anaesth. 2003;47(2):116–119.
2. Campos JH. Current techniques for perioperative lung isolation in adults. Anesthesiology.
2002;97(5):1295–1301.
3. Campos JH. An update on bronchial blockers during lung separation techniques in adults.
Anesth Analg. 2003;97:1266–1274.
4. Ransom ES, Carter L, Mund GD. Univent tube: A useful device in patients with difficult
airways. J Cardtothorac Vasc Anesth. 1995;9(6):725–727.
5. Campos JH, Kernstine KH. A comparison of a left-sided Broncho-Cath with the torque:
Control blocker Univent and the wire-guided blocker. Anesth Analg. 2003;96:283–289.
6. Takenaka I, Aoyama K, Kadoya T. Use of the Univent bronchial-blocker tube for
unanticipated difficult endotracheal intubation. Anesthesiology. 2000;93(2):590–591.
7. Kernstine KH. The incidence of right upper-lobe collapse when comparing a right-sided
double-lumen tube versus a modified left double-lumen tube for left-sided thoracic surgery.
Anesth Analg. 2000;90:535–540.
8. Uwe K, Karzai W, Bloos F, et al. Role of fiberoptic bronchoscopy in conjunction with the
use of double lumen tubes for thoracic anesthesia: A prospective study. Anesthesiology.
1998;88:346–350.
9. Campos JH, Massa C, Alliaume B, et al. Reliability of auscultation in positioning of double-
lumen endobronchial tubes. Can J Anaesth. 1992;39(7):687–690.
10. Brodsky JB, Lemmens HJ. Left double-lumen tubes: Clinical experience with 1,170
patients. J Cardiothorac Vasc Anesth. 2003;17(3):289–298.
11. Swift J. Placement of double lumen tubes—time to shed light on an old problem. Br J
Anaesth. 2000;84(3):308–310.
• Double lumen tube
• Hypoxic pulmonary vasoconstriction
CLINICAL PEARLS
• Correct positioning of a DLT can be confirmed clinically by auscultation of the lungs during
manual ventilation; breath sounds should be absent distally when clamping the desired
lumen (tracheal, bronchial) (9)[B]. Visualization with a fiberoptic scope is the gold standard
for confirming positioning.
• Patients with severe restrictive lung disease, very low cardiac output, or pneumonia in non-
ventilated lung may be less capable of handling the shunt created in the non-dependent
lung.
OPERATING ROOM FIRES
Jeanna Blitz, MD
Shawna Dorman, MD
BASICS
DESCRIPTION
• An operating room fire is any fire that ignites in the operating or procedure room.
• Anesthesia providers should be aware of the treatment and prevention of surgical and
airway fires.
– Surgical fires are defined as those that occur on or around a patient.
– Airway fires are defined as surgical fires that ignite within the patient’s airway or
breathing circuit.
• All fires require the triad of an ignition, oxidizer, and fuel. Thus, prevention in high-risk
scenarios should aim at reducing or eliminating one of these elements.
EPIDEMIOLOGY
Incidence
• Difficult to accurately assess because there is no FDA mandate requiring operating room
staff to report a fire
• In the US, there are approximately 550–650 surgical fires per year.
• 21% of surgical fires involve the airway.
Morbidity
Disfiguring or disabling injuries from operating room fires is estimated to occur in 20–30
patients per year (1).
Mortality
Death from operating room fires occur in ~1–2 patients per year (mostly airway fires)
• Fire triad
– Ignition: Electrocautery, lasers, fiberoptic light source, defibrillators, high-speed burrs
– Oxidizers (gases that can support combustion): Oxygen and nitrous oxide
– Fuel: Alcohol-based surgical preps, ETT, breathing circuits, drapes, body hair, nasal
cannula, face masks, intestinal gases
• High-risk surgical procedures are defined as anytime an ignition source may come in close
proximity to an oxygen-rich environment.
– Procedures above the xiphoid, sedation with open oxygen source (face mask, nasal
cannula)
Cataract
Carotid endarterectomy (cervical block)
Removal of skin lesions
Face lifts
Blepharoplasty
– Procedures that “enter" the airway
Tracheostomy
Biopsy (vocal cords, tracheal)
Removal of lesions
Oropharyngeal procedures
• Oxygen lowers the temperature at which a fuel will ignite.
– Even materials that will not burn in room air will do so in an oxygen-enriched
environment.
– Oxygen-enriched fires are hotter, more intense, and spread more rapidly.
• Oxygen-enriched environments are defined as any atmosphere in which the oxygen
concentration is >21% or the partial pressure is >160 mm Hg (2).
– Drapes promote trapping or pooling of oxygen from open sources (blow by, face mask,
nasal canula).
– Airway procedures enter an enclosed, oxygen-enriched environment
• Nitrous oxide supports combustion by dissociating and releasing heat and oxygen.
• Most, if not all, operating room, surgical, and airway fires are preventable.
• Deliver safe room air sedation.
– Select patients with normal pulmonary function
– Judiciously administer hypnotics, sedative, and opioids
– Use of a pulse oximeter AND end-tidal CO2 to monitor the patient’s oxygenation and
ventilation can decrease hypoxic events by allowing earlier diagnosis of hypoventilation.
– Oxygen saturations of 92% can be safe and acceptable; <90% is undesirable because the
steep portion of the oxyhemoglobin dissociation curve puts the patient at risk for rapid
desaturation.
• Maintain supplemental oxygen <30% when administered via an open oxygen source in any
head or neck surgery (3)[C].
– Nasal cannula can be used at flow rates <4 L/minute if ignition sources are >10 cm from
the oxygen outlet and the head is not draped (2)[C].
– Venturi masks entrain room air to lower the FiO2 that is delivered.
– “Blow by" with a hose is used when masks are not appropriate to the clinical situation.
The use of a color adapter may be helpful to indicate the FiO2 that is delivered. Confirm
that the device is properly sampling the area exposed to the ignition source.
– Air–oxygen blenders are devices that mix medical air and oxygen into a gas source
ranging from 21% to 100% oxygen. They are precise and reliable, but not always readily
available in the operating room.
– In-line oxygen sampling can be utilized to provide a more controlled oxygen delivery
system. The connector of a 5.0 ETT can be attached to the Y- piece of a circuit, and the
nasal cannula or face mask can then be connected to it. The pop-off valve needs to be
closed completely and fresh gas flows (oxygen and air) can be adjusted accordingly. Be
careful not to deliver nitrous oxide.
– Adherent tape may be used to isolate the incision from the oxygen-enriched atmosphere.
• Maintain a low threshold to convert to general anesthesia if the patient cannot maintain an
oxygen saturation >92% with an FiO2 <30%, rather than just increasing the FiO2. An ETT
or supraglottic device will confine enriched oxygen to the breathing circuit and lungs of the
patient.
• Drapes should not be placed until all flammable preps have dried fully.
• Coating hair and facial hair with water-soluble surgical lubricating jelly renders the hair
nonflammable.
• Bipolar instead of monopolar electrocautery should be encouraged in high-risk surgeries.
Bipolar devices create little or no sparking and have not been recorded to start any surgical
fires.
• Procedures that enter the airway or involve oropharyngeal tissue. Fires may be reduced by:
– Placing moistened sponges around tissue and the endotracheal tube.
– Using a laser-proof ETT. Polyvinyl chloride tubes can be readily penetrated by a laser to
release oxygen within the lumen; additionally, they can burn in oxygen concentrations as
low as 25%. Thus, they are considered the least safe option (4)[C].
– Decreasing the FiO2 for 2 minutes prior to entering the airway and flushing air at 5–10
L/min to wash out excess oxygen.
– Encouraging surgeons to enter the airway with a scalpel instead of electrosurgery (5)[C].
– Avoiding nitrous oxide.
DIAGNOSIS
• Usually obvious with the presence of flames or smoke
• Unusual noise or feeling of warmth
TREATMENT
• In the event of a surgical fire:

– Remove burning material from the patient. Discontinue the flow of all airway gases.
– Have another member of the team extinguish the flame.
– Assess the patient’s injuries and treat as necessary.
– Control any bleeding.
– Evacuate the patient if there is danger from the smoke or fire.
– Use an aqueous solution to extinguish non-electrical fires.
However, the fluid resistance of surgical drapes may not allow water to reach the fire.
Use a CO2 fire extinguisher if needed.
– Never use a fire blanket as this will contain the fire on the patient.
• In the event of an airway fire (5)[C]:
– First remove the ETT or LMA.
– Turn off the oxygen or nitrous oxide.
– Remove the drapes.
– Pour saline into the airway to ensure that the fire is extinguished.
– Mask-ventilate the patient with air until all sources of fire are suppressed.
– Re-secure the patient’s airway.
– Inspect the patient for injuries and treat accordingly.
Rigid bronchoscopy should be performed after an airway fire.
FOLLOW-UP
• Once the fire has been extinguished, evaluate the extent of the fire damage. Discuss with the
surgeons whether or not to continue with the case. Each decision should be made based on
fire damage, urgency of the surgery, and patient stability.
• Maintain a very low threshold of leaving the patient intubated as smoke inhalation injury
may have occurred, but edema may be delayed.
• If the patient was awake when the fire erupted, he/she may recall the smell of the flames
and the resulting pain. Consider psychiatry consult, be empathetic, and explain the event.
• Consult the plastic surgeon for the management of skin and airway burns (4).
CLOSED CLAIMS DATA
• ASA currently has only task guidelines; however, there will soon be mandates that everyone
must follow.
• 17% of anesthetic malpractice claims are related to burns from surgical fires (4).
REFERENCES
1. Yardley IE, Donaldson LJ. Surgical fires, a clear and present danger. Surgeon. 2010;8:87–
92.
2. Orhan-Sungur M, Komatsu R, Sherman A, et al. Effect of nasal cannula oxygen
administration on oxygen concentration at facial and adjacent landmarks. Anaesthesia.
2009;64:521–526.
3. ECRI. New clinical guide to surgical fire prevention. 2009;314–329.
4. Nishiyama K, Makiko K, Kodaka M, et al. Crisis in the operating room: Fires, explosions
and electrical accidents. J Artif Organs. 2010;13(3):129–133.
5. American Society of Anesthesiologists Task Force on Operating Room Fires. Practice
advisory for the prevention and management of operating room fires. Anesthesiology.
2008;108(5):786–801.
ADDITIONAL READING
• Bhananker SM, Posner KL, Cheney FW, et al. Injury and liability associated with monitored
anesthesia care: A closed claims analysis. Anesthesiology. 2006;104:228–234.
• www.ecri.org
• Electrical safety
• Airway fires
• Thyroidectomy
• Cataract
• Burr hole
CLINICAL PEARLS
• The majority of surgical fires are preventable.
• Recognize which surgical procedures are high risk for operating room and airway fires
(tonsillectomy, tracheostomy, cataract, creation of burr hole, carotid endarterectomy).
• Vigilance is of utmost importance when caring for a patient undergoing a high-risk
procedure with a natural airway and open oxygen source. Minimizing or eliminating
enriched oxygen delivery is fundamental in preventing fires.
• Convert quickly to GA with a secured airway if the patient is not able to tolerate an FiO2
<30%.
• Consider the possibility of smoke inhalation injury that can result from thermal injury to the
airways, particulate irritation, and gaseous-related injury.
OXYGEN ANALYZERS ON ANESTHESIA MACHINES
BASICS
DESCRIPTION
• Modern anesthesia workstations include the anesthesia machine, a ventilator, vaporizers,
monitors, and alarms; together with the breathing and scavenging system, it constitutes the
anesthesia delivery system. To ensure adequate oxygen delivery, several safety mechanisms
are built into the system.
• The 2 largest manufacturers of anesthesia delivery systems in North America are Drager
Medical, Inc. (Telford, PA) and Datex-Ohmeda, a division of GE Healthcare (Madison, WI).
Despite differences between the 2 manufacturers, current guidelines mandate the following
oxygen safety systems:
– Multiple oxygen sources
– Oxygen supply and pressure alarms
– Inspired oxygen concentration monitor
– Hemoglobin oxygen saturation monitor (1,2)
• Multiple oxygen sources exist including a pipeline, cylinder, and auxiliary supply.
• Pipeline supply:
– The primary gas source for the anesthesia machine and provides oxygen (and other gases)
to the system at approximately 50 psig.
– Diameter-Indexed Safety System (DISS) is a specific and nationally standardized, gas-
specific, system that ensures appropriate connection of all supply pipelines to the
anesthesia machine. It prevents the wrong pipeline attachment and inadvertent delivery of
a hypoxic gas mixture.
• Cylinder supply:
– A backup supply in the event of depleted or malfunctioning pipeline supply
– Pin Index System (PIS) is a specific, nationally standardized, pin configuration on the
cylinder yoke that corresponds to the appropriate cylinder valve on the machine. It
prevents the wrong cylinder from being attached to the wrong valve and inadvertent
delivery of a hypoxic gas mixture.
• Auxiliary oxygen supply:
– Located on the anesthesia machine and can provide supplemental oxygen with a nasal
cannula, facemask, or Ambu bag; functions even if the anesthesia machine is off.
– There is no oxygen analyzer in this set-up, and a misconnection could result in a hypoxic
gas being delivered to the patient from this source.
• Preventing the delivery of a hypoxic gas mixture is a major consideration in the design of
anesthesia delivery systems. An adequate oxygen supply is ensured via several systems—the
fail-safe valve, the oxygen–nitrous oxide proportioning system, a pressure regulation and
threshold system, an oxygen concentration monitor, and an oxygen saturation monitor.
• Fail-safe valve:
– Located downstream from the nitrous oxide source. Depending on the manufacturer, it has
the ability to shut off or decrease the supply of nitrous oxide if oxygen pressure decreases.
An oxygen supply failure alarm is also activated. It should be noted that the fail-safe valve
operates according to oxygen pressure, not flow. A hypoxic gas can still be delivered if the
pressure is unchanged or if a system leak develops distal (downstream) to the fail-safe
valve.
– In Datex-Ohmeda systems, the fail-safe valve is a pressure sensor shut-off valve (PSSV)
that completely stops the flow of nitrous oxide and other gases when oxygen pressure falls
below a predetermined threshold of 20 psig.
– In Drager systems, the oxygen failure protection device (OFPD) proportionately decreases
the flow of other gases as oxygen pressure decreases until a threshold is reached after
which gas flow ceases.
• Oxygen–nitrous oxide proportioning system:
– Ensures that a minimum level of 25% oxygen is flowing when nitrous oxide is used. Since
this system is linked only to nitrous oxide, if other gases are used, a hypoxic mixture may
be given.
– In Datex-Ohmeda systems, the Link-25 Proportion Limiting Control System connects the
oxygen and nitrous oxide flow meters via a steel link chain such that as the flow of nitrous
oxide increases, so does the oxygen flow.
– In Drager systems, an Oxygen Ratio Monitor Controller (ORMC) limits the flow of nitrous
oxide with flow resistors and diaphragms according to the flow of oxygen.
• Pressure regulation and thresholds: These are designed such that oxygen is the last flow to
decrease should a machine failure occur.
• Inspired oxygen concentration monitor:
– Aids in detecting the delivery of a hypoxic gas mixture (1). It is the only device that
confirms the presence of oxygen in the inspired gas mixture.
– Depending upon the machine type and manufacturer, the inspired oxygen concentration is
measured by an oxygen sensor or analyzer:
An oxygen sensor is a galvanic fuel cell located near the inspiratory unidirectional valve.
A multi-gas analyzer incorporates a paramagnetic oxygen analyzer and samples gas near
the circuit Y-piece.
• Pulse oximetry
FIGURE 1. Diagram of a generic 2-gas anesthesia machine.
ANATOMY
• Gases enter the anesthesia system and flow through 3 pressure circuits: High, intermediate,
and low (3).
• High-pressure circuit: Consists of the gas cylinders and their primary pressure regulators
– E cylinders for oxygen and nitrous oxide are initially 2,200 and 745 psig, respectively, and
are downregulated to provide gases at approximately 45 psig.
• Intermediate pressure circuit: Consists of the regulated pipeline/cylinder supplies to the flow
control valves
– In most Datex-Ohmeda machines, a second stage regulator further decreases oxygen
pressure to a range of 12–19 psig and nitrous oxide to 26 psig.
• Low-pressure circuit: Consists of the flow control valves to the common gas outlet
– The oxygen flow meter is typically downstream of all other gases because in the event of a
flow meter leak, a hypoxic gas mixture is least likely (but not prevented) with this
configuration.
• Numerous situations can occur that may lead to an inadequate oxygen concentration. These
include:
– A hypoxic gas delivered from the oxygen pipeline or tank
– A disconnection of the fresh gas hose with use of a hanging bellows ventilator
– Oxygen flow control valve turned off
– Malfunction of the fail-safe system
– Failure of the nitrous oxide-oxygen proportioning system
– An oxygen leak in the low pressure system
– Use of inadequate oxygen flow rate with a closed circuit (4)
• While adverse outcomes related to gas delivery equipment are rare, the associated injuries
can be severe. In one review of claims between 1961 and 1994, gas delivery equipment
problems accounted for 2% of all equipment-related adverse events, 72 of 3,791 claims.
However, death or brain damage was the result in 76% of these claims (5).
Recommended Essential Steps in a Pre-Anesthesia Checkout Procedure. Feldman JM, Olympio MA, Martin D, Striker A.
New guidelines available for pre-anesthesia checkout. APSF Newsletter. 2008;23:6–7.
Recommended Essential Steps in a Pre-Anesthesia Checkout Procedure.

Feldman JM, Olympio MA, Martin D, Striker A. New guidelines available for pre-anesthesia checkout. APSF Newsletter.
2008;23:6–7.
• With improved monitoring devices and additional safeguards on modern systems, adverse
events have decreased. In a more recent review of claims the reported number and severity
of adverse events related to anesthesia gas delivery equipments decreased to 1% and 30%,
respectively (4).
• In order to ensure the proper function of the anesthesia delivery system and decrease the
risk for a serious adverse event, equipment checklists have been developed and modified
over the last several decades:
– The 1993 Food and Drug Administration (FDA) Anesthesia Apparatus Checkout
Recommendations (6). This checklist is most often used and contains 14 items that should
be completed prior to initial machine use and can be abbreviated between anesthetics (7).
– The 2008 Recommendations for Pre-Anesthesia Checkout Procedures (8). These are new
guidelines developed to address changes in anesthesia workstations and contain 15 items
applicable to all modern anesthesia systems. The initial machine check can also be
abbreviated between anesthetics (8).
• Regardless of which list is used, the most important preoperative checks are: Oxygen
analyzer calibration, low-pressure circuit leak test, and circle system test.
• Oxygen analyzer calibration:
– One of the more important monitors on the anesthesia machine because it is the only
device that evaluates the function of the low-pressure circuit and detects problems
downstream of the flow meters.
– It should read 21% with room air and 90% or greater when the system is flushed with
oxygen.
– The low oxygen concentration alarm should be enabled.
• Low-pressure circuit leak test:
– A test for leaks is essential to ensure system integrity because the components in the low-
pressure circuit are quite susceptible to breakage and leaks, and the low-pressure circuit is
downstream from all safety devices except the oxygen analyzer.
– Methods for testing the low-pressure circuit vary between manufacturers.
– In general, the presence or absence of a check valve near the common gas outlet greatly
influences which method is used.
Most Datex-Ohmeda systems have this check valve and are tested with a negative-
pressure leak test using a suction bulb.
Drager machines do not have a check valve and are tested with a positive-pressure leak
test with flow from the anesthesia machine or a bulb.
• Circle system test:
– This test evaluates the integrity of the breathing circuit and the unidirectional valves from
the common gas outlet.
– Occluding the Y-piece, closing the APL valve then pressurizing and holding the system to
30 cm H2O tests for circuit leaks. Inhaling and exhaling into the appropriate circuit limbs
test the function of the unidirectional valves.
REFERENCES
1. Standard Specification for Particular Requirements for Anesthesia Workstations and their
Components ASTM F1850-2005.
2. West Conshohocken, PA: American Society for Testing and Materials, 2005.
3. tandards for Basic Anesthetic Monitoring. Park Ridge, IL: American Society of
Anesthesiologists, 2010.
4. Check-Out: A Guide for Preoperative Inspection of an Anesthesia Machine. Park Ridge, IL:
American Society of Anesthesiologists, Inc., 1987.
5. Eisenkraft JB. Hazards of the anesthesia workstation. ASA Refresh Course Anesthesiol.
2009;37(1):37–55.
6. aplan RA, Vistica MF, Posner KL, et al. Adverse anesthetic outcomes arising from gas
delivery equipment: A closed claims analysis. Anesthesiology. 1997;87:741–748.
7. Anesthesia Apparatus Checkout Recommendations. Rockville, MD: US Food and Drug
Administration, 1993.Brockwell RC, Andrews JJ. Understanding your anesthesia
workstation. ASA Refresh Course Anesthesiol. 2007;35(1):15–29.
8. Feldman JM, Olympio MA, Martin D, et al. New guidelines available for pre-anesthesia
checkout. APSF Newsletter. 2008;23:6–7.
ADDITIONAL READING
• Eisenkraft JB. Anesthesia machine basics. Semin Anesth Perioperative Med Pain.
2005;24:138–146.
CLINICAL PEARLS
• Differences exist between manufacturers and models; therefore, it is essential to be aware of
the function of the particular anesthesia system in use, including its alarms and safety
features.
• An anesthesia system pre-use checklist should be completed prior to the use of the
anesthesia machine and between anesthetics as necessary. Though equipment checklists are
helpful, it is important to remember that they are recommendations and may not contain
specific instructions for all anesthesia machines. Anesthesia providers should refer to system
manuals for design-specific features.
• Backup sources for oxygen and emergency airway equipment must be immediately available
should a machine failure occur.
OXYGEN TOXICITY
Julie Marshall, MD
BASICS
DESCRIPTION
• Oxygen toxicity can result from exposure to high concentrations of inhaled oxygen and is
also known as oxygen toxicity syndrome, oxygen poisoning, or oxygen intoxication. It can
result from either:
– Full body immersion in high oxygen concentration conditions (e.g., hyperbaric chambers)
– Inhalation exposure (e.g., mechanical ventilation, prematurity)
• High blood partial pressures of oxygen can result in the generation of free radicals that
interrupt cellular processes and damage tissue components such as the lungs, central
nervous system, and eye.
• Oxygen is an “oxidizing” agent and accepts electrons transferred from other compounds; in
doing so, it is “reduced.” This occurs most commonly in the electron transport chain, which
couples electron transfer from NADH to oxygen and generates ATP across the mitochondrial
membrane.
• “Reduced” oxygen forms reactive oxygen species (ROS) that are natural byproducts of
oxygen metabolism (i.e., electron binding). Other metabolic pathways that contribute to the
formation of ROS include oxidative–reductive processes: Cytochrome P450 activity, nitric
oxide synthases, and inflammatory pathways.
• ROS play an important role in cell signaling, via a process called oxidative signaling. For
example:
– Iron uptake occurs via anion exchange protein 2 and is dependent on superoxide anion
(O2-).
– Hydrogen peroxide modifies cellular function and response to insults.
– Platelet recruitment
– Apoptosis
• ROS are normally buffered by endogenous antioxidants such as superoxide dismutase,
catalases, and glutathione peroxidases. Other in vitro antioxidants include Vitamins E and C
and uric acid.
ANATOMY
• The mitochondria generate most of the ROS in cells as a result of the oxidative–reductive
process.
• Free radicals may also be generated at other locations in the cell, such as the plasma
membrane and cytoplasmic enzyme systems.
• Oxygen reduction and the formation of ROS is a normal physiologic function. However,
exposure to high concentrations of inspired oxygen can result in excessive production of
ROS and overwhelm the native antioxidant supply.
• The remaining active free radicals can react with components of the cell, causing cellular
damage or dysfunction. Injury to proteins, lipids, or nucleic acids may cause cell death or
dysfunction. ROS may also:
– Create additional free radical compounds in cells, activating pro-death signals in cells
– Inactivate nitric oxide reactions involved in vascular and bronchial responsiveness
• Lung damage. The time to clinical emergence is inversely proportional to the FiO2
concentration (higher concentrations contribute to lung pathology at a faster rate)
– Acute tracheobronchitis
Can occur after 4–24 hours of 95% FiO2 at normal atmospheric pressure; may occur in 3
hours at 3 atmospheres of pressure.
May see cough with substernal pain or a burning sensation in the chest
Reduction of tracheal mucociliary transport with erythema and swelling of the bronchial
lining.
Symptoms decrease a few hours after terminating oxygen therapy.
Complete resolution of symptoms occurs within days.
– Diffuse alveolar damage
Usually takes >48 hours of oxygen therapy to develop
Similar clinical picture to acute respiratory distress syndrome (ARDS), including reduced
pulmonary compliance, increased P(A–a)O2 gradient, decreased vital capacity, and
decreased carbon dioxide diffusion
– Pulmonary fibrosis may occur after prolonged ventilation.
– Bronchopulmonary dysplasia (BPD)
Thought to be caused by direct damage to pulmonary epithelium by ROS
The chance of developing bronchopulmonary dysplasia may be increased in premature
infants exposed to high oxygen environments.
ROS may further impair the development of the premature lung. This may be due to
impairment of nitric oxide signaling involved in lung maturation.
• Central nervous system toxicity may occur above normal atmospheric pressures, either
underwater or in hyperbaric chambers.
– Early manifestations include twitching of perioral and hand muscles, as well as cogwheel
breathing from diaphragmatic twitching.
– Further exposure may lead to vertigo, nausea, behavioral changes, and generalized tonic–
clonic seizures.
• Eye
– Retinopathy of prematurity (ROP)
The second most common cause of blindness in children in the US.
Premature infants <30 weeks postconceptual age or <1,500 g are at higher risk.
ROP is a multifactorial condition; however, hyperoxia plays an important role in
development of this condition.
Initially, the high oxygen concentration halts growth of vessels in the eye by suppressing
vascular endothelial growth factor (VEGF).
As the eye grows, the retina outgrows the blood supply, and the retinal tissues become
hypoxic. Abnormal vascular growth occurs in response, eventually leading to vision
impairment or blindness.
– Reversible myopia
Direct oxygen contact with the lens (as in a hyperbaric chamber) can cause local toxic
effects on the lens.
May also occur, to a lesser extent, from inhalation of high oxygen concentrations.
– Cataract formation may occur after repeated hyperbaric oxygen therapies.
• While there is animal data and theoretical concern that high intraoperative FiO2
concentrations may cause lung injury, there is no strong clinical evidence this occurs with
routine intraoperative procedures (1)[C].
• Addition of PEEP may improve oxygenation without increasing FiO2 concentrations.
• Patients coming from intensive care units on mechanical ventilation may have lung changes
from oxygen toxicity. This may make intraoperative oxygenation and ventilation more
challenging. In severe cases of diffuse alveolar damage, using the patient’s intensive care
unit ventilator may be advisable.
• In patients being treated in the intensive care unit, decreasing FiO2 concentrations may lead
to lower mortality rates (2)[B].
– Reperfusion injury may occur after cardiopulmonary bypass when the ischemic heart is
exposed to high oxygen concentrations.
– Exposure of the ischemic heart to hyperoxic conditions may generate oxygen-free radicals
and lead to myocardial damage.
– Normal oxygen tensions after cardiopulmonary bypass may decrease oxidative myocardial
damage (3)[A].
• Bleomycin
Risk factors associated with developing lung damage:
Pre-existing lung injury from bleomycin
Exposure to bleomycin in the last 2 months (4)[C]
– If the clinical situation allows, consider administering a low FiO2 (<30%) for anesthesia
or intensive care unit ventilation.
– There are reports of ARDS following general anesthesia in patients who have a history of
bleomycin exposure; however, there is variable evidence for this association in reports (4)
[C].
• Amiodarone
– It is proposed that exposure to high levels of oxygen therapy and resultant ROS generation
may contribute to amiodarone-induced lung injury.
– As with bleomycin, exposure to high oxygen concentrations should be avoided if clinically
possible.
– Limit oxygen concentration to patients <32 weeks postconceptrual age.
– Consider accepting lower SpO2 levels to limit hyperoxia for premature infants (5)[A].
Equations
• PAO2 = PiO2 – (PaCO2/R); where PAO2 is the partial pressure of oxygen in the alveoli, PiO2
is partial pressure of inhaled gas, PaCO2 is the partial pressure of carbon dioxide in the
artery, and R is the respiratory coefficient (normally 0.8).
• Alveolar–arterial gradient: PAO2 – PaO2; where PAO2 is the partial pressure of oxygen in the
alveoli, and PaO2 is the partial pressure of oxygen in the artery.
REFERENCES
1. night PR, Holm BA. Three components of hyperoxia. Anesthesiology. 2000;93(1):3–4.
2. De Jonge E, Peelen L, Kijzers PJ, et al. Association between administered oxygen, arterial
partial oxygen pressure and mortality in mechanically ventilated intensive care unit
patients. Crit Care. 2008;12(6):R156.
3. hnken K, Winkler A, Schlensak C, et al. Normoxic cardiopulmonary bypass reduces
oxidative myocardial damage and nitric oxide during cardiac operations in the adult. J
Thorac Cardiovasc Surg. 1998;116(2):327–334.
4. Mathes DD. Bleomycin and hyperoxia exposure in the operating room. Anesth Analg.
1995;81:624–629.
5. Chen ML, Guo L, Smith LEH, et al. High or low oxygen saturation and severe retinopathy of
prematurity: A meta-analysis. Pediatrics. 2010;125(6):1483–1492.
6. Auten RL, Davis JM. Oxygen toxicity and reactive oxygen species: The devil is in the
details. Pediatr Res. 2009;66(2):121–127.
7. Bitterman H. Bench-to bedside review: Oxygen as a drug. Crit Care. 2009;13:205.
• Donaldson L, Grant IS, Naysmith MR, et al. Acute amiodarone-induced lung toxicity.
Intensive Care Med. 1998;24(6):626–630.
• Jackson RM. Pulmonary oxygen toxicity. Chest. 1985;88(6):900–905.
• Patel DN, Goel A, Agarwal SB, et al. Oxygen toxicity. J Indian Acad Clin Med.
2003;4(3):234–237.
• Waid-Jones MI, Coursin DB. Perioperative considerations for patients treated with
bleomycin. Chest. 1991;99(4):993–999.
CODES
ICD9
987.8 Toxic effect of other specified gases, fumes, or vapors
ICD10
• T41.5X4A Poisoning by therapeutic gases, undetermined, init encntr
• T41.5X4D Poisoning by therapeutic gases, undetermined, subs encntr
• T41.5X4S Poisoning by therapeutic gases, undetermined, sequela
CLINICAL PEARLS
• Clinical signs of pulmonary toxicity are rarely seen with a routine general anesthetic.
• In the intensive care unit, attempts should be made to limit prolonged periods of hyperoxia
in order to reduce the chance for pulmonary damage. Alternative ventilation techniques or
application of PEEP may assist in minimizing the exposure to high oxygen concentrations.
• Keep FiO2 low for premature infants if clinical situation allows, in order to minimize the
contribution to retinopathy of prematurity and bronchopulmonary dysplasia.
• The clinical concerns with hyperbaric oxygen therapy include central nervous system
toxicity, pulmonary toxicity, reversible myopia, and cataract formation.
• If clinically possible, avoid exposing a patient with a history of bleomycin or amiodarone
therapy to high oxygen level concentrations.
PACEMAKER DEPENDENT
Peter M. Schulman, MD
Marc A. Rozner, PhD, MD
BASICS
DESCRIPTION
• No universally established definition (1). Pacing dependence can occur in a patient with a
conventional pacemaker (PPM) or an implanted cardioverter-defibrillator (ICD).
• Indications for pacing (whether a conventional PPM or ICD) include either a slow or
inadequate intrinsic rate or the need for profound beta blockade:
– Slow or inadequate HR: Sinus node disease, atrioventricular node disease,
neurocardiogenic syncope, long QT syndrome
– Beta blockade: Tachycardia syndromes, hypertrophic obstructive cardiomyopathy
• Indications for biventricular pacing (cardiac resynchronization therapy (CRT)) include
cardiomyopathy with a left ventricular ejection fraction ≤35% (2)
• Absolute Pacing Dependency (PD) is defined as an absence of intrinsic heart rhythm
(asystole) following cessation of ventricular pacing
• Functional Pacing Dependency is defined as symptoms resulting from inadequate intrinsic
heart rhythm following cessation of ventricular pacing or failure to pace both ventricles
correctly in a patient with cardiac resynchronization therapy (CRT)
• Preoperatively, the patient with a cardiac implantable electronic device (CIED) will likely
require additional information gathering and care to determine current programmed
parameters, especially pacing mode and rate. The identification of pacing dependence will
alert the perioperative team to the high risk of hemodynamic embarrassment, serious injury,
or death from device malfunction or failure. Care should be directed toward minimizing the
chance of perioperative electromagnetic interference (EMI), as it can interfere with CIED
function, possibly resulting in ventricular over-sensing and pacing inhibition.
EPIDEMIOLOGY
Prevalence
• Variable and dependent on definition and testing technique used (1)
• Increasing yearly in the general population; the adjusted implantation incidence of
permanent PPMs has increased 2.7-fold over 30 years (3)
• Patients with high-grade AV block (AVB) have a higher incidence of PD than patients with
sinus node disease (SND) (4). In older studies, the incidence of PD was 24–50% in AVB and
6–12% in SND. In more recent studies with different diagnostic criteria the incidence was
much less (1).
• In a recent study, the annual rate of new onset PD in PPM patients was 1.6% (4)
• Following cardiac surgery 1–3% of patients need PPMs of which many develop PD (1)
Prevalence
• In PPM patients, the reported prevalence of PD is highly variable with a historical published
range from 5–30%
• In one recent study, 2.1% of PPM patients were PD, and patients with AV block had a higher
prevalence than patients with sick sinus syndrome or atrial fibrillation (AF) (5)
Morbidity
• Impossible to quantify, however, PD might confer increased morbidity (6)
• Risk of significant symptoms following an abrupt cessation of pacing, such as profound
ventricular bradycardia, hypotension, syncope, inadequate perfusion, death.
Mortality
• Impossible to quantify
• Possible association between PD and cardiovascular as well as overall mortality (5,7)
• Risk of cardiac arrest following an abrupt cessation of pacing
• Sinus node disease (can include PD)
• Advanced heart block (can include PD)
• AV node ablation for treatment of drug refractory AF (almost always PD)
• Neurocardiogenic syncope (rarely PD)
• Cardiac surgery (can include PD)
• Previous myocardial infarction (MI) (can include PD)
• Temporary pacing prior to permanent pacemaker implant (can include PD)
• Pacing systems are comprised of a pulse generator and leads. The pulse generator houses the
battery and electronic/computer equipment; it is most frequently implanted in the pre-
pectoral fascia just inferior to the clavicle. Most current systems employ transvenously
placed leads which contact the endocardium. The same electrodes are used to sense intrinsic
electrical impulses from the heart as well as deliver an electrical stimulus to depolarize the
myocardium in the appropriate chamber. The atrial lead is positioned with its tip in the
right atrial appendage. The right ventricular lead is positioned with its tip in the right
ventricular apex or outflow tract. For biventricular pacing (CRT), a third lead is placed in
the coronary sinus to pace the left ventricle. Sometimes, this lead is placed on the
epicardium.
• Basic settings include:
– Pacing mode; denoted by position (8)
1st position: Chamber(s) paced
2nd position: Chamber(s) sensed
3rd position: The response to sensing
4th position: The presence or absence of rate modulation programming
5th position: Multisite pacing, if present
– Lower rate
– Upper tracking rate (for dual-chamber (DDD) pacing)
– Upper sensor rate (for rate modulation)
– AV delay
• Demand mode. Refers to pacing without regard to the underlying rhythm. It is not available
in an ICD unless shock therapy is disabled. Examples include:
– AOO: Asynchronous atrial only pacing
– VOO: Asynchronous ventricular only pacing
– DOO: Asynchronous AV sequential pacing
• Rate modulation. Describes the ability to detect exercise and increase the pacing rate
(present in all new devices). Various sensors include both mechanical and electronic
elements. Knowledge of sensor type and settings can prevent inappropriate treatment and
patient injury when iatrogenic sensor stimulation from skin preparation or electrical
interference might increase the paced heart rate in the perioperative period (9).
• AV sequential pacing (DDD mode, also called p-wave synchronous ventricular pacing)
represents the most common pacing mode in the US. It preserves AV synchrony, avoiding
atrial contraction against a closed AV valve, which can create vertigo or pulsating
symptoms called pacemaker syndrome.
• Battery depletion can result in pacing system failure and failure to deliver high voltage
therapy for an ICD. Low battery voltage also puts the device at-risk for EMI-induced reset.
Pacing mode changes are designed to limit batter current drain; some CIEDs convert from
dual chamber to single chamber pacing when elective replacement battery voltage is
detected.
• Outright lead detachment is rare after the first 6 weeks of implant. However, lead tip
fibrosis resulting in sensing or pacing threshold issues and lead fracture or insulation failure
remain important long-term issues.
• Reprogramming to an asynchronous mode can prevent inappropriate pacing inhibition from
EMI. For PPM (but not for ICD), most generators will respond to the placement of a magnet
by converting to asynchronous pacing at a manufacturer-specific rate that identifies battery
performance. Placing a magnet over an ICD usually suspends or disables anti-tachycardia
detection or therapy, but rarely alters pacing (only ICDs from Sorin Corporation change
pacing rate, but not mode, when exposed to a properly placed magnet). ICD patients
requiring asynchronous pacing will therefore always require formal device reprogramming.
Note that many CIEDs can have their magnet switch programmed off.
• Minimizing intraoperative EMI:
– Bipolar electrocautery should be used if possible
– Short, intermittent bursts of electrocautery should be used at the lowest possible energy
• The electrosurgery current-return (“grounding”) pad should be positioned so that the
electrosurgery current path does not cross the chest or pacer system (6)[C].
• Testing for PD is performed by the cardiology/pacemaker team during each regular device
follow up. Various testing protocols exist that establish the presence of an inadequate or
absent intrinsic rhythm at a low pacing rate. Testing is done by temporarily programming a
low ventricular base rate (30–40 bpm) and assessing for the presence or absence of an
underlying rhythm and/or the onset of associated symptoms.
• According to the Heart Rhythm Society (HRS)/American Society of Anesthesiologists (ASA)
Consensus statement (10), CIED clinic records should be obtained for every patient prior to
any elective case to reduce or eliminate confusion regarding CIED function, and the
patient’s CIED physician should be contacted. In the absence of records, the HRS/ASA
statement suggests a preoperative interrogation to ensure appropriate device function and
programming with respect to the upcoming procedure. Some parameters (such as a reduced
pacing rate for nighttime or a long AV delay) might need to be changed for an operative
procedure, especially if large blood loss or fluid shifts are expected. In general, patient
reports should not be trusted; many report a pacemaker check after only a simple 12 lead
electrocardiographic evaluation and patients rarely understand or are informed about CIED
or lead alerts.
TREATMENT
Temporary pacing modalities in the perioperative period may be used to stabilize a patient
with urgent or emergent pacing indications: transesophageal, transcutaneous, and
transvenous pacing. Esophageal pacing (EP) utilizes a specially constructed esophageal
stethoscope with two stainless steel rings, designed to stimulate the left atrium. EP requires
intact atrial and AV nodal function; thus it is absolutely contraindicated in the presence of AF
or flutter, as well as significant AV nodal disease. Transcutaneous pacing utilizes 2 cutaneous
pads with pacing achieved via an external defibrillator. Transvenous pacing is achieved by
placing a temporary pacing wire through a central vein so that its tip lies in the right
ventricle. It is more reliable and can therefore be used for a longer duration than EP or
transcutaneous pacing.
FOLLOW-UP
• PPM patients should have a comprehensive device interrogation at least annually. ICD
patients should undergo a comprehensive device interrogation every 3–6 months, and CRT
patients should be checked every 3 months. For some low risk, non PD patients with the
latest generators, telephone interrogations can replace office visits.
• Postoperatively, care must be taken to ensure that a CIED continues to function
appropriately. CIEDs exposed to EMI, especially if pacing inhibition was observed or blood
transfused, should be checked. The HRS/ASA states that for any high-risk patient, or where
preoperative or intraoperative programming was performed, or where a question arose
about pacing or ICD function, that a postoperative check should be performed prior to
discharge from a monitored environment. For a low-risk patient, a CIED could be checked in
an ambulatory clinic after patient discharge from the PACU. The site of the postoperative
check should be established during the preoperative process, since the patient’s CIED
physician should be involved in the perioperative planning.
CLOSED CLAIMS DATA
Analyses of pacing systems show failures at multiple levels. The 1990–2002 FDA Data
Analysis (11) showed that there were 2.25 million PPMs and 415,780 ICDs implanted in US.
The annual malfunction replacement rate for PPMs was 4.6 per 1,000 implants and 20.7 per
1,000 implants for ICDs. 61 deaths were attributed to generator malfunction. Mechanical
problems with device leads were common; the reported failure rate of ICD leads at 8 years
was 28–40% (1).
REFERENCES
1. orantzopoulos P, Letsas P, Grekas G, et al. Pacemaker dependency after implantation of
electrophysiological devices. Europace. 2009;11:1151–1155.
2. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator
for congestive heart failure. N Engl J Med. 2005;352:225–237.
3. Uslan DZ, Tleyjeh IM, Baddour LM, et al. Temporal trends in permanent pacemaker
implantation: A population-based study. Am Heart J. 2008;155: 896–903.
4. Nagatomo T, Abe H, Kikuchi K, et al. New onset of pacemaker dependency after permanent
pacemaker implantation. Pacing Clin Electrophysiol. 2004;27:475–479.
5. Lelakowski J, Majewski J, Bednarek J, et al. Pacemaker dependency after pacemaker
implantation. Cardiol J. 2007;14:83–86.
6. American Society of Anesthesiologists. Practice advisory for the perioperative management
of patients with cardiac implantable electronic devices: Pacemakers and implantable
cardioverter-defibrillators: An updated report by the American society of anesthesiologists
task force on perioperative management of patients with cardiac implantable electronic
devices. Anesthesiology. 2011;114:247–261.
7. Tang AS, Roberts RS, Kerr C, et al. Relationship between pacemaker dependency and the
effect of pacing mode on cardiovascular outcomes. Circulation. 2001;103:3081–3085.
8. Bernstein AD, Daubert JC, Fletcher RD, et al. The revised NASPE/BPEG generic code for
antibradycardia, adaptive-rate, and multisite pacing. North American Society of Pacing and
Electrophysiology/British Pacing and Electrophysiology Group. Pacing Clin Electrophysiol.
2002;25:260–264.
9. Lau W, Corcoran SJ, Mond HG. Pacemaker tachycardia in a minute ventilation rate-
adaptive pacemaker induced by electrocardiographic monitoring. Pacing Clin
Electrophysiol. 2006;29:438–440.
10. Crossley GH, Poole JE, Rozner MA, et al. The Heart Rhythm Society (HRS)/American
Society of Anesthesiologists (ASA) Expert Consensus Statement on the Perioperative
Management of Patients with Implantable Defibrillators, Pacemakers and Arrhythmia
Monitors: Facilities and Patient Management This document was developed as a joint
project with the American Society of Anesthesiologists (ASA), and in collaboration with the
American Heart Association (AHA), and the Society of Thoracic Surgeons (STS). Heart
Rhythm. 2011;8:1114–1154.
11. Maisel WH, Moynahan M, Zuckerman BD, et al. Pacemaker and ICD generator
malfunctions: analysis of Food and Drug Administration annual reports. JAMA.
2006;295:1901–1906.
12. Maisel WH, Hauser RG, Hammill SC, et al. Recommendations from the Heart Rhythm
Society Task Force on Lead Performance Policies and Guidelines Developed in
collaboration with the American College of Cardiology (ACC) and the American Heart
Association (AHA). Heart Rhythm. 2009;6:869–885.
ADDITIONAL READING
• Moses HW, Mullin JC. A Practical Guide To Cardiac Pacing. 6th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2007.
• Cardiac Pacemaker Cells
• Bradycardia
• Hypertrophic Cardiomyopathy
CODES
ICD9
• V45.01 Cardiac pacemaker in situ
• V45.02 Automatic implantable cardiac defibrillator in situ
ICD10
• Z95.0 Presence of cardiac pacemaker
• Z95.810 Presence of automatic (implantable) cardiac defibrillator
CLINICAL PEARLS
• PD patients are at high risk for serious injury or death in the event of pacing system
malfunction.
• Perioperative pacing system malfunction from EMI and other factors is difficult to predict
and occurs commonly.
• A key preoperative consideration is establishing the presence or absence of PD in PPM
patients if EMI is likely to be present. When EMI is likely (such as intraoperative monopolar
electrosurgery), PD patients might require reprogramming to an asynchronous pacing mode
or application of temporary pacing modalities.
PANCREATIC TRANSPLANTATION
Catherine Ifune, MD, PhD
BASICS
DESCRIPTION
General
• Transplantation of the pancreas is the surgical treatment for insulin dependent diabetes
mellitus. It can be performed
– Simultaneously with a kidney transplant (Simultaneous Pancreas-Kidney, SPK); most
commonly performed. Indicated in diabetic patients with imminent or established end-
stage renal disease (ESRD).
– Following a kidney transplant (Pancreas After Kidney, PAK). May be indicated in diabetic
patients who have received a renal transplant.
– Alone (Pancreas Transplant Alone, PTA); rarely performed. Indicated for severe metabolic
complications of diabetes, intolerance to exogenous insulin therapy, and failure of insulin
therapy to prevent acute complications.
• Preparation of the graft includes removing the recipient’s spleen and mobilizing the portal
vein. This is followed by reconstructing the donor’s superior mesenteric and splenic arteries
to form a Y graft using the donor iliac artery bifurcation.
• Arterial anastomosis is to the recipient’s iliac artery and the venous anastomosis is either to
the recipient’s iliac vein (systemic drainage, technically easier) or portal vein (portal
drainage, more physiologic since insulin undergoes first pass metabolism in the liver,
avoiding hyperinsulinemia).
• Drainage of exocrine secretion is by anastomosing the donor’s duodenal segment to either
the recipient’s bladder (bladder drainage, BD) or small bowel (enteric drainage, ED). BD is
used more frequently in PTA to monitor urine amylase levels as an indicator for rejection.
ED is used more frequently for SPK.
• Exclusion criteria include:
– Insufficient cardiac reserve
– Age >65 years
– Obesity (>50% ideal body weight)
– Malignancy
– Active infection
– Ongoing drug or alcohol abuse
– History of non-compliance
– Psychological instability
• An evolving, less invasive treatment for insulin dependent diabetes mellitus is percutaneous
islet cell transplantation into the portal vein; however, the risk of immunosuppression may
not justify the current outcome benefit. On the other hand, autografts of islet cells after
pancreatic resection for pancreatitis maintains normoglycemia for several years;
additionally, no immunosuppression is necessary.
Position
• Supine, with arms abducted <90°
• Protect dialysis access site
Incision
• Transperitoneal midline incision
• Sometimes 2 separate lower quadrant incisions for SPK
Approximate Time
3–8 hours if combined transplant
EBL Expected
250–500 mL
Hospital Stay
Intensive care unit for 24–48 hours
Major abdominal surgery equipment
EPIDEMIOLOGY
Incidence
1,500–1,800 per year worldwide
Prevalence
30,000 pancreatic transplants performed worldwide from 1966–2008
Morbidity
• Immediate surgical complications 13%
• Graft rejection 5–25%, peaks between 3 and 12 months post-transplant
Mortality
Patient survival of >90% at 3 years and 67% at 10 years.
• Maintain adequate graft perfusion by optimizing volume status and perfusion pressure.
• Maintain euglycemia
SYMPTOMS
• Hyperglycemia: Polyuria, polydipsia, weight loss, nausea, vomiting, and abdominal pain if
ketoacidotic
• Hypoglycemia: Sweating, anxiety, tremor, CNS symptoms including seizures or loss of
consciousness
• In chronic diabetics, symptoms of end-organ involvement need to be assessed
History
• Diabetes mellitus, mostly Type I; Type II in 6–7%
• Rarely, total pancreatectomy
• Renal failure; assess hemodialysis duration, schedule, complications (hyperkalemia,
hypotension)
Signs/Physical Exam
• Airway exam
• Assessment of volume status and of veins for peripheral IV placement.
• Assessment of AV fistula or dialysis access site.
MEDICATIONS
• Insulin
• Treatment for end-organ impairment
Labs/Studies
• CBC
• Basic metabolic panel
• Type and cross match blood
• Screening for ischemic heart disease: EKG, stress test, coronary angiography, if necessary.
• Macrovascular complications of diabetes
– Coronary artery disease
– Peripheral vascular disease
– Stroke
• Microvascular complications of diabetes
– Diabetic nephropathy
– Neuropathy
– Retinopathy
• Autonomic neuropathy, gastroparesis
• Anemia
TREATMENT
Premedications
• Consider aspiration prophylaxis
• Continue cardioprotective medications
• Invasive monitoring lines
• Postoperative ventilatory support
• Second generation cephalosporin. Repeat dosing may be necessary.
• Antifungal usually started postoperatively
INTRAOPERATIVE CARE
• Postoperative systemic heparinization contraindicates epidural catheter placement for
postoperative pain management.
Monitors
• Arterial line prior to induction if significant cardiac disease or autonomic dysfunction (avoid
site of AV fistula)
• One large bore peripheral IV
• Central venous catheter placement for volume status monitoring, infusion of antithymocyte
globulin, possible vasoactive infusion and postoperative hyperalimentation.
• Foley catheter
• Nasogastric tube
• Mechanical DVT prophylaxis
• GERD and gastroparesis are common. Consider a RSI. IV access is generally preferred in
older children/adolescent patients meeting “full stomach” criteria.
• Potential for difficult airway due to glycosylation of joints (stiff-joint syndrome) affecting
temporomandibular and atlanto-occipital joints.
Maintenance
• Balanced technique with muscle relaxation.
• Avoid nitrous oxide. Consider the use of atracurium or cisatracurium for muscle relaxation.
Use narcotics with limited active metabolites such as hydromorphone.
• Start immunosuppressive therapy after induction of anesthesia. Most transplant centers use
induction therapy with a single high dose of corticosteroids followed by alemtuzumab or an
infusion of antithymocyte globulin intraoperatively. Of note, the antithymocyte globulin can
cause hypotension and in some cases the infusion rate must be reduced to maintain
adequate BP.
• Hemodynamics
– Maintain an elevated central venous pressure (CVP) (12–14 mm Hg) and systolic BP
(around 140 mm Hg) with fluid administration, and inotropes if necessary.
– Goal is optimal perfusion of the transplanted organs. This is balanced by the need to avoid
graft and bowel edema which can complicate the pancreas transplant as well as
abdominal closure at the end of the case.
– Expect hypotension and acidosis at reperfusion and prepare to promptly optimize
hemodynamics, to maintain graft blood flow.
• Correct acid-base status and normalize electrolytes
• Consider mannitol for free radical scavenging before reperfusion.
• Glycemic control
– Check blood glucose every hour initially and every half-hour post reperfusion.
– An insulin infusion may be used to keep blood sugars between 100 and 200 mg/dL. Tight
glycemic control enhances graft survival by decreasing metabolic demand on islet cells
until reperfusion injury has resolved.
– Octreotide is a somatostatin analogue which reduces gastrointestinal, biliary, and
pancreatic secretions and may also be used to transiently rest islet cells.
– Continuous D5W infusion to provide intracellular nutrition and decrease free fatty acid
production avoiding the potential for adverse cardiac events.
• Maintain normothermia.
• Fully awake, following standard criteria
• Avoid hypertension
POSTOPERATIVE CARE
BED ACUITY
• Surgical intensive care unit. Careful monitoring of volume status, hemodynamics,
electrolytes and glucose.
• Monitor for bicarbonate loss in BD.
• Immunosuppression: Maintenance therapy is started postoperatively with a calcineurin
inhibitor (usually tacrolimus), mycophenolate mofetil, and corticosteroids. Studies have
shown that this triad provides excellent graft survival of 86% at 1 year and 53% at 10 years.
ANALGESIA
Moderate pain is consistent with abdominal surgery. Usually IV opioid PCA is used.
COMPLICATIONS
• Assess for postoperative cardiac dysfunction
• Surgical
– Technical failure due to decreased vascularity of the pancreas
– Thrombosis requires graft removal; seen in 6% of cases. Routine postoperative
antithrombotic prophylaxis may decrease the incidence.
– Infection 2–3%
– Pancreatitis 2–3%. Early presentation is possibly from ischemia reperfusion injury;
whereas late presentation can be from urinary reflux into the graft if BD. Treatment
consists of supportive measures.
– Bleeding <1%
• Acute rejection can occur after 7 days. Heavy immunosuppression is necessary.
PROGNOSIS
• Improved life expectancy. At 5 years, diabetics on dialysis have a survival of 30–40% versus
78% after kidney transplant and 82% after SPK.
• Improved quality of life
• Improved renal graft function
• Regression of atherosclerosis with reduced rates of MI and acute pulmonary edema
• Arrested deterioration of retinopathy
• Rejection occurs for both organs simultaneously and is monitored by creatinine levels
REFERENCES
1. Larson-Wadd K, Belani KG. Pancreas and islet cell transplantation. Anesthesiology Clinics
of North America. 2004;22:663–674.
2. Koehntop DE, Beebe DS, Belani KG. Perioperative anesthetic management of the kidney-
pancreas transplant recipient. Current opinion in Anesthesiology. 2000;13:341–347.
3. Gruessner AC, Sutherland DER, Gruessner RWG. Pancreas transplantation in the United
States: A review. Current Opinion in Organ Transplantation. 2010;15:93–101.
4. American Diabetes Association. Pancreas and Islet Transplantation in Type I Diabetes.
Diabetes Care. 2006;29(4):935.
5. White SA, Shaw JA, Sutherland DER. Pancreas transplantation. Lancet. 2009;373:1808–
1817.
ADDITIONAL READING
• Beebe DS, Kendall DM, Gruessner RWG, et al. Pancreas transplantation. In: Anesthesia and
transplantation. Sharpe MD, Gelb AW, eds. Boston: Butterworth-Heinmann; 1999:217–240.
• Heilman RL, Mazur MJ, Reddy KS. Immunosup-pression in simultaneous pancreas-kidney
transplantation. Drugs. 2010;70(7):793–804.
• Renal Transplantation
• Diabetes Mellitus
• Hyperglycemia
CLINICAL PEARLS
• Check immunosuppression regimen and start immunosuppressive therapy soon after
induction of anesthesia.
• Prepare for tight blood glucose control intraoperatively.
• Careful fluid and hemodynamic management to optimize perfusion of the transplanted
organs
• Anticipate and treat hemodynamic changes at reperfusion
PAO2
Matthew Ellison, MD
Erik Olness, MD
BASICS
DESCRIPTION
• PaO2 is the partial pressure of oxygen in the arterial blood. Although PaO2 is in equilibrium
with dissolved (blood) and bound (oxyhemoglobin) oxygen, these other states do not exert
partial pressure.
• Although normal values can be estimated by the use of a simple equation, accurate values
must be determined by laboratory arterial blood gas (ABG) analysis.
• Hypoxemia is defined as decreased PaO2 in blood whereas hypoxia is defined as low oxygen
availability to the body or to individual organs/tissues
• PAO2 is the alveolar partial pressure of oxygen. In contrast to PaO2, it is a calculated value.
• The partial pressure of a gas is defined as the pressure exerted independently by that gas in
a mixture of gases
– According to Dalton’s Law, the total pressure of a mixture of gases is equal to the sum of
the partial pressures of each individual gas
• The partial pressure of a gas dissolved in a liquid is the partial pressure that would be
exerted by the gas while in a gaseous phase and while in equilibrium with the liquid
– According to Henry’s Law, if one were to double the pressure of a gas, then the
concentration of that gas in solution would be doubled as well
• Solubility is the ability of a substance (O2) to dissolve in a solute (blood). The solubility
coefficient of a gas is the volume of the gas that can be dissolved in a certain volume of
solvent at a specified temperature and pressure
– At standard body temperature, the solubility coefficient (and the solubility) of CO2 is
approximately >20 times that of O2; therefore, diffusion abnormalities should not result
in hypercapnia
• The net diffusion of a gas, such as O2, is dependent on the:
– Partial pressure gradient. Since the partial pressure of O2 in the alveoli (PAO2) is greater
than the partial pressure of the dissolved O2 in the blood, more O2 molecules will diffuse
from the alveoli into the pulmonary capillary blood. It is also dependent on
Diffusion coefficient. Based on the solubility and molecular weight of the gas in question
Thickness and surface area of the pulmonary capillary membrane. Because of its
tremendous size and microscopic thickness (0.4–0.5 μm), a normal pulmonary capillary
membrane provides almost no resistance to the diffusion of lipid soluble gases such as
O2 and CO2
Transit time. The rate limiting step in the transport of O2 from the alveoli to the blood is
typically the loading of O2 onto Hb, not the diffusion of O2 across the pulmonary
capillary membrane
• Diffusion capacity is the amount of gas (O2) that can be transferred from the alveoli to the
blood across the alveolar-capillary membrane. The O2 diffusing capacity at rest in an adult
male is ∼21 mL/min/mm Hg and may increase to 65 mL/min/mm Hg with strenuous
exercise
• PaO2 will be <Pc’O2 (pulmonary end-capillary O2) because it will be diluted with mixed
venous blood called the venous admixture. Normally, the venous admixture consists of
blood from the bronchial-pulmonary venous communication, the Thebesian circulation, and
low V/Q areas in the lung
ANATOMY
• Hemoglobin is a molecule consisting of 4 heme and 4 protein subunits. Heme is an iron-
porphyrin compound comprising an essential part of O2 binding sites; only the divalent (+2
charge) form of iron can bind O2. Hemoglobin A1 (normal adult hemoglobin) consists of 2α
and 2β chains held together by weak bonds between the amino acid residues. Theoretically,
each gram of Hb can carry up to 1.39 mL of O2.
• Peripheral chemoreceptors include the aortic and carotid bodies; PaO2 has a minimal effect
on central chemoreceptors
– The aortic bodies (found in the aortic arch and its branches) have predominantly
circulatory effects, while the carotid bodies (located at the bifurcation of the common
carotid artery) have predominantly ventilatory effects
– Neural output from the aortic bodies travels to the medullary centers via the vagus (CN X)
nerve, while output from the carotid bodies reaches the central respiratory centers via the
afferent glossopharyngeal (CN IX) nerve
– Both carotid and aortic bodies are stimulated by decreased PaO2, but not by decreased
SaO2 or CaO2
– Neural activity from these receptors begins to increase when the PaO2 falls to <100 mm
Hg. When PaO2 levels reach 60–65 mm Hg, neural activity is substantially augmented to
increase the minute ventilation
– Patients that depend on hypoxic ventilatory drive (those with COPD, for example) have
PaO2 values in the mid 60s; this must be considered when weaning these patients from
mechanical ventilatory support as spontaneous ventilation will not resume until the PaO2
falls to <65 mm Hg
• The oxygen–hemoglobin (also known as the oxyhemoglobin) dissociation curve is the
graphical illustration of the measured relationship between PaO2 and SaO2.
– SaO2 is a measure of the percentage of hemoglobin binding sites occupied by O2. A normal
PaO2 of 100 mm Hg results in a SaO2 of about 98%
– The curve is sigmoidal in shape; it represents conformational changes to Hb as more O2
molecules bind to, or dissociate from, it. These changes accelerate the loading, or
unloading, of the fourth O2 molecule.
– The “S” shape also minimizes the effects of changes in PaO2 on the SaO2, while in the
normal range. However, there is a “steep” vertical section where small changes in PaO2
result in significant drops in the SaO2; it also corresponds to the PaO2 level where
chemoreceptors begin firing.
– P50 (the point at which Hb is 50% saturated) normally falls at a PaO2 of 26.7 mm Hg.
– If the oxyhemoglobin curve is shifted to the left (reduced P50), then hemoglobin has a
higher than normal affinity for O2, resulting in decreased O2 unloading. Circumstances
causing a leftward shift include: Abnormal hemoglobin (fetal), alkalosis,
carboxyhemoglobin, decreased 2,3-DPG, hypothermia, and methemoglobin. When the
curve is shifted to the right (increased P50), Hb has a lower affinity for O2 leading to
increased O2 unloading in the periphery. Shifting of the curve to the right may be caused
by: Abnormal hemoglobin, acidosis, hyperthermia, increased 2,3-DPG, and increased CO2
• The most common mechanism for hypoxemia is an increased alveolar-arterial gradient
• The diffusion of O2 can be slowed when the thickness of the pulmonary capillary membrane
becomes pathologically thickened. This may occur in diseases such as pulmonary fibrosis,
pulmonary edema (accumulation of interstitial fluid in the membrane), and pneumonia
(inflammatory fluid accumulation in the membrane)
• Dissolved oxygen usually has very little impact on the total arterial oxygen content because
most of the oxygen in blood is carried by hemoglobin (see equation )
• Pulse oximetry is listed an American Society of Anesthesiologists Standards for Basic
Anesthetic Monitoring. It is a safe, noninvasive, continuous method to measure oxygenation
and rapidly detect hypoxia. Oximetry readings provide an estimation of the PaO2, based on
the oxygen–hemoglobin curve.
– Values are based on the Lambert–Beer law stating that oxyhemoglobin and
deoxyhemoglobin absorb different quantities of red and infrared light
– Oxyhemoglobin (HbO2) absorbs more infrared light at a wavelength of 940 nm and
therefore, appears red to the human eye
– Deoxyhemoglobin (Hb) absorbs more red light at 660 nm, appearing blue or cyanotic
– Oxygen saturation is calculated by a microprocessor that compares the ratio of light
absorption at the red and infrared wavelengths
– Functional oximetry is defined as HbO2 divided by the sum of HbO2 and Hb; it does not
include COHb and MetHb which, in normal physiological states, are present in small
concentrations. The operating room and ICU pulse oximeter are functional pulse
oximeters.
– Fractional oximetry is defined as the ratio of HbO2 to the total Hb (all 4 species: HbO2,
Hb, COHb, MetHb). It is measured by laboratory co-oximeters.
– The pulse oximeter isolates the pulsatile component of blood based on plethysmography,
in an attempt to eliminate false readings from venous blood or tissue
– Pulse oximeters also measure heart rate based on this pulsatile flow in addition to the
SpO2
• Although generally very accurate at SpO2 readings from 70 to 100%, pulse oximeters have
several potential problems
– Values reflect an average value over a time span of 5–8 seconds; this delay can translate
into a delay in treatment.
– Artifacts may be caused by fingernail polish, ambient light, methylene blue dye, and
motion.
– Low perfusion states such as cardiac arrest, hypothermia, increased SVR, severe anemia,
cardiac bypass, or tourniquet placement may affect the ability to obtain a reading
– Carboxyhemoglobin (COHb) absorbs light in a similar manner to HbO2, resulting in a
falsely high reading in patients with CO poisoning
– Methemoglobin absorbs light equally at red and infrared wavelengths, providing a
constant pulse oximeter reading of ∼85%. SpO2 may be falsely high or low depending on
the actual SaO2
– Unable to distinguish between PaO2 values greater than 100 mmHg – will all have oxygen
saturations of 100%
• ABG analysis measures PaO2 values as well as arterial pH, PaCO2, HCO3−, and base deficit.
It allows for an assessment of oxygenation (PaO2), ventilation based on the PaCO2, and
provides insight into the acid–base status with pH measurement and base deficit.
• Normal range of PaO2 in an adult is 60–100 mm Hg and is dependent on multiple factors
including alveolar ventilation, FiO2 (inspired O2 concentration), SvO2 (mixed venous O2
saturation), and ventilation–perfusion ratio
– If PaO2 is <60 mm Hg, then hypoxemia is present
– If hypoxemia is present, calculation of the A-a gradient will help to determine the cause
– Normal A-a gradient may result from hypoventilation or low FiO2
– Increased A-a gradient can be caused by V/Q mismatching, increased right to left
shunting, and diffusion abnormalities
EQUATIONS
• Approximation of arterial oxygen tension based on age = PaO2 = 102 – Age/3
• Alveolar gas equation = PAO2 = FiO2 (PB – PH2O) – PACO2 / R; PACO2/R is used an as
indirect measure of VO2/VA where VO2 is O2 consumption and VA is alveolar ventilation
• Arterial Oxygen Content = CaO2 = O2 bound to Hb + O2 dissolved in blood = [SaO2 × (Hb ×
1.34)] + [PaO2 × 0.0031]
• Oxygen Delivery = DO2 = CO × CaO2
• Dalton’s Law = Ptotal = Pgas1 + Pgas2 + PgasN
• Henry’s Law = Cg = k × Pg, where Cg is concentration of the gas in solution, k is a
solubility constant, and Pg is the partial pressure of the gas
• Diffusion Capacity for O2 = DLO2 = Oxygen Uptake / (PAO2 – PC’O2)
• Functional Oximetry = SpO2 = HbO2 / (HbO2 + Hb)
• Fractional Oximetry = SaO2 = HbO2 / (HbO2 + Hb + COHb + MetHb + other
hemoglobins)
REFERENCES
1. Boemke W, Krebs MO, Rossaint R. Blood gas analysis. Anaesthesia. 2004;53(5):471–492.
2. ilber HC, Vender JS. Arterial blood gas monitoring. Crit Care Clin. 1995;11(1):233–248.
3. Story DA. Alveolar oxygen partial pressure, alveolar carbon dioxide partial pressure and
the alveolar gas equation. Anesthesiology. 1996;84(4):1011.
ADDITIONAL READING
• Sherwood, Lauralee. Human Physiology: From Cells to Systems. 3rd ed. Belmont:
Wadsworth, 1997.
• Mixed Venous Oxygen Saturation
• Hemoglobin
• Pulse Oximetry
• Alveolar Arterial Gradient and Ratio
CLINICAL PEARLS
• PaO2 is a measured value obtained from an ABG and PAO2 is a calculated value
• The A-a gradient for O2 is typically <15 mm Hg but increases up to 30 mm Hg as one ages
– Increased A-a gradient can be caused by V/Q mismatching, increased right to left
shunting, and diffusion abnormalities
• The majority of O2 transported in the blood is carried by Hb and not dissolved in the blood
• The oxyhemoglobin dissociation curve is a sigmoidal shaped curve portraying the
relationship between PaO2 and SaO2
– Causes of a leftward shift include: Abnormal hemoglobin (fetal), alkalosis,
carboxyhemoglobin, decreased 2,3-DPG, hypothermia, and methemoglobin
– Causes of a rightward shift: abnormal hemoglobin, acidosis, hyperthermia, increased 2,3-
DPG, and increased CO2
• PaO2 stimulates ventilation via the peripheral chemoreceptors with minimal effect on the
central receptors
• Operating room pulse oximeters emit light at wavelengths or 660 and 940 nm and work
based on Lambert–Beer law
PARATHYROIDECTOMY
Joe C. Hong, MD
BASICS
DESCRIPTION
General
• Parathyroidectomy is indicated for the management of hyperparathyroidism.
• The biochemical diagnosis of hyperparathyroidism is made in the setting of elevated serum
calcium and parathyroid hormone (PTH) levels (1).
• Causes of hyperparathyroidism include:
– Primary: Direct hyper-functioning of the parathyroid gland due to parathyroid adenoma or
glandular hyperplasia.
– Secondary: Parathyroid hyperplasia caused by chronic renal disease or vitamin D
deficiency.
– Multiple endocrine neoplasia syndromes.
– Parathyroid carcinoma.
• When a single gland adenoma is suspected, localizing imaging studies (neck ultrasonography
and 99mTc-Sestamibi scan) can aid with a limited and focused parathyroidectomy (2).
• Multiple gland disease requires bilateral neck dissection and 4-gland bilateral exploration.
Position
• Supine with arms tucked bilaterally.
• A roll is placed transversely beneath the scapulae to facilitate mild neck extension, and
thereby optimizes surgical exposure.
• In patients with cervical spine disease, range of neck extension should be carefully assessed
preoperatively.
Incision
• Focused parathyroidectomy: 2–3 cm transverse incision lateralized towards the side of the
suspected adenoma.
• Bilateral exploration or redo: 4–6 cm transverse midline neck incision.
Approximate Time
• Typically 30–60 minutes for focused parathyroidectomy.
• Up to 2+ hours for bilateral exploration or redo parathyroidectomy.
EBL Expected
• Focused: Minimal
• Bilateral exploration: 25–100 mL
Hospital Stay
• Depends on patient comorbidities.
• Focused parathyroidectomy can be done on an ambulatory basis to 24-hour overnight stay.
• Bilateral exploration or redo surgery usually requires a 24–48+ hour hospital course.
• Some surgeons prefer an electromyography (EMG) endotracheal tube for recurrent laryngeal
nerve monitoring (3).
• For deep neck dissections, an esophageal temperature probe may aid in the digital palpation
of landmarks.
EPIDEMIOLOGY
Incidence
• In the US: 100,000 cases of primary hyperparathyroidism per year
• Single gland adenoma: ~80–85%
• Multiple gland hyperplasia: ~10–15%
• Double gland adenoma: ~2–5%
• Parathyroid carcinoma: ~1%
Prevalence
• In the US population: 1:500–1:1,000 have a history of hyperparathyroidism.
• Female > male (4:1)
• Increases with age
• Peak incidence in the 6th decade of life
Morbidity
• Recurrent laryngeal nerve injury:
– Unilateral injury leads to hoarseness.
– Bilateral partial injury can lead to complete airway obstruction or stridor and the need for
intubation or tracheostomy.
• Neck hematoma
• Hypocalcemia
• Operative failure to resect all sources of hypersecreting tissue (multiple gland hyperplasia or
double adenoma).
Mortality
Extremely rare
• Severe symptomatic hypercalcemia with resulting intravascular volume depletion and
cardiac dysrhythmia should be medically managed and optimized prior to surgery.
• Preoperatively, consider IV hydration as this will restore intravascular volume and
temporize hypercalcemia.
• Furosemide, after volume resuscitation, will further decrease plasma calcium concentration
prior to surgery.
• Intraoperatively, the need for recurrent laryngeal nerve monitoring will preclude the use of
non-depolarizing muscle relaxants.
• Dexamethasone is commonly used to temporize postoperative airway edema.
• Bucking on emergence should be minimized to decrease the likelihood of neck hematoma
formation.
SYMPTOMS
• “Painful bones, renal stones, abdominal groans, and psychiatric moans.”
• Often asymptomatic except for biochemical evidence of hypercalcemia and elevated PTH
levels.
History
• Often asymptomatic; discovered after routine laboratory examination reveals hypercalcemia.
• Non-specific history of bone pain, kidney stones, abdominal distress, anxiety, fatigue, and
depression.
• For secondary hyperparathyroidism, history of chronic renal insufficiency, end-stage renal
disease.
• Personal or family history of multiple endocrine neoplasia syndromes.
Signs/Physical Exam
• Skeletal “painful bones”:
– Osteoporosis
– Skeletal demineralization
– Spontaneous fracture
– Bone pain
• Renal “kidney stones”:
– Nephrolithiasis
– Nephrocalcinosis
– Reduced glomerular filtration
– Polydipsia
– Polyuria
• Gastrointestinal “abdominal groans”:
– Abdominal distress
– Gastroduodenal ulcer
– Gastroesophageal reflux disorder
– Anorexia
– Vomiting
– Pancreatic calcification
• Neuropsychiatric: “Psychiatric moans”:
– Fatigue
– Anxiety
– Depression
– Psychosis
– Somnolence
– Coma
• Cardiovascular:
– Hypertension
– Short QT interval
– Intravascular volume depletion
• Neuromuscular:
– Muscle fatigue
– Hypotonia
MEDICATIONS
• Bisphosphonates
• Calcimimetics
• Estrogen therapy in postmenopausal women
Labs/Studies
• Elevated serum calcium and PTH levels
• Per routine labs based on comorbidity
• EKG (short QT interval)
• Renal insufficiency secondary to nephrolithiasis and nephrocalcinosis
• Cardiac dysrhythmias and short QT interval secondary to hypercalcemia
TREATMENT
Premedications
• Ensure adequate IV hydration as hyperparathyroid patients are often intravascularly volume
depleted
• Midazolam may be titrated to comfort, as anxiety is a prominent symptom of hypercalcemia.
• Patients with bone pain may benefit from fentanyl premedication.
• Regional/local with sedation versus general anesthesia and the possibility of conversion
from MAC to general anesthesia.
• Possibility of postoperative intubation in rare cases of partial bilateral recurrent laryngeal
nerve injury.
First generation cephalosporins, such as cefazolin, is recommended prior to surgical skin
incision. Clindamycin is an alternative for patients with a cephalosporin allergy.
INTRAOPERATIVE CARE
• For bilateral neck dissection, 4-gland exploration, and redo operations, a general
endotracheal anesthesia is indicated.
• MAC sedation +/− a superficial cervical plexus block or local infiltration is appropriate
when well-localized single gland disease is expected (2). MAC should be avoided in obese
patients or those with claustrophobia.
• Even when general anesthesia is employed, a superficial cervical plexus block provides
excellent postoperative analgesia.
Monitors
• Invasive monitoring is dictated by patient comorbidities.
• EMG endotracheal tube per surgeon request.
• Induction and airway management is dictated by preoperative airway assessment.
• Parathyroid pathology is rarely severe enough to cause compressive effects on the airway.
However, review of available radiographic studies and discussion with the surgeon can
delineate potential difficulties.
Maintenance
• Balanced technique is most commonly employed.
• Since focused parathyroidectomies are short ambulatory procedures, the use of low-
solubility inhalational anesthetics such as desflurane or sevoflurane with or without nitrous
oxide will result in rapid emergence.
• Total intravenous anesthesia may be utilized to optimize EMG monitoring.
• Coughing/bucking on emergence should be minimized to decrease the likelihood of neck
hematoma formation. Preintubation tracheal lidocaine can provide airway analgesia.
• Communication with the surgeon regarding the likelihood of partial bilateral recurrent
laryngeal nerve injury needs to take place prior to emergence and extubation. If present, the
patient must remain intubated until a new tracheostomy is placed.
POSTOPERATIVE CARE
BED ACUITY
• For uncomplicated procedures, a standard floor bed is usually adequate.
• Patients for focused parathyroidectomy may be discharged on an ambulatory basis after
adequate time of postoperative observation.
ANALGESIA
• Preoperative superficial cervical plexus block provides excellent postoperative analgesia.
• Patients with bilateral neck dissection who are not blocked may be placed on patient-
controlled analgesia.
COMPLICATIONS
• Intraoperative complications include massive bleeding and possible stroke when injury to
the nearby carotid artery occurs.
• Intraoperative carotid sinus irritation may lead to hemodynamic fluctuations and
bradyarrhythmia.
• Respiratory compromise from an occult pneumothorax resulting from lower neck surgical
dissection.
• The SLN innervates the cricothyroid, a vocal cord (VC) tensor; whereas the RLN innervates
the posterior cricoarytenoid (VC abductor) and the rest of the intrinsic laryngeal muscles
(VC adductors).
– Injury to the SLN: The cricothyroid muscle is unable to tense the VCs, giving a weak and
husky voice.
– Injury to RLN: Abductors are more vulnerable to injury. Therefore, partial nerve damage
may result in a selective abductor paralysis while a complete transection paralyzes both
adductors and abductors. Unilateral complete transection: Paralyzed VC that lies midway
between adduction and abduction, just lateral to the midline (results in hoarseness).
Unilateral partial transection: When abductors are more severely paralyzed than
adductors, the affected VC lies in the midline adducted position. Bilateral complete
transection: VCs are positioned midway between abduction and adduction. Breathing is
still possible with a glottic opening smaller than normal. Bilateral partial transection:
When abductor are more severely affected than adductors, both VCs meet in the midline
and this results in complete airway obstruction.
• Neck hematoma.
• Hypocalcemia.
• Hypoparathyroidism.
• Failure to resect all hypersecreting parathyroid tissue resulting in persistent hypercalcemia.
PROGNOSIS
Surgical cure rate for primary hyperparathyroidism is above 95%.
REFERENCES
1. raser WD. Hyperparathyroidism. Lancet. 2009; 374(9684):145–158.
2. Shindo ML, Rosenthal JM, Lee T. Minimally invasive parathyroidectomy using local
anesthesia with intravenous sedation and targeted approaches. Otolaryngol Head Neck
Surg. 2008;138(3):381–387.
3. Miller MC, Spiegel JR. Identification and monitoring of the recurrent laryngeal nerve
during thyroidectomy. Surg Oncol Clin N Am. 2008; 17(1):121–144.
ADDITIONAL READING
• Adler JT, Sippel RS, Chen H. New trends in parathyroid surgery. Curr Probl Surg.
2010;47(12):958–1017.
• Felger EA, Kandil E. Primary hyperparathyroidism. Otolaryngol Clin North Am.
2010;43(2):417–432.
• Thyroidectomy
• Hypocalcemia
• Recurrent Laryngeal Nerve
• Carotid Sinus
• Deep Extubation
• Vocal cord palsy
CLINICAL PEARLS
• Severe symptomatic hypercalcemia from hyperparathyroidism is a medical emergency.
Management consists of IV hydration and furosemide prior to surgical resection.
• Intraoperatively, the need for recurrent laryngeal nerve monitoring will preclude the use of
non-depolarizing muscle relaxants.
• Superficial cervical plexus block provides excellent analgesia for postoperative pain
management. This regional technique can be the primary anesthetic in a focused
parathyroidectomy.
• Bucking on emergence should be minimized to decrease the likelihood of neck hematoma
formation.
PARKINSON’S DISEASE
BASICS
DESCRIPTION
• Parkinson’s disease is a common chronic, progressive, neurodegenerative disease with
hallmarks of hypokinesia, rigidity, resting tremor, and postural instability.
• Profound and selective loss of nigrostriatal dopaminergic neurons and the presence of alpha-
synuclein proteinaceous inclusions (Lewy bodies)
EPIDEMIOLOGY
Prevalence
• Overall: 13.4 per 100,000 persons
• North America: ∼1 million people
Prevalence
• Increases with age: 1% in 60-year olds, 4–5% in those aged 85 years and above.
• Race: Hispanics > non-Hispanic Whites > Asians > Blacks
• Gender: Men slightly > women
Morbidity
See concomitant organ dysfunction
Mortality
• Comparable to the general population, although may be increased with male gender, gait
disorder, and absent rest tremor
• Pneumonia is most often the terminal event
• Etiology is unknown, but believed to be multifactorial and likely a combination of polygenic
inheritance, environmental exposure, and gene-environment interaction
• Genetic factors (substantial): Multiple gene loci have been identified (Park1-17, SPG11,
ACA2, 3). The majority are sporadic; family history comprises 20% of all cases
• Environmental factors and neurotoxins: Pesticides (paraquat), herbicides, metals; chemical
products (paints, glues, solvents, printing products, gasoline, asbestos, varnishes or stains);
well water; living in rural areas within industrialized countries; farming (men only)
• Idiopathic: Pathologic protein aggregation (alpha-synuclein, ubiquitinated proteins);
oxidative stress; mitochondrial dysfunction; disturbed intracellular signal transmission;
dysregulation of manganese homeostasis; neuroinflammation
• Parkinson’s disease manifests from the degeneration of heterogeneous populations of
neurons, most notably in the substantia nigra pars compacta (SNpc) and aminergic brain-
stem nuclei. This causes unopposed activity of GABA nuclei in the basal ganglia with
resultant inhibition of thalamic nuclei and consequent suppression of the motor cortex.
Clinical effects appear when there is 80% loss of striatal dopamine and 50% loss of nigral
neurons.
• Lewy bodies are concurrently found; they are intraneuronal cytoplasmic inclusions that are:
Spherical, eosinophilic protein aggregates, and composed of numerous proteins (alpha-
synuclein, parkin, ubiquitin, synphilin, and neurofilaments). They are believed to interfere
with normal cellular processes and sequester proteins important for cell survival
(alternatively, it has been postulated that they are protective and sequester harmful protein
aggregates).
• Patients are at risk for postoperative pulmonary complications, primarily due to aspiration.
Anesthetic management with appropriate dosing of drugs aims at a fully awake patient with
positive protective reflexes at the time of emergence.
• Cardiovascular instability may result from drug–drug interactions, malnutrition, and
autonomic nervous system dysfunction
• Patients may be more prone to hypothermia secondary to malnutrition and autonomic
nervous system dysfunction.
SYMPTOMS
• Motor symptoms: Bradykinesis, hypokinesis, rigidity, tremors, postural instability, dysphagia
• Dystonias from L-dopa
• Confusion, dementia
History
‘Shaking palsy’, first described in 1817 by Dr. James Parkinson (London)
Signs/Physical Exam
Reduced mouth opening from rigidity
TREATMENT HISTORY
• Surgery: Gpi-pallidotomy, VL-thalamotomy
• Deep brain stimulation
– VIM (tremor)
– STN and GPI (rigidity, dyskinesia)
• Experimental therapies: Stem-cell therapy, fetal tissue transplantation, adrenal medullary
transplants
MEDICATIONS
• Goals: Increase dopamine in basal ganglia (not periphery), decrease side effects of
acetylcholine on neurons
• Levodopa (with peripheral inhibitor of dopa decarboxylase carbidopa or benserazide): Most
effective medication to improve motor symptoms; however has a short half-life. Side effects:
Motor fluctuations, peak dose dyskinesia and freezing, and acute dopaminergic side effects
(nausea, vomiting, orthostatic hypotension, hallucinations, psychosis)
• COMT inhibitors (entacapone, tolcapone): Extends half-life of levodopa by preventing its
metabolism. Side-effect: Hepatic failure
• Dopamine agonists. Ergots and non-ergots directly stimulate receptors in the striatum. Ergot-
related side effects: Pulmonary fibrosis, cardiac valve fibrosis, erythromelalgia, and
dopaminergic side effects (nausea, vomiting, orthostatic hypotension, hallucinations,
impulse control disorders, sleep attacks, leg edema)
• Anticholinergic drugs. Most effective on tremor; however, use is limited by cognitive side
effects such as confusion and hallucinations, urinary retention, tachycardia, dry mouth, and
eyes
• NMDA antagonists (amantadine). Releases dopamine from central neurons and delays
uptake; also an anticholinergic. Side effects: Hallucinations, confusion, leg edema, urinary
retention
• MAO-B inhibitors (selegiline, rasagiline, deprenyl). Increase dopamine through blockade of
MAO-B oxidation of dopamine. Side effects: Serotonergic syndrome, dietary restrictions
Labs/Studies
• Electrolytes, serum albumin/transferrin: Might be deranged through malnutrition
• Blood glucose: If taking selegiline
• Hepatic enzymes: If taking tolcapone
• ECG: For assessment of arrhythmias, and if taking amantadine (long QT)
• CXR, PFTs, possibly ABG: If respiratory dysfunction present
• Neuropsychiatric symptoms: Olfactory deficits (70–100%); fatigue (40–70%); depression
(25–50%); psychosis (16–40%), mostly visual and increased with dopaminergic
medications; dementia (25–35%); apathy; impulsive and compulsive behavior (sexual
disinhibition); cognitive dysfunction; sleep disturbances; restless legs.
• Pain (40–70%) secondary to dystonia and myogelosis
• Ophthalmologic disturbances: Decreased lash reflexes, dry eyes, saccadic eye movements
• Motor:
– Bradykinesia/hypokinesia: Dysarthria, dysphagia, reduced movements, small steps,
propulsion and retropulsion, micrographia, hypomimia, freezing
– Rigidity: Neck, jaw, contractures
– Tremors: At rest (distally), postural
– Postural instability: Falls, decreased movement in large joints, loss of balance
• Airway and respiratory systems: Diminished cough reflex; abnormal control and function of
intrinsic laryngeal and pharyngeal muscles due to rigidity; bradykinesia; decreased
coordination; and an obstructive ventilatory pattern in up to 1/3rd of patients.
• Autonomic nervous system: Postural instability, urinary incontinence, gastroparesis,
defective cardiovascular control, impaired temperature regulation, disturbance of sweating
• Cardiovascular system: Arrhythmias, leg edema, orthostatic, or drug-induced hypotension
• Gastrointestinal function: Dysphagia, hypersalivation (70–80%), due to reduced automatic
swallowing; weight loss; and malnutrition
Insufficient medical therapy with prolonged off-phases may hamper extubation
CLASSIFICATIONS
• Hoehn and Yahr staging of PD from 1 to 5
• Unified Parkinson Disease Rating Scale (UPDRS):
– Mentation, behavior, mood
– Activities of daily living
– Motor symptoms
TREATMENT
Premedications
• Benzodiazepines: Increased sensitivity, prolonged effects
• Continue Parkinson’s medications as close to time of surgery (except in DBS procedures)
• Beta-blockers: Suppress tremor
• Anticholinergics: Diphenhydramine can decrease tremors and provide sedation.
Dementia in up to 35%; may need to acquire consent from family or power of attorney.
INTRAOPERATIVE CARE
• Regional anesthesia: Should be considered when feasible as it has the benefit of avoiding
airway instrumentation. Neuraxial techniques, however, can cause hypotension due to
sympatholysis
• General anesthesia: Hemodynamic instability may occur secondary to hypovolemia,
norepinephrine-depletion, autonomic dysfunction, malnutrition, and drug-induced
hypotension
Monitors
• Foley catheter if urinary incontinence
• Invasive monitors may be indicated depending on the severity of disease, comorbidities, and
surgical procedure
• Induction medications should be chosen and titrated carefully due to the risk of
hypotension. Thiopentone and etomidate have been demonstrated to be clinically safe;
propofol may cause dyskinesia and abolish tremors (avoid during DBS placement), however
effects are unpredictable; ketamine may provoke an exaggerated sympathetic response,
although in low-dose, it can be titrated to effect with good control of tremor and dysarthria.
• Increased risk for arrhythmias during induction if electrolytes are deranged
• Aspiration risk: Consider a rapid sequence (or modified) induction if gastroparesis,
hypersalivation, dysphagia are present. Avoid succinylcholine due to the potential for
hyperkalemia
• Difficult airway should be anticipated based upon an airway exam (small mouth opening),
neck rigidity.
Maintenance
• Lower anesthetic requirements
• Opioids: Fentanyl and morphine have been shown to cause muscle rigidity and alfentanil
can result in an acute dystonic reaction; these effects can be reversed with naloxone.
Meperidine is contraindicated with selegiline (MAO inhibitor) and can cause hyperthermia
and muscle rigidity. Remifentanil has been shown to suppress tremor.
• Volatile anesthetics: Can inhibit dopamine reuptake and increase spontaneous and
depolarization-evoked dopamine release. Halothane can cause arrhythmias due to
sensitization of the heart to catecholamines. Isoflurane, enflurane, sevoflurane, and
desflurane have been shown to be clinically safe; however, pre-existing hypotension may be
amplified through peripheral vasodilation.
• Muscle relaxants: Non-depolarizing agents have been shown to be clinically safe.
• Dexmedetomidine has been shown to be well suited, even during DBS placement; however,
it has a risk for hypotension.
• Postoperative nausea and vomiting may be treated with 5-HT3A medications or steroids.
Avoid antidopaminergics such as butyrophenones (haloperidol and droperidol),
phenothiazines, and metoclopramide can reverse dopamine effects in the basal ganglia and
are contraindicated.
• Laryngospasm due to hypersecretion: Consider glycopyrrolate to decrease secretions and
avoidance of coughing during emergence.
• Airway obstruction secondary to pharyngeal muscle discoordination.
• Delirium with confusion and hallucinations
FOLLOW-UP
BED ACUITY
ICU bed if the patient requires postoperative intubation, or may need reintubation.
• NSAIDs: Good adjuncts
• Resume Parkinson’s medications as soon as possible; may be necessary to place an NG tube
for administration
COMPLICATIONS
• Severe hypotension
• Aspiration, respiratory failure, respiratory insufficiency due to impaired cough reflex
• Psychosis: Low-dose benzodiazepines or neuroleptics (clozapine, but also olanzapine,
risperidone, and quetiapine)
• Post-extubation laryngospasm
• Drug–drug interaction with additive effects on blood pressure and with MAOI
REFERENCES
1. ew M.Overview of Parkinson’s disease. Pharmacotherapy. 2007;27(12 Pt 2):155S–160S.
2. Bekris LM. The genetics of Parkinson disease. J Geriatr Psychiatry Neurol. 2010;23(4):228–
242.
3. Gárdián G, Vécsei L. Medical treatment of Parkinson’s disease: today and the future. Int J
Clin Pharmacol Ther. 2010;48(10):633–642.
4. Nicholson G, Pereira AC, Hall GM. Parkinson’s disease and anaesthesia. Br J Anaesth.
2002;89:904–916.
ADDITIONAL READING
• Kalenka A, Schwarz A. Anaesthesia and Parkinson’s disease: How to manage with new
Therapies. Curr Opin Anaesthesiol. 2009;22:419–424.
• Gagne JJ, Power MC. Anti-inflammatory drugs and risk of Parkinson disease: A meta-
analysis. Neurology. 2010;74(12):995–1002.
• Alzheimer’s disease
CODES
ICD9
332.0 Paralysis agitans
ICD10
G20 Parkinson’s disease
CLINICAL PEARLS
• Thorough preoperative assessment is indispensable.
• In non-Parkinson surgery, drug therapy needs to be maintained precisely.
• For longer surgeries, levodopa may be administered via a gastric tube or apomorphine can
be given subcutaneously (with antiemetic).
• Precipitating factors and drugs need to be avoided.
• Substantial additive effects on pre-existing arterial hypotension through anesthetics are
common.
• Avoiding respiratory complication (especially aspiration), should be a key anesthetic goal.
PARTIAL PRESSURES
BASICS
DESCRIPTION
• There are 3 states of matter: Solid, liquid, and gas. Matter, regardless of its state, is
composed of atoms and molecules (molecular theory) (1,2).
– Solids (drugs and electrolytes) and liquids (water) achieve equilibrium by diffusion based
upon concentration gradients or differences.
– Gases achieve equilibrium based upon partial pressure gradients or differences.
• The partial pressure of a gas describes the pressure exerted by those gas molecules against
the walls that it is contained within (e.g. alveoli, anesthetic circuit, blood vessels).
• Perioperatively, the anesthesia provider and intensivist utilize the concept of partial
pressures to describe gas molecules in air (alveoli) as well as liquid (blood).
• Molecules dissolved in a liquid are described as “concentrations”: The amount or mass of the
particular molecule per a specified volume (e.g. mg/mL, g/L) (1,2).
– Molecules in plasma and extracellular fluid attain equilibrium based upon their
concentration gradient; drugs, and electrolytes distribute in this manner.
• Molecules in the gaseous state, however, possess a high kinetic energy, low density and
viscosity, as well as the ability to expand indefinitely.
– Thus, the term “concentration” cannot be used to describe gases.
– Instead, the term “partial pressure” is used to describe the “amount” or distribution of a
particular gas molecule
• Partial pressures implement the concept of volume and pressure
– Volume describes the 3-dimensional area that molecules occupy whether solids, liquids
and gases.
– Since gas molecules expand indefinitely, volume cannot be used to accurately or
completely describe the amount of gas.
– Pressure, however, can be measured. Gas molecules in a closed container (defined
volume) exert a measurable force against the walls of the container.
• Partial pressures are used to describe a particular gas “concentration.”
– In a mixture of gases, each gas bestows a “partial” contribution to the pressure and is
termed the partial pressure of the gas.
– It is a function of the number of molecules that exert pressure against the walls of the
container (fraction).
– Partial pressure gradients drive gas diffusion and the attainment of equilibrium.
• In the alveoli and breathing circuit, each gas exerts a partial pressure against the walls that
it is contained in (due to indefinite expansion) and based upon the number of molecules of
the particular gas.
• In the blood, gas molecules are present either in the following states:
– Gaseous form above the level of the liquid. Only gas molecules in their gaseous form exert
a partial pressure; diffusion and equilibrium is based upon partial pressures.
– Dissolved based upon their individual solubility characteristics. They do not exert a partial
pressure, but are in equilibrium with molecules in their gas form
– Bound to substances (hemoglobin, proteins); does not exert a partial pressure.
– Transformed to form other compounds based on the chemical reaction; does not exert a
partial pressure.
– Oxygen and carbon dioxide in the blood are present in all the above-mentioned forms;
however, they are usually measured and discussed as partial pressures (gaseous form).
• Solubility affects the amount of gas dissolved in liquid (blood, cerebrospinal fluid, water)
– The solubility coefficient (λ) is the milliliters of gas dissolved per milliliters of liquid per
atmosphere (1 atm = 760 mm Hg) partial pressure of the gas at any given temperature.
– In other words, gas solubility is directly proportional to the pressure of that gas above the
surface of the solution.
– Increased partial pressures “force” gas molecules into the solution
– This is the concept behind carbonated beverages. Bottling is done under pressure to
increase the carbon dioxide that is dissolved in solution. Thus, when the bottle is opened,
the pressure above the solution decreases and carbon dioxide bubbles out or effervesces.
Hyperbaric oxygen therapy also functions in this manner.
• Temperature affects the amount of gas dissolved in liquid (blood, cerebrospinal fluid, water)
– Increases in kinetic energy enhance the motion of molecules and breaks intermolecular
bonds, allowing escape from solution.
– This results in an increased total pressure of all gases (increased total force exerted against
the walls of a container).
– Critical temperature is the temperature above which a gas cannot be liquefied regardless
of the pressure applied. The critical temperature of nitrous oxide is 36.5°C. Below an
ambient temperature of 36.5°C, nitrous oxide exists as a heterogenous mixture of gas and
liquid within a cylinder. The critical temperature for oxygen is −119°C.
• Partition coefficient describes the ratio of concentrations of a substance in 2 heterogenous
phases in equilibrium with each other; it is dependent upon the partial pressures and
solubility of the gas in the 2 phases. Anesthesia providers frequently utilize this concept
when discussing volatile agents (blood:gas, brain:blood, fat:blood, oil:gas ratios).
• Oxygen enters the body as a gas via the alveoli. Blood in pulmonary capillary arteries “pick
up” the oxygen and carry it to tissues bound to hemoglobin molecules or in the gaseous or
dissolved forms.
– Hemoglobin binds oxygen to form oxyhemoglobin. Each gram of normal hemoglobin
molecule has a binding coefficient of 1.39 mL O2/dL.
– Oxygen solubility in blood. At 37°C, O2 has a solubility coefficient of 0.003 mL O2/dL of
blood/mm Hg PaO2. Thus, a normal blood gas PaO2 of ∼100 mm Hg equates to 0.3 mL
O2/dL of blood. This is based on Henry’s law of solubility of gases.
– Oxygen cascades down its partial pressure gradient from a PaO2 of ∼100 mm Hg in the
pulmonary capillaries and ultimately through the blood and tissue to the intracellular
mitochondria (PO2 ∼ 2 mm Hg).
– Solubility and temperature: Increases in temperature result in increases in kinetic energy
of the gas molecule and reduced solubility. Conversely, decreased temperature reduces the
kinetic energy of the gas molecule and increases solubility.
– Saturation or dissociation curves are used to describe oxygen and carbon dioxide in blood.
It plots the concentration of the gas molecule in blood (y-axis) against the gas molecule’s
partial pressure (x-axis).
• Carotid and aortic body chemoreceptors carefully regulate respiratory function in response
to changes in pH, PaO2, and PaCO2 (2,3). Hypoxemia, hypercapnia, and acidemia lead to an
increase in chemoreceptor activation and receptor firing; ultimately serving to increase
minute ventilation. The threshold for chemoreceptor activation is a PaO2 < 80 mm Hg,
PaCO2 > 40 mm Hg, or pH < 7.4.
• Absorption atelectasis (3): The tendency for airways to collapse if proximally obstructed in
the setting of 100% oxygen administration.
– Alveolar space primarily consists of oxygen and nitrogen. In the setting of proximal airway
obstruction, the alveolar gases diffuse into the blood along their concentration gradient.
The diffusion of nitrogen is limited by its poor solubility in plasma and thus it remains in
the alveolar space (functions as a “space holder”).
– In the setting of a high inspired concentration of oxygen and/or nitrous oxide, the
“splinting” or “stenting” effects of nitrogen are lost and absorption atelectasis can occur.
• Nitrous oxide expansion of an enclosed space. Air is composed of nitrogen (79%) and
oxygen (21%). Nitrous oxide is poorly soluble in blood and will rapidly enter air spaces to
reach equilibrium. However, nitrogen is 20 times less soluble in blood than nitrous oxide,
and slowly diffuses/exits out of an air space into blood to reach a new equilibrium.
Consequently, air spaces can increase in size (e.g., bowel causing difficulty with surgical
visualization or closure); and closed air space expansion may be harmful (e.g., endotracheal
tube cuff tracheal ischemia, venous air embolism enlargement, pneumothorax expansion,
etc).
• Diffusion hypoxia: When a low FiO2 is inhaled at the conclusion of a nitrous oxide
anesthetic, an abrupt decrease in alveolar oxygen tension can occur. Nitrous oxide diffuses
from the blood into the alveoli, diluting the oxygen available for pulmonary gas exchange.
• Concentrating effect: Increasing the inspired concentration of a gas increases both the
alveolar concentration and the rate of rise (FA/Fi) of alveolar concentration.
– If 50% of an inhalation anesthetic is taken up by the pulmonary circulation, an inspired
concentration of 20% (20 parts of anesthetic in a total volume of 100 parts gas) will result
in an alveolar concentration of 11% (10 parts anesthetic in a remaining gas volume of 90
parts).
– If the inspired concentration is increased to 80%, and the pulmonary uptake is unchanged
at 50%, the resulting alveolar concentration will be 67% (40 parts of anesthetic remaining
in a total volume of 60 parts of gas).
• Calculating the contents of a nitrous oxide cylinder using the cylinder weight and
Avogadro’s law (1):
– The molecular weight of nitrous oxide is 44 g and a full nitrous oxide cylinder weighs 3.4
kg. According to Avogadro’s hypothesis, 1 mole of nitrous oxide weighs 44 g and 1 mole
of nitrous oxide occupies 22.4 L. Therefore, 3.4 kg (3400 g) of nitrous oxide will occupy
1730 L ([3400 g/44 g] × 22.4 L).
• Vaporizers and altitude change: Vaporizers deliver a set percentage of saturated vapor
pressure to the fresh gas flow. Every potent inhalation anesthetic has a different saturated
vapor pressure, which is independent of atmospheric pressure.
– In areas of higher altitude, and thus lower atmospheric pressure, (i.e., Denver, Colorado),
the saturated vapor pressure of a particular inhalational agent will contribute a higher
percentage of the total pressure (Dalton’s law). Thus, for a given percentage of anesthetic
administered, the partial pressure and depth of anesthesia should be greater.
– In areas of lower altitudes, and thus higher atmospheric pressure (i.e., Death Valley), the
vapor pressure contributes to a lesser percentage of the total pressure. The output for a
given percentage setting on the vaporizer is reduced.
• The alveolar gas equation allows a determination of the composition of alveolar gases. The
inspired air in the alveoli is mainly composed of nitrogen (79%), oxygen (21%), carbon
dioxide (0.03%), and water vapor. Based on Dalton’s and Henry’s law, at one atmospheric
pressure of 760 mm Hg: The partial pressure of oxygen in dry air is 0.21 × 760 = 160 mm
Hg.
– The partial pressure of water vapor at one atmosphere when the air is fully saturated with
vapor is 47 mm Hg. Inspired air that is fully saturated with water vapor reaching the
lungs has a partial pressure = PatmO2 – Patm H2O = 160−47 = 113 mm Hg.
– The Alveolar partial pressure of oxygen at room air may be calculated using the Alveolar
Gas equation: PAO2 = PiO2–(PaCO2/R), where PAO2 = partial pressure of oxygen in the
alveolar gas; PiO2 = partial pressure of oxygen in the inspired gas; PaCO2 = pressure of
carbon dioxide in the artery, R = respiratory quotient
– The Alveolar partial pressure at varying FiO2 can be calculated as follows: PAO2 = [(Pbaro
– PH20)(FiO2) – PaCO2/R]
• Blood gas analysis: Measures the partial pressure of the gases in the arterial or venous blood
that mainly include carbon dioxide and oxygen. The partial pressure of a gas in the blood
determines the amount of gas that may be dissolved in the blood and attached to
hemoglobin, and hence available to tissue. Alpha stat and pH stat are discussed at length
elsewhere.
• Hyperbaric oxygen chamber has 2 components that increase oxygen delivery: Increased
hydrostatic pressure and increased oxygen pressure. The hydrostatic pressure reduces
bubble volume, and the absence of inspired nitrogen increases the gradient for elimination
of nitrogen and reduces hypoxia in downstream tissues. Increased oxygen pressure at the
tissue level is the primary therapeutic goal. At 1.3 atm, the Alveolar gas equation is as
follows: [{(760 × 1.3) – (47)}FiO2 – (PACO2/0.8)]
• Deep sea divers suffer from a condition called ‘Bends’ if they do not readjust slowly to the
lower pressure at the surface (1). Deep sea divers breathe compressed air and are subject to
high pressures when submerged; thus, the amount of nitrogen dissolved in blood and other
tissues increases. If the diver returns to the surface too rapidly, the nitrogen forms bubbles
in the blood as it becomes less soluble due to a decrease in pressure. The nitrogen bubbles
can cause great pain and possibly death. To alleviate this problem, artificial breathing
mixtures of oxygen and helium are used. Helium is only 1/5th as soluble in blood as
nitrogen. As a result, there is less dissolved gas to form bubbles. Treatment with hyperbaric
oxygen serves to “re-pressurize” the bubbles and dissolve them back into the blood.
EQUATIONS
• Ideal gas law. PV = nRT (1)
• Boyle’s law. P1V1 = P2V2
• Charles’ law. V1/T1 = V2/T2
• Third gas law. P1/T1 = P2/T2
• Avogadro’s law. V1/n1 = V2/n2
• Dalton’s law. PT = Pa + Pb+ Pc
• Henry’s law of solubility. Pi = k × Ci
REFERENCES
1. avis PD, Kenny GNC. Basic Physics and Measurement in Anaesthesia, 5th edition,
Butterworth-Heinemann; 2003.
2. anong WF. Review of Medical Physiology. 22nd edition, copyright © The McGraw-Hill
Companies, Inc. 2005.
REFERENCES
3. West JB. Respiratory physiology, the essentials; 8th edition, copyright © Lippincott
Williams and Wilkins; 2008.
• Hyperbaric Oxygen Therapy
• PaO2
• PaCO2
• Arterial blood gases
• pH Measurements
CLINICAL PEARLS
• Partial pressure is defined as the pressure exerted by a gas on the walls of the enclosed space
in a mixture of gases.
• The amount of gas dissolved is based upon the gas molecule, the liquid, the partial pressure
of the gas, and the temperature.
PARTIAL THROMBOPLASTIN TIME (PTT)
BASICS
DESCRIPTION
• PTT is a screening test for hemostasis and is one of the most frequently ordered tests in
coagulation medicine.
• PTT measures the integrity of the intrinsic and final common pathways of the coagulation
cascade (Figure 1).
FIGURE 1. Schematic of coagulation cascade. HMWK = high-molecular-weight kininogen; PK = prekallikrein.
FIGURE 2. Approach to a prolonged PTT.

• It represents the time (in seconds) for the patient’s plasma to clot after the addition of
phospholipid (an intrinsic pathway activator) and calcium.
• PTT measures coagulation factors in the intrinsic and common pathways. These factors (in
order of their role in the coagulation cascade) are:
– High-molecular-weight kininogen (HMWK)
– Prekallikrein (PK)
– Factor XII
– Factor XI
– Factor IX
– Factor VIII
– Factor V
– Factor X
– Factor II
– Fibrinogen
• Normal range: depends on the reagent and instrument combinations each laboratory uses.
– Deficiencies or inhibitors of clotting factors within the intrinsic and final common
pathways result in prolongation of the PTT. Etiologies can result from:
– Anticoagulation: Heparin, low-molecular-weight heparins, warfarins.
– Systemic disease
– Coagulation factor deficiencies
– Presence of an inhibitor
– Artificial causes
• Anticoagulation
– Heparin binds to antithrombin III, causing a conformational change that accelerates its
action 1000–3000-fold. Activated antithrombin III inactivates thrombin and Factor X
(common pathway) that clot blood; dose-related prolongation of PTT is seen.
– Low-molecular weight heparins (LMWHs) accelerate anti-factor X activity and can cause a
mild prolongation of PTT (rarely <40 seconds)
– Warfarin inhibits vitamin K epoxide reductase which is responsible for Factor II, VII, IX,
and X (common, instrinsic, extrinsic pathway).
• Systemic disease:
– Liver disease: All coagulation factors are made in the liver except for vWF. Thus, the PTT
time is a good indicator of liver metabolic function. It should be noted, however, that the
PT is a better indicator of early liver failure; factor VII, which is a part of the extrinsic
pathway, has the shortest half-life and is affected first.
– Connective tissue disease: Lupus anticoagulants.
– Amyloidosis: Factor X deficiency.
– Myeloproliferative disease: Factor V deficiency.
– Disseminated intravascular coagulation and fibrinolysis.
• Coagulation factor deficiency:
– Hemophilia A: X-linked recessive transmission of Factor VIII deficiency.
– Hemophilia B: X-linked recessive transmission of Factor IX deficiency.
– Hemophilia C: Factor XI.
– Factor II, V, X: Autosomal inheritance.
– von Willebrand’s disease: A hereditary or acquired coagulation abnormality that can result
in a qualitative or quantitative deficiency of von Willebrand factor (vWF). vWF is a
protein required for platelet adhesion. As von Willebrand’s disease may be accompanied
by factor VIII deficiency, PTT could be prolonged in these patients.
• Presence of an inhibitor:
– Specific factor inhibitor: Directed against specific clotting factors (e.g., factor VIII or factor
V inhibitor) or excess heparin in the specimen (blood collected from heparinized
catheter).
– Nonspecific inhibitors (e.g., lupus anticoagulants).
• Artificial causes:
– Lipemic, icteric, and hemolyzed plasma samples (interferes with light transmission)
– High hematocrit in patients with erythrocytosis (more plasma to anticoagulant ratio)
– Even in the absence of the above conditions the test needs to be repeated.
• Prolonged PTT in the perioperative period:
– Nasal airway/intubation is generally avoided in the presence of a coagulopathy.
– Esophageal and gastric instrumentation should be minimized due to the risk of bleeding.
– Central line placement in the thorax can result in life-threatening hemothorax. Adequate
compression of large vessels in the event of arterial or venous bleeding is difficult, if not
impossible. If placement is attempted in the neck, ultrasound technique may reduce
inadvertent carotid artery puncture.
• Prolonged PTT and neuraxial anesthesia techniques can increase the risk of bleeding around
the spinal cord.
– It is considered the most significant hemorrhagic complication in regional anesthesia due
to the catastrophic nature of bleeding into a fixed and noncompressible space.
– Incidence: Actual incidence of neurologic dysfunction from hemorrhagic complications
associated with neuraxial blockade is unknown. Although the incidence cited in the
literature is estimated to be <1 in 150,000 epidural placements and <1 in 220,000 spinal
anesthetics, recent epidemiologic surveys suggest that the frequency is increasing and may
be as high as 1 in 3,000 in some patient populations.
– Management: The decision to perform spinal or epidural anesthesia/analgesia and the
timing of catheter removal in a patient receiving antithrombotic therapy should be made
on an individual basis. The risk of a spinal hematoma must be weighed against the
benefits of regional anesthesia for a specific patient. If spinal or epidural needle/catheter
placement is performed, the patient’s coagulation status should be optimized during
placement, duration of epidural catheterization, and removal of the catheter.
• In plexus and peripheral nerve blockade:
– The associated risk of bleeding remains undefined.
– Neurologic deficits: The expandable nature of the peripheral site decreases the chance of
irreversible neural ischemia (unlike the epidural space).
– Massive hemorrhage: Bleeding into the neurovascular sheath (especially in plexus blocks)
may result in a significant decrease in the hematocrit.
– Incidence: Due to the rarity of the complications and lack of randomized studies, the
information available is based on case reports. The overall incidence of bleeding
complications associated with peripheral nerve blocks is low.
– Management: The decision to perform peripheral nerve or plexus blocks (single injection
or continuous catheter infusion) is at the discretion of the anesthesiologist after weighing
the benefits of regional anesthesia against the risk of neural damage from hematoma or
bleeding complications. In superficial limb blocks, anatomical landmarks are generally
well defined or easily visualized with ultrasound imaging, and a developing hematoma
can be easily accessed and compressed. On the other hand, bleeding complications may
not be easily diagnosed in deeper blocks such as the posterior lumbar plexus block,
especially with the use of a continuous catheter technique.
REFERENCES
1. amal AH, Tefferi A, Pruthi RK. How to interpret and pursue an abnormal prothrombin
time, activated partial thromboplastin time, and bleeding time in adults. Mayo Clinic
Proceedings. 2007; 82(7):864–873.
2. Muilenburg DJ, Singh A, Torzilli G, et al. Surgery in the patient with liver disease.
Anesthesiology Clinics. 2009;27(4):721–737.
3. Horlocker TT, Wedel DJ, Rolingson JC, Enneking FK, Kopp SL, Benzon HT, Brown DL, Heit
JA, Mulroy MF, Roenquist RW, Tryba M, Yuan C. Regional anesthesia in the patient
receiving anitthrombotic or thrombolytic therapy. American Society of Regional Anesthesia
and Pain Medicine Evidence-Based Guidelines (Third Edition). Regional Anesthesia and
Pain Medicine. 2010;35(1):64–101.
4. Ho M, Ganapathy S. Is peripheral/plexus block safe in the anticoagulated patient?
Techniques in Regional Anesthesia and Pain Management. 2006:10:56–61.
• Epidural Hematoma
• Prothrombin Time (PT)
• Cirrhosis
CLINICAL PEARLS
• Routine coagulation studies are not indicated unless clinical or medication history suggests
the potential for a coagulopathy.
• It is important to recognize bleeding disorders that will not be detected by PTT assays.
These disorders include:
– Qualitative and quantitative platelet defects, which require specialized platelet function
testing.
– von Willebrand disease, which requires assays for von Willebrand factor.
– Factor XIII deficiency, which requires specialized factor XIII screening or functional
assays.
– Deficiency of plasminogen activator inhibitor 1, which requires specific assays.
PATENT DUCTUS ARTERIOSUS
Swati Patel, MD
BASICS
DESCRIPTION
• In utero, the ductus arteriosus is a vascular connection that shunts blood from the main
pulmonary artery (PA) to the descending aorta thereby decreasing pulmonary blood flow
and increasing placental perfusion.
• The ductus arteriosus closes functionally within 15 hours of birth and closes permanently 2–
3 weeks after birth. Spontaneous closure is brought on by increasing oxygen concentrations
and decreased circulating placental prostaglandins.
• Persistent patent ductus arteriosus (PDA) occurs when the ductus arteriosus fails to close
after birth resulting in a pathologic left-to-right shunt from the aorta to the main PA.
EPIDEMIOLOGY
Prevalence
• Term infants: 1 per 2,500 live births
• Preterm infants: 33 per 100 live births
• Spontaneous closure ∼0.6% per year
Prevalence
The National Birth Defects Prevention Network cites a wide range: 8–99 per 10,000 live
births
Morbidity
PDA in preterm infants is associated with bronchopulmonary dysplasia (BPD), chronic lung
disease (CLD), myocardial dysfunction, congestive heart failure (CHF), pre-renal azotemia,
necrotizing enterocolitis, and interventricular hemorrhage.
Mortality
Untreated PDAs have a mortality rate of approximately 1/3rd by 30 years of age and 2/3rd by
60 years of age.
• More common in preterm infants.
• Female to male ratio is 3:1.
• Often present in complex congenital heart defects. It provides a source of blood flow
between pulmonary and systemic circulations in infants with single ventricles prior to
palliative interventions.
• Can be associated with chromosomal abnormalities such as Down’s syndrome.
• The ductus arteriosus closes spontaneously after birth in response to increased oxygen
concentrations and decreased circulating placental prostaglandins including PGE2 and PGI2.
The ductus arteriosus in preterm infants has been shown to have decreased sensitivity to
oxygen concentrations and increased sensitivity to prostaglandins perhaps leading to an
increased incidence of PDA in preterm infants.
• PDA causes a left-to-right shunt at the level of the great arteries (aorta to main pulmonary
artery). The amount of shunting depends on the size of the PDA and the ratio of resistances
between the pulmonary and systemic vasculature.
– The ratio of pulmonary vascular resistance (PVR) to systemic vascular resistance (SVR) is
the driving force that determines the direction and volume of flow through the shunt.
– The length and diameter of the PDA also affect shunt flow, with short and wide PDAs
having the greatest flow.
• A large PDA, and hence left-to-right shunt, causes increased PA blood flow, increased return
from the pulmonary veins to the left atrium, pulmonary compliance, and if left untreated,
eventually left heart failure, CHF, and CLD.
– Over time, increased PVR can become irreversible, leading to pulmonary hypertension and
right heart failure.
– If PVR > SVR there can be a reversal of shunt (now right-to-left) leading to Eisenmenger’s
syndrome (cyanosis, polycythemia).
• A large PDA also causes a decrease in aortic diastolic BP due to backward flow of blood
from the aorta to the PA during diastole or diastolic runoff. Diastolic runoff can lead to
decreased coronary perfusion and myocardial ischemia.
• The combination of CHF, myocardial ischemia, and diastolic runoff can lead to decreased
cardiac output and systemic hypoperfusion putting the infant at risk for acidosis, renal
failure, and necrotizing enterocolitis.
• Anesthetic technique should depend on the patient’s presenting clinical condition,
prematurity, birth weight, co-existing disease and surgical procedure.
• Special attention should be given to maintaining adequate ventilation and cardiac perfusion.
SYMPTOMS
• Vary depending on the size of the PDA, severity of shunt, shunt direction, and range from
asymptomatic to severe.
• Increased work of breathing or shortness of breath, poor weight gain, feeding intolerance,
fatigue, cyanosis, and decreased urinary output
History
• Birth history: pregnancy or birth complications, prematurity, and birth weight.
• Past medical history: length of NICU stay, pulmonary status (history of intubation, length of
intubation, BPD, CLD, recent chest x-ray), cardiovascular condition (history of other
congenital cardiac anomalies, recent EKG or echocardiogram), other congenital anomalies,
and history of blood product transfusions.
• Past surgical history and history of anesthesia or airway complications.
• Family history of congenital anomalies or malignant hyperthermia.
• Feeding history: growth retardation, failure to thrive.
• Current clinical condition: Evidence of myocardial ischemia, systemic hypoperfusion, or
respiratory insufficiency. When applicable, ventilator settings and endotracheal tube size
and position as well as any problems ventilating patient, recent or current need for
ionotropes, vascular access and invasive monitoring should be determined.
Signs/Physical Exam
• Tachycardia, tachypnea
• Continuous machine-like heart murmur heard best at the left upper sternal border
• Laterally displaced apical impulse
• Widened pulse pressure, bounding pulses
• Differential cyanosis and BP: Pre-ductal pulse oximetry and BP are often higher then post-
ductal measurements
• Patients with CHF may have signs of systemic hypoperfusion including diminished
peripheral pulses, decreased capillary refill, hypotension, or acidosis.
TREATMENT HISTORY
• First-line treatment for failed spontaneous closure involves pharmacologic efforts with cyclo-
oxygenase (COX) inhibitors (i.e., Ibuprofen or Indomethacin).
• Surgical closure can also be performed via thoracotomy, VATS (video assisted thoracic
surgery), or robot assisted VATS.
• Transcatheter closure may be performed if the size and shape are amenable to device
closure.
MEDICATIONS
As above (COX inhibitors)
Labs/Studies
• Arterial Blood Gas (ABG): may show cyanosis, hypoxemia, hypercapnia or acidosis.
• CBC: Anemia, polycythemia if cyanosis present.
• Comprehensive Metabolic Panel (CMP): Metabolic acidosis, pre-renal azotemia,
hypoglycemia, or other electrolyte abnormalities.
• Chest Radiography: Enlarged heart and increased pulmonary circulation.
• Echocardiography: Presence of PDA, shunt direction, evidence of volume overload,
myocardial function, other cardiac anomalies.
• Lungs- BPD, CLD, increased PVR and decreased pulmonary compliance leading to increased
work of breathing and difficulties ventilating patient.
• Renal failure (pre-renal azotemia)
• Necrotizing enterocolitis
• Interventricular hemorrhage
• Unstable premature infants with poor feeding and difficult ventilation often require
facilitated PDA closure in order to stop pulmonary over-circulation and improve feeding,
weight gain, and extubation. If on high frequency oscillatory ventilation or too unstable for
transport, PDA ligation can take place in the NICU at the bedside.
• Acute illness (upper respiratory infection with fever or pneumonia) in stable outpatients that
are undergoing elective closure may need to be delayed until resolution.
CLASSIFICATIONS
• Symptomatic or asymptomatic
• Direction of the shunt (left-to-right versus right-to-left shunt).
TREATMENT
Premedications
Patients needing premedication (usually >6 months of age) may be premedicated with
midazolam (0.05–0.1 mg/kg IV or 0.5–1.0 mg/kg PO)
Premature infants and low birth weight infants are at increased risk for anesthetic and
surgical complications as well as remaining intubated after surgery.
INTRAOPERATIVE CARE
• Choice of anesthetic should depend on the clinical condition at the time of surgery,
prematurity, birth weight, co-existing disease, and surgical procedure. General endotracheal
anesthesia is always needed.
• High spinal, epidural or caudal anesthesia in conjunction with general anesthesia may be
used to provide postoperative pain control.
Monitors
• Pre-ductal and post-ductal pulse oximetry. Pre-ductal measured in the right upper extremity.
Post-ductal measured in the left upper or either of the lower extremities.
• Invasive or non-invasive monitoring of the arterial BP in both pre-ductal and post-ductal
locations; consider invasive monitoring if the patient has CHF or other co-existing
conditions.
• Central venous monitoring for patients with CHF or other co-existing conditions.
• Inhalational induction with sevoflurane is appropriate for stable patients without
intravenous access.
• Intravenous induction with fentanyl, muscle relaxants, and possibly etomidate is appropriate
in severe or decompensated CHF patients who may not tolerate the cardiodepressent effects
of inhalational anesthesia.
• Prior to the start of surgery, patients should have adequate IV access and blood products
available in order to treat possible intraoperative blood loss.
• Hypothermia should be avoided by actively warming the patient as well as intravenous
fluids and/or blood products.
Maintenance
• Inhalational anesthesia with sevoflurane is appropriate for stable patients.
• Unstable patients with CHF or decreased myocardial function may not tolerate inhalational
maintenance. Fentanyl and muscle relaxants can be used in conjunction with very low-dose
sevoflurane.
• A decrease in post-ductal pulse-oximetry is seen if either the aorta or the main pulmonary
arteries are inadvertently ligated.
• Blood pressures. The diastolic BP should increase after ductus ligation with cessation of
diastolic run off to the lungs. If post-ductal BP decreases or is absent following duct ligation,
the descending aorta may have been ligated. If a pre- and post-ductal BP gradient exists, an
aortic coarctation may be present or was created operatively.
• Dependent on age, birth weight, co-existing disease, pre-operative clinical condition, and
surgical course or complications.
• Consider leaving intubated if already intubated prior to ligation (due to pulmonary over-
circulation) or in premature infants with a history of CLF or PBD to optimize pain control,
fluid, and ventilatory management.
• Consider extubating if stable, not intubated before surgical repair, and uncomplicated
surgical course.
FOLLOW-UP
BED ACUITY
• Determined by age, weight, comorbidities, and post-operative condition.
• Preterm infants often require at least 24-hour post-operative admission with apnea
monitoring.
• Symptomatic patients often require admission in either a neonatal or pediatric intensive care
unit.
• Asymptomatic patients or patients undergoing transcatheter closure may not necessarily
require intensive care admission post-operatively and often can go home the same day after
follow-up echo.
• Dependent on age of patient, pre-operative status and/or other comorbidities.
• CBC to evaluate hematocrit after surgical blood loss and intra-operative volume shifts.
• Blood gas may be drawn to assess oxygenation and ventilation as well as possible post-
operative acidosis.
COMPLICATIONS
• Complications if left untreated can include: Pulmonary hypertension, CHF, Eisenmenger’s
syndrome, endocarditis, or arrhythmias.
• Intraoperative complications may include: Hemorrhage, infection, damage to the left
recurrent laryngeal nerve, pulmonary edema, or diaphragmatic paralysis from damage to
the phrenic nerve.
REFERENCES
1. amrick S, Hansmann G. Patent ductus arteriosus of the preterm infant. Pediatrics.
2010;125:1020–1030.
2. Koch J, Hensley G, Roy L, et al. Prevalence of spontaneous closure of the ductus arteriosus
in neonates at a birth weight of 1000 grams or less. Pediatrics. 2006;117(4):1113–1121.
3. Schneider DJ, Moore JW. Patent ductus arteriosus. Circulation. 2006;114(17):1873–1882.
4. Fortescue EB, Lock JE, Galvin T, McElhinney DB. To close or not to close: The very small
patent ductus arteriosus. Congenital Heart Disease. 2010; 5(4):354–365.
ADDITIONAL READING
• Andropoulos DB, Stayer SA, Russell IA, Mossad EB. Anesthesia for Congenital Heart Disease.
• Cote CJ, Lerman J, Todres ID. A Practice of Anesthesia for Infants and Children.
• Fetal Cardiovascular Physiology
• Atrial Septal Defect
CODES
ICD9
747.0 Patent ductus arteriosus
ICD10
Q25.0 Patent ductus arteriosus
CLINICAL PEARLS
• A persistent PDA causes a left-to-right shunt at the level of the great arteries leading to
increased PVR, pulmonary edema, decreased pulmonary compliance, and left heart volume
overload.
• If left untreated, PDA can lead to myocardial dysfunction, CHF, pulmonary hypertension and
CLD.
• Hypothermia, hypoxia, and acidosis in the neonate may temporarily increase PVR compared
to SVR and cause shunt reversal with resultant cyanosis and decreased cardiac output.
PEDIATRIC CARDIAC PHYSIOLOGY
Johanna C. Schwarzenberger, MD
BASICS
DESCRIPTION
• Since cardiac catheterization is a difficult undertaking in the newborn and growing infant,
most physiologic data about the cardiovascular system of the fetus, neonate, and pediatric
patient is derived from invasive studies in sheep. Molecular function of the developing
cardiac muscle has been investigated across many mammalian species, yet human data is
lacking.
• The pediatric cardiovascular system undergoes vast changes from fetal life to adolescence
and knowledge about the specific developmental stages is crucial in understanding
cardiovascular compromise in the pediatric patient.
• Series circulation. Following birth, the neonatal heart adapts to the new loading conditions
resulting from a series circulation. As the lungs replace the low resistance placenta for gas
exchange, the pulmonary vascular resistance drops continuously in the first days of life.
Pulmonary blood flow becomes 20 times higher than during fetal circulation. In addition,
the right ventricle is no longer exposed to the high afterload during fetal circulation.
Remodeling of the pulmonary vascular bed occurs as a result of many factors:
– Exposure to oxygen, a pulmonary vasodilator
– Ventilation indirectly changes alveolar surface tension and thus affects perivascular tissue
pressures
– Changes in the metabolic milieu of the lung: Prostaglandins, bradykinins, histamine,
angiotensin II
• Cardiac output (CO). Overall CO per kilogram of body weight of the neonate is high when
compared with the adult heart. In the newborn, CO reaches close to 200 mL/kg/minute.
This high value mirrors the high oxygen consumption of neonates for processes such as
thermoregulation, growth, and work of breathing. CO requirements are reduced to normal
adult levels as lung mechanics become more effective in gas exchange. By adolescence, the
CO is equivalent to that of an adult heart (2.5–3 liters/minute/m2).
• Structural and cellular aspects of cardiac function
– Fetal. Initially, neonatal myocytes contain immature myofibrils that are arranged in a
disordered fashion featuring an incomplete sarcomere. To allow growth of the cardiac
muscle, myocyte division during fetal life is traded for myocyte hypertrophy shortly after
birth. In addition, the heart has an immature calcium transport due to an underdeveloped
transverse tubular system and sarcoplasmic reticulum
– Neonatal. At birth, developmental changes in myofibril size and structure begin and
continue through childhood until their organized adult shape is attained. This involves:
A reduction of the size of the nuclei but an increase in cellular mass.
With an increase of the cell surface area, the sarcolemma and T-tubule system develop
after birth. Invagination of the T-tubule is vital for effective excitation-contraction
coupling.
Maturation of the sarcoplasmic reticulum and its calcium release channels occur at the
same time as T-tubule development
• Neonatal contractility. Despite the cellular development, the effective contractile mass of the
neonatal myocardium is 50% that of the adult. As a result, the neonatal heart improves
cardiac output by increasing heart rate rather than by improving its loading conditions with
an increased preload.
• Neonatal wall tension (a function of preload and afterload). The Frank Starling principle
defines afterload as the weight against which myocardial fibers contract; decreases in
afterload increase fiber shortening. In vivo, afterload is affected by the wall stress exerted
onto the cardiac muscle as much as the impedance of the vasculature and the ejection
pressure the heart has to pump against. LaPlace’s law defines wall stress: The
circumferential wall stress (T) is equal to the pressure (P) times the radius (r) divided by
twice the wall thickness (h). Consequently, afterload is also preload dependent. An increase
in the left ventricular end diastolic volume increases the radius. It also affects the inertial
mass against which the muscle has to pump. Venous return is determined by right atrial
pressure. If right atrial pressure is increased, passive venous return has to overcome this
pressure. In the pediatric heart, the left ventricular performance is reduced, making the
restricted LV prone to ischemia and reperfusion injury.
• The neonatal heart and the effects of neural, hormonal, and local mediators on vascular
tone.
– Neural innervation and responsiveness of the vasculature undergo developmental changes
from the neonate to the adult. The sympathetic nervous system is incomplete at birth
whereas the parasympathetic nervous system is complete. The developed systemic
vasculature embraces a vast network of afferent and efferent signals with multiple effector
site on the heart, smooth muscle vasculature, and endocrine system (e.g., adrenal gland).
In addition, there are sophisticated feedback loops initiated by baroreceptors and
chemoreceptors that are located in the carotid body, aortic arch, and atrial walls.
– Local regulation of vascular tone occurs in response to hypoxemia, hypercarbia, low flow,
and acidosis. The endothelium releases hormonal mediators with autocrine, paracrine, and
endocrine action. Mediators include prostaglandin, nitric oxide, ATP sensitive potassium
channels, and endothelin.
– Glucocorticoid receptors also partake in maintaining vascular tone. Low cortisol may
cause impaired cardiac performance and low vascular tone.
ANATOMY
• In utero the circulatory pattern is in parallel. There are 3 vascular beds (pulmonary,
systemic, and placental) that are connected by shunts in the fetal circulation altering the
specific tasks of the left and right ventricle compared to their work in adult life. The right
ventricle performs two-thirds of the contractile work and thus becomes the dominant
ventricle; it develops greater muscle mass compared to the left ventricle.
– Placenta. Oxygenated blood from the placenta enters the umbilical veins and flows
through the ductus venosus into the inferior vena cava to enter the right atrium.
– Right atrium. The cardiac output is divided to either pass through the open foramen ovale
to the left atrium or through the tricuspid valve into the pulmonary vasculature. The
majority of blood enters the left atrium and joins blood returning from the pulmonary
veins which then passes through the mitral and aortic valve to the coronaries, ascending
aorta, the head vessels and lastly through the descending aorta. Of the blood that enters
the tricuspid valve, only 7% passes through the lungs due to the high vascular resistance;
the remainder is shunted via the ductus arteriosus (PDA) to the descending aorta
• At birth, the placenta is clamped and the foramen ovale and PDA are closed, thereby
establishing an adult cardiac circulatory pattern that pumps blood in series.
• A transitional circulation with right-to-left shunting through an open foramen ovale and/or
PDA may persist in the presence of congenital heart disease or severe lung disease
(meconium aspiration, diaphragmatic hernia, sepsis). It manifests clinically as hypoxia,
hypercarbia, and acidosis. The underlying pathophysiology increases the pulmonary
vascular resistance with resultant increases in right atrial pressures. This facilitates right-to-
left intracardiac shunting via the patent foramen ovale as well as extra-cardiac shunting via
the patent ductus arteriosus.
• Congenital heart disease may present as:
– Decreased systemic perfusion. Low systemic output may be either due to a failing systemic
ventricle or a predominant left-to-right shunt resulting in Qp > Qs.
– Tachypnea develops slowly as the pulmonary vascular resistance falls and the hemoglobin
concentration declines. Decreased PVR results in increased pulmonary blood flow
secondary to left-to-right shunting at the level of the heart or the great vessels. Physiologic
anemia results from decreased erythropoietin levels in response to the relatively hyperoxic
environment compared to in utero.
– Cyanosis occurs when there is decreased pulmonary blood flow from right-to-left shunting
(deoxygenated blood bypasses the lungs and enters the systemic circulation).
• Hypercyanotic spells describe the acute reduction in pulmonary blood flow due to a variable
outflow obstruction to the pulmonary vascular bed. This may be seen in infants with
Tetralogy of Fallot and similar physiology. They present with abnormal respiratory pattern,
severe cyanosis, and changes in the level of consciousness.
• As with the adult, adequate oxygen delivery to the tissues is dependent on systemic blood
flow, hemoglobin concentration, and hemoglobin oxygen saturation.
• Parameters that are unique to the pediatric heart include:
– Bradycardic/parasympathetic response to stress. The neonate response to stress is via the
parasympathetic system. Since neonatal cardiac performance is heart rate dependent, it is
imperative that vagal stimulating procedures are either avoided or anticipated. Pre-
treatment with a parasympatholytic, such as atropine, is advisable. The impact of vagal
stimulation is lessened by general anesthesia and deep ICU sedation.
– The high sympathetic output state of the heart makes the neonate prone to cardiovascular
compromise when using beta-blockers or inhalation anesthetics.
– The neonatal heart improves cardiac output by increasing heart rate rather than by
increasing preload. However adequate preload must be maintained by reducing fasting
periods and/or pre-operative intravenous fluid administration.
– Inotropic support may be necessary to (re)establish the balance between venous return,
optimal right atrial pressure, end diastolic ventricular pressure, and ventricular afterload.
It should be noted that the response to inotropes may be decreased secondary to the
incomplete development of the sympathetic nervous system.
– Elevated levels of ionized calcium may be necessary for optimal cardiac performance in
the neonatal heart.
– Hypocortisolism should be considered in the young infant unresponsive to vasopressor
therapy.
EQUATIONS
• Cardiac Output = Heart Rate × Stroke Volume
• Systemic oxygen delivery = Systemic blood flow (Qs) × oxygen content of systemic arterial
blood
• LaPlace’s Law: T = (P × r)/2 h
• Ohm’s Law: R = P/Q
GRAPHS/FIGURES
Table 1 Cardiovascular variables according to age (1)
REFERENCES
1. Flemming S, Thompson M, Stevens R, et al. Normal ranges of heart rate and respiratory
rate in children from birth to 18 years of age: A systematic review of observational studies.
Lancet. 2011;377(9770):1011–1018.
2. Rohan AJ, Golombek SG. Hypoxia in the term newborn: Part one-cardiopulmonary
physiology and assessment. MCN Am J Matern Child Nurs. 2009; 34(2):106–112.
3. Blackburn S. Placental, fetal, and transitional circulation revisited. J Perinat Neonatal Nurs.
2006; 20(4):290–294.
4. Heymann MA. Control of the pulmonary circulation in the fetus and during transitional
period to air breathing. Eur J Obstet Reprod Biol. 1999;84(2):127–132.
ADDITIONAL READING
• Artman M, Mahony L, Teitel DF. “Neonatal Cardiology" 2nd edition, 2011, McGraw-Hill
• Rudolph AM. “Congenital Diseases of the Heart” 3rd edition, 2009, Wiley-Blackwell.
• Cardiac Output
• Afterload
• Preload
• Oxygen Content
• Pediatric Respiratory Physiology
CLINICAL PEARLS
The newborn, immature heart compared to the adult, has:
• A decrease in:
– Force of contraction
– Velocity of fibrous shortening
– Response to exogenous catecholamines
• Increased dependency upon increases in heart rate to enhance cardiac output.
• Hypothermia in the neonate can severely compromise systemic perfusion. Since the
newborn lacks the ability to shiver it resorts to thermogenesis in the brown fat. Neural input
in response to hypothermia releases noradrenalin in brown fat resulting in the oxidation of
triglyceride. This process increases oxygen consumption of the neonate, making it prone to
lactic acid production (metabolic acidosis may ensue). Acidosis combined with the higher
norepinephrine levels increases pulmonary vascular resistance. Hypothermia induced
increases in PVR may revert the neonate’s circulation back to a transitional fetal circulation
with the inability to oxygenate and to maintain adequate systemic perfusion.
PEDIATRIC RESPIRATORY PHYSIOLOGY
Samuel H. Wald, MD
BASICS
DESCRIPTION
• Pediatric patients have age-dependent respiratory physiology that changes with child
development. The younger the patient, the greater the variance from adult physiology.
• In general, pediatric patients have:
– Increased respiratory rate
– Increased oxygen (O2) consumption
– Increased airway resistance
– Decreased functional residual capacity (FRC)
– Decreased lung compliance
– No change in tidal volumes or dead space per kg
• The increased compliance and shape of the neonatal chest leads to increased work of
breathing and decreased FRC. This, in conjunction with increased O2 consumption, can lead
to rapid desaturation during periods of apnea.
• Infant and toddler respiratory systems continue to develop until approximately 10 years of
age.
• Anatomical differences between the pediatric and adult airways as well as increased
sensitivity to anesthetic-induced upper airway obstruction in neonates and infants may
make mask ventilation and intubation more difficult.
– Compliance:
– In utero, pulmonary respiration is performed by the low resistance placenta and the lungs
remain “collapsed.”
– At birth, pulmonary respiration shifts to the neonate’s lungs. The first breaths require
large pressures (40–80 cm H2O) to overcome the surface forces needed to inflate the
lungs. Adequate surfactant, present in term infants, helps to decrease the inflation
pressures.
– Neonates and infants have decreased lung compliance (compared to older children and
adults) due to the increased airway resistance caused by a relative paucity and immaturity
of alveoli and decreased elastin. Alveoli maturation is not complete until 8–10 years of
age.
– In addition to decreased lung compliance, neonates also have increased chest wall
compliance. This increased compliance is due to cartilaginous ribs and limited thoracic
muscle mass. Less elastin leads to decreased chest wall recoil, decreased dynamic FRC,
and increased work of breathing. As children grow, chest wall compliance decreases with
a resultant decrease in the work of breathing and an increase in the FRC.
• FRC: Adult FRC is 50% of the total lung capacity (TLC); however, infants under general
anesthesia have a FRC as low as 10–15% of the TLC.
– When the FRC decreases to less than closing capacity, small airway closure occurs with
tidal volume breathing, leading to worsened atelectasis, ventilation to perfusion
mismatching, and decreased arterial O2 concentrations.
– The decrease in FRC caused by increased chest wall compliance is overcome in
spontaneously ventilating infants by continued diaphragmatic activity in the early
expiratory phase, relative tachypnea (with start of inspiration during preceding expiration
to cause intrinsic PEEP), as well as sustained tonic activity of respiratory muscles.
– Under general anesthesia, especially with muscle relaxants and paralysis, the
compensatory mechanisms that neonates use to increase dynamic FRC are abolished,
increasing the risk of atelectasis and respiratory insufficiency.
• Ventilation: Neonates have an elevated respiratory rate that will gradually decrease to near
adult levels by adolescence.
– The carbon dioxide (CO2) response curve in neonates is shifted to the right and has a
decreased slope. Thus, a higher arterial CO2 is required to stimulate an increase in minute
volume and the response is also dampened compared to older children and adults.
– The slope of the CO2 response curve increases with postnatal age.
• Oxygenation: Neonates and infants have increased metabolism and O2 consumption.
– Neonates have a bimodal response to hypoxemia. Initially there is a transient increase in
ventilation followed by a sustained decrease in ventilation. This decrease is believed to be
secondary to direct suppression of the medullary respiratory centers and is more
pronounced in premature infants.
– The predominance of fetal hemoglobin (Hgb) in the neonatal circulation shifts the O2–Hgb
dissociation curve to the left. Hgb F has decreased 2,3-DPG causing increased Hgb–O2
affinity and a resultant left shift of the O2–Hgb dissociation curve with a lower P50 (partial
pressure of O2 at which Hgb is 50% saturated).
Neonatal P50 = 19 mm Hg
3 months of age P50 = 27 mm Hg
9 months of age P50 peaks at 29–30 mm Hg
Adult P50 = 27 mm Hg
– Increased concentrations of Hgb may be necessary to maintain adequate O2 delivery in
neonatal patients.
ANATOMY
• The pediatric airway, especially in Neonates and infants have: Neonates and infants can be
more technically challenging for mask ventilation and intubation due to the anatomical
differences when compared to adult airways.
– A proportionally larger occiput and tongue.
– A more cephalad larynx (C2-C4 level compared to C6 in adults).
– A more anterior attachment of the vocal cords.
– A long horse shoe-shaped epiglottis.
– A short trachea and neck.
• The cricoid cartilage is the narrowest point of a pediatric airway until approximately 5 years
of age. In adults, the narrowest point is the glottis.
• Infants are obligate nasal breathers until 5 months of age.
• The neonatal chest wall is composed of cartilaginous ribs with a more horizontal attachment
to the vertebral column. This causes increased chest wall compliance and less efficient
ventilation with increased work of breathing.
• Pediatric patients have much smaller absolute diameters of their upper and lower airways.
Poiseuille’s law for laminar flow (R = 8 Ln/πr4, where R is resistance and r is radius) shows
that even a small decrease in airway radius, when put to the fourth power, will cause a
large reduction in airway caliber (1–2 mm of edema will cause a proportionately larger
obstruction in pediatric patients versus adults, given the smaller diameter of their trachea
and airways).
• Neonates and infants have periodic breathing at baseline. 80% of term infants and 100%
preterm infants will have asymptomatic apnea of <10 seconds without cyanosis or
bradycardia, most often during sleep. General anesthesia increases the frequency of periodic
breathing or “postoperative apnea.”
– The younger the infant, the greater the risk for postoperative apnea; premature infants
have the greatest risk. After general anesthesia, neonates may require postoperative apnea
monitoring for 24 hours depending on post conceptual age.
– Factors associated with postoperative apnea include extent of surgery, anesthesia
technique, anemia, and postoperative hypoxia.
• Pediatric patients frequently suffer from upper respiratory infections (URI) and may present
the day of surgery with recent history of URI.
– During and up to 6 weeks following a URI, pediatric patients may have reactive airways
and are more prone to bronchospasm, laryngospasm, and respiratory complications
following general anesthesia.
– Risk factors for respiratory complications in patients with/following URI:
The younger the age of the patient.
Active symptoms of fever, nasal congestion, rhinorrhea, or productive cough.
History of reactive airway disease.
• Laryngospasm: Sustained tight closure of the vocal cords by contraction of adductor
muscles. More likely to occur in the setting of light anesthesia, recent or current URI,
airway anomalies, ear/nose/throat procedures, hyperventilation with hypocapnia, and
during induction or upon emergence. Treatment for laryngospasm includes increasing the
depth of anesthesia, positive pressure ventilation, and/or muscle relaxation/paralysis.
• Congenital syndromes can be associated with anatomical anomalies causing a more difficult
mask ventilation or intubation. Syndromes known to be associated with difficult airways
include:
– Pierre Robin
– Treacher Collins
– Goldenhar
– Mucopolysaccharidosis
– Down
– Edwards
– Freeman–Sheldon
– Kenny–Caffey
– Schwartz–Jampel
– Cri du chat
• Infants are more prone to desaturation and hypoxia during induction of general anesthesia.
– More sensitive to anesthetic-induced upper airway obstruction.
– Decreased FRC and increased O2 consumption lead to rapid desaturation during periods of
apnea.
• Pediatric airway anatomy can make mask ventilation and intubation more technically
difficult.
– Careful positioning and a shoulder roll can often improve mask ventilation and
endotracheal intubation.
– Proper mask size, an oral airway, and a chin lift or jaw distraction can improve mask
ventilation.
– Blade selection and endotracheal tube (ETT) size are important during pediatric
intubation.
ETT size can be approximated by [(Age in years)/4] + 4
Depth can be estimated by 3 × (ETT size)
See Table 2
– Given that the narrowest point of the pediatric airway is the cricoid cartilage, which is
past the glottis, it is important to check for an airway leak around the ETT at
approximately 20–25 cm H2O to ensure that the ETT is not putting pressure on the
trachea causing airway edema and possible postoperative croup or obstruction.
• Barotrauma. The developing lung in neonates and infants are more prone to barotrauma.
– While either pressure control (PC) or volume control (VC) ventilation can be used
intraoperatively, PC is more commonly used to prevent barotrauma.
• High concentrations of O2 can be damaging to neonates, especially premature neonates.
– The lowest FiO2 possible to maintain adequate oxygenation should be used to prevent
retinopathy of prematurity in susceptible neonates.
– 100% FiO2 can lead to absorption atelectasis after 5 minutes of preoxygenation.
• Positive end expiratory pressure (PEEP) can help counteract the decrease in FRC in infants
under general anesthesia.
– PEEP of 6 cm H2O is recommended in children <6 months of age.
– PEEP of 6 cm H2O can also help combat absorption atelectasis caused by high
concentrations of inspired O2.
• Premature infants are prone to more anesthetic complications including difficulty with
intubation, mask ventilation, and both intraoperative and postoperative ventilation.
Premature neonates have:
– A smaller airway, making intubation technically more difficult.
– Decreased surfactant, immature alveoli, and small lower airway diameters that decrease
lung compliance and ability to ventilate.
– Immature chest wall development that can lead to decreased FRC.
– Underdeveloped respiratory centers with a decreased hypoxic ventilatory response and
higher apneic threshold.
– The possibility of developing persistent pulmonary hypertension from chronic or frequent
hypoxia and hypercapnia. Increased resistance to flow through the pulmonary vasculature
can result in right-to-left shunting via the foramen ovale or ductus arteriosus.
– Increased risk for postoperative apnea.
EQUATIONS
• ETT size = [(Age in years)/4] + 4
• Depth of ETT (cm) = 3 × ETT size
• Poiseuille’s law for laminar flow: R = 8 Ln/πr4
– R = resistance
– L = length
– n = viscosity
– r = radius
GRAPHS/ FIGURES
Table 1 Age-Related Pulmonary Physiology
Table 2 Age-Related Airway Sizes
REFERENCES
1. Colin A, McEvoy C, Castile R. Respiratory morbidity and lung function in preterm infants
32–36 weeks gestational age. Pediatrics. 2010;126:115–128.
2. Von Ungern-Sternberg B, Regli A, Schibler A, et al. The impact of positive end-expiratory
pressure on functional residual capacity and ventilation homogeneity impairment in
anesthetized children exposed to high levels of inspired oxygen. Anesth Analg.
2007;104:1364–1368.
3. Flick R, Wilder R, Peiper S, et al. Risk factors for laryngospasm in children during general
anesthesia. Paediatr Anaesth. 2008;18:289–296.
ADDITIONAL READING
• Cote CJ, Lerman J, Todres ID. A Practice of Anesthesia for Infants and Children. 4th ed.
Philadelphia, PA: Elsevier; 2009.
• Upper respiratory infection, preoperatively
• Laryngospasm
• Work of breathing
• Respiratory system compliance
CLINICAL PEARLS
• Pediatric patients have age-dependent respiratory physiology, with premature infant and
neonatal physiology differing the most from adult respiratory physiology.
– Increased O2 consumption
– Decreased FRC leading to rapid O2 desaturation during periods of apnea
– Immature respiratory centers with decreased ventilatory responses to hypoxia, right
shifting of the CO2 response curve, and decreased apneic threshold
– Increased risk for laryngospasm, postoperative apnea, and respiratory complications of
general anesthesia.
• Premature infants and neonates are at increased risk for laryngospasm, postoperative apnea,
and respiratory complications of general anesthesia.
PERICARDIAL TAMPONADE
Lori Gilbert, MD
BASICS
DESCRIPTION
• Pericardial tamponade is a clinical syndrome caused by accumulation of fluid in the
pericardial space; this creates an increase in intrapericardial pressure that restricts cardiac
filling and decreases cardiac output. Tamponade can result from the accumulation of blood,
pus, or air as a result of effusion, trauma, or rupture of the heart.
• Cardiac tamponade can be due to slow or rapid compression of the heart. Large, slowly
progressing chronic effusions are frequently well tolerated due to compensatory stretching
of the pericardial sac. However, even with compensation, there is a critical point where the
effusion reduces the volume of the cardiac chambers, increases intracavitary pressures, and
causes drastic reduction in preload and cardiac output. Acute collections are a medical
emergency and can be fatal if not quickly recognized and treated.
EPIDEMIOLOGY
Prevalence
• In the US: 2 cases per 10,000 people
• In patients with large pericardial effusions (defined as >10 mm on echocardiogram), 35–
47% will progress to tamponade.
• In patients with end-stage renal disease (ESRD), there is an increased incidence of
pericarditis and pericardial effusions leading to tamponade.
• Malignant effusions are the most common cause of pericardial tamponade.
Prevalence
• Most commonly seen in middle-aged and older populations.
• Tamponade related to trauma or HIV is more common in young adults.
• In regions endemic to tuberculosis, pericarditis is a prominent cause of effusion and
tamponade.
Mortality
Cardiac tamponade is an emergency; it is universally fatal if left untreated.
• Idiopathic (large pericardial effusion)
• Iatrogenic: Postcardiac surgery, electrophysiology procedures (atrial fibrillation and other
ablations), percutaneous valve repair, percutaneous coronary intervention
• Malignancy
• Trauma
• ESRD/uremia
• Drugs: Hydralazine, procainamide, isoniazid, minoxidil
• Less common causes: Collagen vascular disease (lupus, scleroderma), tuberculosis, radiation,
bacterial and fungal infections, HIV infection
• The pericardial sac consists of the visceral and parietal layers that surround the heart. The
pericardial sac normally contains up to 50 mL of serous fluid that minimizes friction on the
epicardium and thus helps to equalize hydrostatic pressures over the heart surface.
Therefore, the pericardium has a small reserve volume and once the critical volume is
reached, intracardiac filling pressures increase and diastolic volumes decrease. This results
in a dramatic impairment of cardiac filling and a concomitant reduction in cardiac output.
• In an effort to prevent chamber collapse, ventricular diastolic, right atrial, and wedge (left
atrial) pressures all rise to equal pericardial pressures. This equalization of pressures is
highly characteristic of tamponade.
• Pulsus paradoxus is an exaggeration of the normal drop in systemic BP with inspiration
(>10 mm Hg). With inspiration, there is increased venous return to the right, “full” heart.
The increased volume pushes the intraatrial and intraventricular septums into the left heart.
This results in decreased volumes of the left heart which manifests as a decrease in systemic
cardiac output and a drop in systemic BP.
• “Full, fast, forward:" Avoid decreases in volume, bradycardia, vasodilation, and cardiac
depression. The primary derangement is a decrease in stroke volume from impaired preload
secondary to decreased ventricular chamber size.
– Maintain filling pressures to overcome diastolic filling restrictions
– Heart rate is a critical determinant of CO, as stroke volumes are significantly decreased
(CO = SV × HR)
– Increased vascular tone is necessary to maintain perfusion to the heart and brain, as
SV/CO is decreased
– Contractility is necessary to maintain efficient ejection of the stroke volume
• Anesthetic technique should maintain a high sympathetic output until tamponade is
relieved.
SYMPTOMS
• Dyspnea, tachycardia, tachypnea, chest pain, syncope
• Weight loss, fatigue, anorexia may be seen in patients with malignancy or systemic disease
• Musculoskeletal pain or fever may be present with connective tissue disorder
• Night sweats, fever, weight loss can occur in patients with tuberculosis
• Feeling of impending doom
History
• Recent cardiovascular surgery, coronary intervention, or trauma
• Malignancy
• Renal failure (uremic pericarditis)
• IV drug abuse or opportunistic infections (HIV)
• Recent chest wall radiation
• Lupus/drug-induced lupus
• Recent pacemaker lead implantation
Signs/Physical Exam
• Elevated jugular venous pressure (JVP): Kussmaul’s sign describes a paradoxical rise in JVP
on inspiration (instead of the normal decrease)
• Pulsus paradoxus: Inspiratory systolic fall in arterial pressure of 10 mm Hg or more during
normal breathing
• Muffled heart tones
• Hypotension, tachycardia; diaphoresis, dyspnea
• Ewart’s sign: Bronchial breathing and dullness on percussion at the lower angle of the left
scapula in pericardial effusion.
• Y-descent on the central line waveform is abolished due to decreased diastolic filling of the
ventricles (they are “full”). The X-descent is accentuated.
TREATMENT HISTORY
• Needle pericardiocentesis may be performed to relieve intracardiac pressures; the use of
imaging such as fluoroscopy, CT or echocardiographic techniques may be utilized. The most
common approach for pericardiocentesis is the paraxiphoid, between the xiphoid and the
left costal margin.
• In hypotensive patients, volume expansion may be used as a temporizing measure; however,
volume expansion in someone with active tamponade has been associated with increased
intra-pericardial pressures, RA pressure and LV end-diastolic pressure.
• Pericardiectomy (pericardial window) may also be indicated for hemodynamically unstable
patients or in patients with recurrent tamponade.
• Treat the underlying cause.
MEDICATIONS
• Ibuprofen, aspirin for pericarditis
• Stomach acid reducer (H2 blocker, proton pump inhibitor)
Labs/Studies
• Doppler echocardiography can reveal chamber collapse of the right atrium, which may also
be seen in hypovolemia without tamponade. Right ventricular collapse is a more specific
finding for tamponade.
• CXR
• CBC to evaluate for infective or anemic causes
• ESR to evaluate for inflammatory causes
• Cardiac enzymes
• ECG can reveal low voltage QRS complexes, PR segment depression, or electrical alternans,
which describes alternate-beat variation in the direction or amplitude of any ECG waveform
segment.
• Pericardiocentesis fluid for culture and cytology.
• Cardiac catheterization (Swan–Ganz)
• Renal failure (uremic pericarditis)
• Pulmonary disease (e.g., tuberculosis)
• Joint disease (e.g., lupus, rheumatoid arthritis)
• Hypothyroidism
Pericardiocentesis under local anesthesia prior to induction of general anesthesia with
sternotomy.
CLASSIFICATIONS
• Acute tamponade (immediately life threatening): Trauma, aortic rupture, or as a
complication of an invasive diagnostic or therapeutic intervention.
• Sub-acute tamponade (chronic): Malignancy, uremia, tuberculosis, or idiopathic pericarditis.
Large amounts of pericardial fluid are tolerated until the critical ‘knee’ is reached on the
pressure/volume curve of the heart.
• Low pressure tamponade: Hemodialysis, traumatic hemorrhage, or over-diuresis; patients
may be severely hypovolemic. Intracardiac and pericardial diastolic pressures are only 6 to
12 mm Hg. Patients may require a fluid challenge of 1 L isotonic saline to elicit tamponade
dynamics.
TREATMENT
Premedications
• Epinephrine or other vasopressors, inotropes/chronotropes may be needed.
• Low-dose ketamine can be started with midazolam if local anesthesia with sedation is to be
used.
• Prep and drape the patient before induction if tamponade has not been relieved by needle
pericardiocentesis.
• In large, chronic effusions and minimal degrees of tamponade, the patient is often capable of
giving consent on their own.
• Acute tamponade is considered immediately life threatening and the decision to proceed is
dictated by common sense even without formal consent.
INTRAOPERATIVE CARE
• Local anesthesia with sedation to maintain spontaneous ventilation
• General anesthesia with spontaneous ventilation
• General anesthesia with positive pressure ventilation; surgeon must be prepared to
emergently perform a sternotomy and relieve pressure.
Monitors
• Large bore IV access
• Arterial line
• Continuous transesophageal echocardiography (TEE) if possible to assess ventricular filling
and contractility.
• General anesthesia with spontaneous ventilation: Mask induction with volatile agents
and/or ketamine may be considered.
• General anesthesia with positive pressure ventilation: Select agents that minimize depression
of cardiac function and cause the least vasodilation and hypotension, such as ketamine or
etomidate. Despite the benefit of maintaining spontaneous ventilation, patients are often
induced, made apneic, intubated, and ventilated with positive pressure. When this occurs,
the patient must be prepped and draped and the surgeons immediately prepared to perform
a sternotomy.
• Awake intubation that maintains spontaneous ventilation can lead to coughing or bucking,
which increases intrathoracic pressure.
Maintenance
• Mechanical ventilation with positive pressure (increased intrathoracic pressures) will further
decrease cardiac output by decreasing preload as well as increasing right ventricular
afterload (decreases right ventricular outflow and forward flow).
• Volume: Maintain filling pressures high enough to overcome diastolic filling restriction. CVP
or PCWP may need to be >20–30 mm Hg.
• Avoid vasodilation, bradycardia and maintain a high sympathetic output until tamponade is
relieved. Inotropes and chronotropes may be needed
Extubation/ Emergence
• Patients are still at risk for pulmonary venous congestion or pulmonary edema from a
sudden increase of pulmonary vascular return to the left atrium.
• Patients with pre-existing left ventricular dysfunction, coronary artery disease, or valvular
dysfunction should be observed.
• Extubation is guided by individual cases: Traumatic, medical, or other causes of tamponade
may lead one to keep the patient intubated depending on hemodynamics.
• Treat hypertension appropriately.
FOLLOW-UP
BED ACUITY
The patient should be sent to the ICU where adequate monitoring for signs of re-accumulation
of fluid, myocardial infarction, and other pathology can be observed and rapidly treated.
• EKG, echocardiogram
• Treat sudden increases in SVR/hypertension
• Cardiac enzymes
• Consults: Cardiology, cardiothoracic surgery
COMPLICATIONS
A possible post-drainage complication is pulmonary edema, which occurs most frequently in
patients with chronic pericardial effusion who have had large volume pericardiocentesis.
REFERENCES
1. O’Connor C, Tuman K. The Intraoperative management of patients with pericardial
tamponade. Anesthesiol Clin. 2010;28:87–96.
2. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:684–690.
3. Khandaker M, Espinosa RE, Nishimura RA, et al. Pericardial disease: Diagnosis and
management. Mayo Clinic Proceedings. 2010;85(6):572–593.
4. Aye T, Milne B. Ketamine anesthesia for pericardial window in a patient with severe COPD.
Can J Anesth. 2002;49(3):283–286.
ADDITIONAL READING
• www.cardiosource.org (American College of Cardiology)
• Uremia
CODES
ICD9
423.3 Cardiac tamponade
ICD10
I31.4 Cardiac tamponade
CLINICAL PEARLS
• The differential diagnosis for cardiac tamponade is constrictive pericarditis, pulmonary
embolism, and tension pneumothorax.
PERIOPERATIVE BLINDNESS
John L. Ard Jr., MD
BASICS
DESCRIPTION
• Vision loss after nonocular surgery is a devastating complication that is most often
associated with:
– Spine surgery (1)
– Cardiac surgery (1)
– Head and neck operations (1)
• The most common diagnoses include:
– Posterior ischemic optic neuropathy (PION)
– Anterior ischemic optic neuropathy (AION)
– Central retinal artery occlusion (CRAO)
– Occipital infarct (cortical blindness)
• Although a minority of patients recover some partial vision, the improvement is often
clinically insignificant. In addition, there are no proven treatment options.
EPIDEMIOLOGY
Prevalence
Depends on the type of surgery
• Cardiac surgery: 8.64 cases/10,000 surgeries (2)
• Spinal fusion: 3.09 cases/10,000 surgeries (2)
• Appendectomy: 0.12 cases/10,000 surgeries (2)
• Age range: 5–81 years
• Male > female
Morbidity
Depends on the diagnosis
• ION (anterior and posterior)
– Usually bilateral, painless vision loss
– Afferent pupil defect or nonreactive pupil
– No light perception
– Color vision is decreased or absent
• CRAO
– Unilateral vision loss
– No light perception
– Afferent pupil defect
– After prone spine surgery, it is often associated with periorbital or eyelid edema,
chemosis, proptosis, ptosis
• Cortical blindness
– Patients have reduced vision with normal pupil reaction, intact corneal reflexes, and
normal eye movement.
• Ischemic optic neuropathy (posterior): The etiology or cause of this complication is
unknown but it is presumably a vascular injury caused by arterial hypoperfusion or possibly
elevated venous pressures secondary to prone positioning and/or interstitial tissue edema.
– Occurs most commonly in prone spine surgery of long duration (>6 hours) and large
blood loss (>1 L).
– Also occurs in cardiac surgery, head and neck surgery, but rarely in other types of surgery.
– Other associated factors (not necessarily causative)
Hypotension
Anemia
Excessive fluid administration
Vasopressors
Elevated venous pressure
• Ischemic optic neuropathy (anterior): The etiology is unknown, but like posterior ION, it is
presumably a vascular injury caused by arterial hypoperfusion or possibly elevated venous
pressure. Occurs most frequently after cardiac surgery but can also occur in prone spine and
head and neck surgeries (3).
• Central retinal artery occlusion: Emboli are the usual cause in cardiac surgery; whereas
direct pressure on the globe causes this injury in the prone spine surgery.
• Cortical blindness: The etiology is ischemia and infarction involving the occipital lobe of the
brain (where the visual cortex is located). It is either due to emboli that occur secondary to
manipulation of the great vessels during cardiac or vascular surgery, or from hypoperfusion
secondary to hypotension. The parieto-occipital region of the brain is a watershed zone for
the middle cerebral and posterior cerebral arteries, and may undergo infarction during
periods of systemic hypotension or if emboli block blood supply. Neuronal cell death is
imminent after approximately 6 minutes of halted blood circulation.
– Risk factors (4)
Hypertension
Diabetes mellitus
Renal insufficiency
Smoking history
COPD
Peripheral vascular disease
Cardiac disease
• Normal anatomy of the optic nerve:
– Contains myelinated axons that arise from the ganglion cells in the retina.
• Nerve fibers traverse from (distal to proximal)
– Head and ocular portions traverse the sclera
– Orbital portion is ~3 cm in length
– Optic canal extends to the optic chiasm; it then travels through the brain
– Visual cortex is found in the occipital lobe of the brain (final destination)
– Arterial blood supply (subject to anatomic variation):
Anterior to the lamina cribrosa: Derived from the short ciliary arteries
Posterior to the lamina cribrosa: Derived from the circle of Zinn
Orbital portion: Derived from the pial circulation which are end branches of the
ophthalmic and retinal arteries.
– Optic nerve venous drainage: The ocular and orbital portions flow primarily into the
central retinal vein.
• ION in prone spine surgery: Since the etiology is uncertain, preventive measures are
speculative.
– Colloids as well as crystalloids should be used for resuscitation in large blood loss cases
(5)[C].
– Head should be positioned level with, or higher than, the heart, if possible (5)[C].
– Head should be in a neutral position (5)[C].
– Consider staging long spinal procedures (5)[C].
• CRAO
– Prone spine surgery: Ensure proper positioning of the head with frequent eye checks to
assure that the eyes are pressure free
– Cardiac surgery: Efforts should be made to reduce the incidence of emboli during surgery
• Patients should be evaluated in the immediate postoperative period. Vision loss usually
manifests as soon as the patient is conscious.
• Urgent ophthalmology consult is mandatory.
– PION: Optic disk appears normal, initially.
– AION: Optic disc edema and hemorrhages on fundoscopic examination.
– CRAO: Macular/retinal edema, cherry red spot, or attenuated retinal vessels are typical on
fundoscopic examination.
• If diagnosis is not apparent after eye examination, then neurological imaging is in order,
preferably MRI with gadolinium and stroke protocol technique (6)[C].
Corneal abrasion
TREATMENT
• ION (anterior and posterior)

– Optimize hemoglobin levels, hemodynamic status, and oxygenation (5)[C].
– Agents that lower intraocular pressure like acetazolamide have been administered
unsuccessfully.
• CRAO
– Optimize hemoglobin levels, hemodynamic status, and oxygenation (5)[C].
• Cortical blindness
– Increase oxygen delivery to the visual cortex by optimizing cerebral perfusion pressure
and hematocrit (6)[C].
FOLLOW-UP
As per ophthalmology
CLOSED CLAIMS DATA
• In 1999, the American Society of Anesthesiologists established the Postoperative Visual Loss
Registry to investigate the mechanism of perioperative ION.
• As of 2006, 93 spine surgery cases had been collected.
– 83 cases were diagnosed with ION
– 10 cases were diagnosed with CRAO
REFERENCES
1. ee LA, Roth S, Posner KL, et al. The American Society of Anesthesiologists Postoperative
Visual Loss Registry: Analysis of 93 spine surgery cases with postoperative visual loss.
Anesthesiology. 2006;105:652–659
2. Yang S, Drum M, Roth S. The prevalence of perioperative visual loss in the United States: A
10-year study from 1996 to 2005 of spinal, orthopedic, cardiac and general surgery.
International Anesthesia Research Society. 2009;109:1534–1545.
3. Roth S. Perioperative visual loss: what do we know, what can we do? Br J Anaes.
2009;103:i31–i40.
4. Berg K, Harrison A, Lee M. Perioperative visual loss in ocular and nonocular surgery. Clin
Ophthalmol. 2010;4:531–546.
5. American Society of Anesthesiologists Task Force on Perioperative Blindness. Practice
advisory for perioperative visual loss associated with spine surgery. A report by the
American Society of Anesthesiologists Task Force on Perioperative Blindness.
6. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol.
2008;145:604–610.
ADDITIONAL READING
• ASA Closed Claims Postoperative Visual Loss Registry:
http://depts.washington.edu/asaccp/eye/index.shtml
• Corneal abrasion
CODES
ICD9
• 362.31 Central retinal artery occlusion
• 377.41 Ischemic optic neuropathy
• 377.75 Cortical blindness
ICD10
• H34.10 Central retinal artery occlusion, unspecified eye
• H47.019 Ischemic optic neuropathy, unspecified eye
• H47.619 Cortical blindness, unspecified side of brain
CLINICAL PEARLS
• Patients undergoing prolonged spinal surgery in the prone position with an expected large
blood loss are at increased risk for postoperative blindness.
– Consider informing these patients of the risk of visual loss in their preoperative visit.
– Consider CVP monitoring.
– Balanced colloid and crystalloid resuscitation.
• Document positioning and eye checks on anesthesia record.
• This injury occurs infrequently so it is difficult to study.
PERIOPERATIVE HYPERTENSION
Cameron J. Ricks, MD
BASICS
DESCRIPTION
• Hypertension:
– Systolic BP >140 mm Hg
– Diastolic BP >90 mm Hg
• Hypertensive crisis or emergency:
– Systolic BP >180 mm Hg
– Diastolic BP >120 mm Hg
– Accompanied by end-organ dysfunction such as hypertensive encephalopathy,
intracerebral hemorrhage, subarachnoid hemorrhage, acute stroke, unstable angina, acute
myocardial infarction, congestive heart failure, acute renal dysfunction, and acute aortic
dissection.
• Hypertensive urgency is defined as a severe elevation in BP without progressive end-organ
dysfunction.
EPIDEMIOLOGY
Prevalence
• In general, the worldwide prevalence of hypertension may be as high as 1 billion people. In
the US, over 50 million people have BP warranting some form of treatment.
• Primary hypertension: 90–95%
• Secondary hypertension: 5–10%
Morbidity
Perioperatively: Diastolic BP >110 mm Hg has been shown to increase cardiac complications
such as bradycardia, tachycardia, and ischemia.
Mortality
• ∼7.1 million deaths can be attributed to hypertension worldwide.
• Perioperatively, hypertensives have a 3.8 times increased odds ratio of postoperative death
compared to normotensives. The 30-day postoperative cardiac mortality is 4 times that of
age-matched controls.
• Primary hypertension: Sedentary lifestyle, stress, obesity (in particular visceral),
hypokalemia, salt sensitivity, alcohol intake, vitamin D deficiency, aging, family history.
Other correlating factors include elevated renin, sympathetic nervous system overactivity,
insulin resistance (Syndrome X or metabolic syndrome), and low birth weight.
• Secondary hypertension: Conditions that affect the kidneys, arteries, heart, or endocrine
systems such as renal stenosis, coarctation of the aorta, pheochromocytoma, preeclampsia,
and Cushing’s disease.
• Systolic BP
– Within the heart, it refers to the pressure during a cardiac contraction and requires
invasive monitoring.
– In the periphery, it can be measured with a non-invasive BP cuff. It measures the resultant
pulsatile pressure against the peripheral vasculature from the blood ejected during cardiac
systole.
– Systole accounts for 1/3rd of the systole–diastole cycle.
• Diastolic BP
– Within the heart, it refers to the pressure of the relaxed ventricles.
– In the peripheral vasculature, it refers to the tone of the arteries.
• Mean arterial pressure is the average pressure in the heart and vasculature. It is calculated
as follows, MAP = 2/3 (diastolic pressure) + 1/3 (systolic pressure).
• Primary hypertension is not well understood.
– During the early stages, there is increased cardiac output and normal total peripheral
resistance.
– With time, the cardiac output drops to normal levels, but the total peripheral resistance
increases.
– Theories include the inability of the kidneys to excrete sodium, causes natriuretic factor to
increase (excretes sodium, but side effect is increased total peripheral resistance);
overactive renin–angiotensin system causing vasoconstriction and retention of sodium and
water (increased blood volume causes hypertension); and overactive sympathetic nervous
system leading to increased stress response.
– The end result is reduced intravascular volume and increased total peripheral resistance.
– With time, this can lead to hemodynamic instability perioperatively (see below) and end-
organ damage.
Central nervous system (CNS)
Cardiac
Renal
Retina
Metabolic
• Preoperatively: Patients can present with anxiety about the procedure/anesthesia or without
taking their scheduled morning antihypertensive.
• Intraoperatively: Induction often produces an exaggerated drop in BP attributed to the
sympatholysis from induction medications combined with the intravascular hypovolemia
from abnormal fluid regulation with hypertension (sympatholytics unmask the relative
hypovolemia). Laryngoscopy often demonstrates an exaggerated increase in BP likely due to
an exaggerated sympathetic response. Hypotension during maintenance often occurs from
direct vascular dilation or sympatholysis.
• Postoperative: The early post-anesthesia period is associated with pain-induced sympathetic
stimulation, hypothermia, hypoxia, and intravascular volume overload. In addition, fluid
mobilization 24–48 hours postoperatively results in intravascular hypervolemia.
• Preoperative evaluation to allay fears and concerns as well as advise about BP medications.
– Preoperative clinic may allow the opportunity, if identified early enough, to optimize
poorly controlled hypertension with the primary care physician
– A phone call the night prior to surgery (along with proper instructions for
antihypertensive medications on the morning of surgery), meeting preoperatively to
discuss the operative course thoroughly, and home anxiolysis can aid in BP control.
• Induction and laryngoscopy: Anticipate instability. These events occur back to back with
widely different hemodynamic responses.
– Propofol decreases preload, afterload, and contractility, hypotension may be avoided with
slower and smaller doses.
– Etomidate may provide more stable hemodynamics. A balanced induction with etomidate
and propofol can avoid hypotension and hypertension.
– Large narcotic doses can reduce induction medications and may blunt the sympathetic
response to laryngoscopy. Although it preserves cardiac contractility, it may blunt
sympathetic drive with resultant bradycardia and vasodilation.
– Administration of vasopressors as appropriate; performing a laryngoscopy and intubation
to “treat” hypotension prior to readiness is a poor practice.
– Lidocaine IV or topical may blunt sympathetic response to laryngoscopy.
– Volatile agents during bag mask ventilation can blunt sympathetic response.
– Airway instrumentation should be performed quickly and effectively.
– Preoperative placement of an arterial line or frequent BP cuff measurements (change
frequency) may improve appropriate titration of medications.
• Intraoperatively: Periods of low stimulation may be met with hypotension or a BP that
precludes adequate perfusion of vital organs.
– Assessment of volume status: NPO, maintenance, insensible and blood loss, other causes
such as sepsis or anaphylaxis. Volume replacement should be performed; avoid
overhydration which can result in postoperative fluid shifting.
– Titrate narcotics and epidural boluses slowly to assess effects and have the opportunity to
treat hypotension.
– Heart rate, and rhythm should be optimized.
– Reduction of volatile or TIVA while maintaining unconsciousness.
– Nitrous oxide can maintain hemodynamics to a greater extent than volatile agents;
additionally, it allows for “titrating down” volatile agents.
– During stimulation, hypertensives may have an exaggerated response. Consider titrating
short-acting medications, particularly if it is felt that the stimulation will be short lived
(e.g., propofol, volatile agents, esmolol, nitroglycerine, calcium channel blockers).
• Emergence: Consider titrating longer-acting antihypertensives if the patient’s BP starts
increasing. Choices include metoprolol, labetalol, and hydralazine.
• Postoperative: Orders for antihypertensive medications should identify titration parameters
and appropriate dosing. If ineffective, consider alternative medications, telemetry, or ICU
admission. Appropriate pain management should be provided (consider regional blocks,
PCA, local infiltration, as appropriate). Pain, anxiety, delirium, hypoxia, and hypercarbia
can result in hypertension and should be appropriately managed.
• Non-invasive BP cuff (forearm, arm, calf) and/or invasive arterial line (radial, brachial,
axillary, femoral, dorsalis pedis).
• Hypertensive crisis
– CNS symptoms include motor, sensory, speech, visual defects from a stroke, or confusion,
headache, and convulsions from hypertensive encephalopathy
– Cardiac symptoms include angina, or angina equivalent (awake patient), EKG changes,
drop in BP, arrhythmias, heart failure and desaturation
– Renal: Hypertensive nephropathy
– Retina: Hypertensive retinopathy
– Metabolic: Elevated sugar levels
• Incorrect reading from poor technique, such as small cuff, or inappropriate placement.
• Cushing’s response from increased intracranial pressure (an adaptive measure that increases
the mean arterial pressure in order to preserve adequate cerebral perfusion; classically
accompanied by bradycardia and irregular respirations).
TREATMENT
• Confirm accuracy with a different limb, ascertaining correct cuff size and proper technique
before administering therapy.
• Determine baseline value from the patient, clinic documents, and/or preoperative
evaluation. Assess for target organ damage as discussed above.
• Hypertensive crisis/emergency
– Cancel surgery
– Place IV line
– Treat with IV medications, boluses or drips; metoprolol, labetalol, hydralazine, diltiazem,
or nitroglycerin.
– Arrange for ER admission or direct admission to telemetry or ICU. It is the anaesthetist’s
responsibility to coordinate a higher level or specialized care. Cancelling the case and
telling the patient to follow up with their primary physician, check BP at home, take
home medications, or drive to the emergency room may be construed as abandonment. In
an ambulatory center, consider calling 911 for hospital transfer.
– Consider arterial line placement.
• Hypertensive urgency
– Review antihypertensive medications.
– Consider having patient take home medication with a small sip of water or administering
the IV equivalent (metoprolol, hydralazine), or another IV antihypertensive.
– Treat anxiolysis with good communication, discussion with the patient, and, if needed,
anxiolytic medications.
– The decision to proceed with the surgery is dependent upon several factors: Urgency of
the procedure (cancer diagnosis), BP measurement, other co-morbidities, anaesthetist’s
personal experience, baseline BP, etc.
• Induction and laryngoscopy are short-lived; derangements in BP should be treated with
short-acting medications to avoid “ups and downs.”
• Intraoperative: Consider phenylephrine, ephedrine or epinephrine boluses to temporize
hypotension. If it is felt that the cause of hypotension is the profound reduction in systemic
vascular resistance from volatile agents, consider phenylephrine infusion to provide alpha
agonism and avoid “swings” in perfusion pressures.
• Postoperative: The early post-anesthesia period can be associated with exaggerated
sympathetic stimulation from pain, hypothermia, hypoxia, and volume overload. Focus on
treatment of the cause.
FOLLOW-UP
• Undiagnosed hypertension: Should follow up with their primary care physician for further
work-up after procedure.
• Hypertensive urgency: Should consider admission to the floor, telemetry, or the ICU for
monitoring and treatment.
• Hypertensive emergency: Should be treated immediately with IV medication to a goal of
MAP reduction no more than 20% and transferred to the ICU for monitoring and IV BP
control.
CLOSED CLAIMS DATA
Not investigated
REFERENCES
1. eventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure. The JNC 7 Report. JAMA. 2003;289:2560–2672.
2. ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac
Surgery (Committee to update the 1996 Guidelines on Perioperative Cardiovascular
Evaluation for Noncardiac Surgery). J Am Coll Cardiol. 2002;39:542–553.
3. Marvik PE, Varon JV. Perioperative hypertension: a review of current and emerging
therapeutic agents. J of Clin Anes. 2009;21:220–229.
ADDITIONAL READING
• Howell SJ, Sear JW, Foex P. Hypertension, hypertensive heart disease and periopeative
cardiac risk. Br J Anaesth. 2004;92(4):570–583.
• Hypertension
CODES
ICD9
• 401.9 Unspecified essential hypertension
• 405.99 Other unspecified secondary hypertension
ICD10
• I10 Essential (primary) hypertension
• I15.9 Secondary hypertension, unspecified
CLINICAL PEARLS
• Careful consideration of the patient’s baseline BP as well as the urgency and type of surgery
should be considered prior to case cancellation.
• Hypercarbia, hypoxia, and pain are common intraoperative and postoperative causes of
hypertension.
PERIOPERATIVE SEIZURES
BASICS
DESCRIPTION
• Perioperative seizures occur mostly in patients with a preexisting seizure disorder. In
particular, those with:
– Frequent seizures at baseline
– Recent seizure activity
– Multiple antiepileptic drugs (AEDs)
• They can also occur in patients with metabolic derangements, local anesthetic systemic
toxicity, or from anesthetic medications. Pathological processes that result in myoclonic
movements may be misconstrued as a seizure.
• Perioperative seizures have not been shown to be influenced by anesthesia type (general,
MAC, regional) or procedure.
EPIDEMIOLOGY
Prevalence
• General population: Occurs in 0.03% for all patients undergoing all types of anesthesia.
• Diagnosis of seizure disorder: Occurs in 2–5.8% undergoing all types of anesthesia.
• Incidence is increased in the pediatric population as well as those who are intellectually and
developmentally delayed.
Prevalence
Related to the patient’s underlying condition, as opposed to the type of anesthesia. It is more
likely to occur in patients who have frequent seizures, especially if they have had seizures
close to the time of the procedure, and if they require multiple antiepileptic medications.
Morbidity
• Perioperative seizures often resolve without medication.
• Injury to the tongue, head, or extremities may result as well as aspiration of stomach
contents.
• Prolonged seizures may result in cerebral ischemia leading to coma and death.
• In the perioperative setting where patients are fasting and anxious, factors that may
contribute to seizures include:
– Antiepileptic medication noncompliance (missed or delayed dosing)
– Altered gastrointestinal absorption of antiseizure medications
– Electrolyte disturbances
– Sleep deprivation
• Anesthetics with pro-convulsant potential:
– Inhaled volatile anesthetics (e.g., enflurane, sevoflurane) with rapid changes in brain
concentration
– Local anesthetics (e.g., lidocaine, bupivacaine) have the potential to be pro-convulsant
even at non-toxic levels.
– Opioids (e.g., fentanyl, alfentanil, sufentanil, meperidine)
– Sedative/hypnotic medications (e.g., propofol, etomidate, ketamine, methohexital)
– Of note, despite the pro-convulsant potential, most anesthetics have both proconvulsant
and anticonvulsant properties.
• The mechanism of anesthetic effect on seizure threshold is speculated to be a result of an
imbalance between excitatory and inhibitory neurotransmission. Most perioperative seizures
occur at induction or emergence when anesthetic levels are changing rapidly.
• The incidence of epilepsy is higher in the intellectually and developmentally disabled
population, and there is increased morbidity and mortality in children with seizures and
neurologic deficits. This group of patients tends to have more frequent seizures and often
requires anesthesia for routine procedures (e.g., radiologic examinations and dental
examinations and treatment) or procedures related to trauma incurred during a seizure that
a healthy patient otherwise would not require.
– The CNS is more sensitive to local anesthetics than the cardiovascular system. Classic early
symptoms include circumoral numbness, metallic taste, lightheadedness, visual and
auditory disturbances, agitation, or tremors. Later symptoms consist of seizures and coma.
– First, a preferential blockade of the inhibitory CNS pathways leaves the excitatory
pathways unopposed. This can manifest as shivering/muscle tremors and proceed to
tonic–clonic seizures. With increasing plasma levels, both inhibitory and excitatory
pathways are blocked. Generalized CNS depression ensues with potential respiratory
arrest.
– Potent, longer acting, and R(+) isomers of local anesthetics such as bupivacaine tend to
be more toxic.
– Hypoxia and hypercarbia can decrease the convulsive threshold.
• Hypoglycemia can result in neuroglycopenia with headache, confusion, mental sluggishness,
seizures, or coma. Patients at greatest risk are those receiving parenteral nutrition with
dextrose-containing solutions that are abruptly stopped. Neonates require dextrose infusions
because they lack glycogen stores due to hepatic immaturity. In addition, in diabetics, long-
acting insulin preparations and oral hypoglycemics can result in hypoglycemia when
combined with NPO status.
• Hypoxia leading to brain ischemia can present as seizures in addition to other neurologic
deficits.
• Electrolyte abnormalities such as hyponatremia and hypocalcemia have been reported to
lower the seizure threshold.
• Febrile seizures: There are no reports of this occurring under anesthesia. The pathogenesis
involves a rapid rise in temperature, usually from a viral infection. Intraoperative
temperatures do not rise that rapidly, especially when monitored.
• Since patients with frequent seizures at baseline are at highest risk of having a seizure in the
perioperative period, it is essential to be prepared to treat seizure activity regardless of the
surgical procedure or anesthetic technique. In addition, avoid missing doses of AEDs and
consider IV dosing if the patient is not tolerating PO intake.
• Patients on parenteral nutrition with dextrose-containing solutions should have their
infusions weaned and not stopped to avoid hypoglycemia. Consider more frequent blood
sugar monitoring.
• Diabetics should have their blood sugars checked prior to surgery as well as be instructed to
hold long-acting insulin preparations and oral hypoglycemics. Ideally, their procedures
should be scheduled early in the morning to avoid excessive fasting periods.
• In patients with febrile seizure history, it is important to monitor temperature and treat with
cooling measures and antipyretics when necessary (per oral or per rectal).
• Initial diagnosis is usually on the basis of clinical signs: Tonic–clonic, tonic, clonic, or
myoclonic movements that do not resolve. The seizure may be associated with a loss of
consciousness and/or postictal sedation.
• Status epilepticus is defined either as simple prolonged seizure, or recurrent seizures, with
decreased consciousness for longer than 30 minutes.
• Delayed awakening should include the possibility of a postictal state, as well as:
– Residual anesthetics (volatile, opioid, benzodiazepine, etc.)
– Coma
• “Seizure-like” or myoclonic activity may be the result of:
– Rigors and shivering
– Sepsis
– Neuromuscular syndrome (NMS)
– Malignant hyperthermia (MH)
– Thyroid toxicosis
– It should be noted that true seizures may also occur with NMS, MH, and thyroid toxicosis.
• Anesthetic drug–induced myoclonic movements have an unknown pathogenesis and this
symptomatic presentation differs from their proconvulsant effects.
TREATMENT
• Perioperative seizures often resolve without therapy.

• Although the cessation of seizure activity is critical, it is also important to discern treatable
causes; for example, hypoxia, metabolic derangements, non-therapeutic AED levels.
• Supportive measures include supplemental oxygen with facemask or assisting ventilation
with a bag mask. Patients at risk for pulmonary aspiration should be placed in the lateral
position. Consider padding areas of potential traumatic injury.
• Seizures lasting longer than 5 minutes can be treated with benzodiazepines. If this therapy
fails, consider the administration of barbiturates or phenytoin. In patients with a history of
epilepsy, the family or caregivers may have experience with treatment options that have
been successful in the past.
• The development of status epilepticus may require the induction and maintenance of
general anesthesia to avoid brain ischemia and coma; consultation with a neurologist should
be performed as soon as possible. Induction with intravenous medications (propofol,
etomidate) should be followed by the placement and continuous monitoring of EEG.
Although the classic teaching has been to utilize volatile agents for maintenance, there have
been reports of the successful use of propofol, etomidate, and even ketamine. Muscle
relaxants stop extremity movement and tongue biting and may be considered to decrease
the risk of injury; however, it should be noted that they have no effect on stopping electrical
seizure activity.
FOLLOW-UP
Consider postoperative EEG monitoring if the patient continues to have seizures, as well as a
neurology consultation.
REFERENCES
1. iesen AD, Jacob AK, Aho LE, et al. Perioperative seizures in patients with a history of a
seizure disorder. Anesth Analg. 2010;111(3):729–735.
2. Benish SM, Cascino GD, Warner ME, et al. Effect of general anesthesia in patients with
epilepsy: A population-based study. Epilepsy Behav. 2010;17(1):87–89.
3. Kopp SL, Wynd KP, Horlocker TT, et al. Regional blockade in patients with a history of a
seizure disorder. Anesth Analg. 2009;109(1):272–278.
4. Cheng M, Tempelhoff R. Anesthesia and epilepsy. Curr Opin Anaesthesiol. 1999;12(5);523–
528.
5. Ren WH. Anesthetic management of epileptic pediatric patients. Int Anesthesiol Clin.
2009;47(3):101–116.
• Seizure disorders
• Hypoglycemia
• Hyponatremia
CODES
ICD9
780.39 Other convulsions
ICD10
R56.9 Unspecified convulsions
CLINICAL PEARLS
• Since patients with frequent seizures at baseline are at highest risk of having a seizure in the
perioperative period, it is essential to be prepared to treat seizure activity regardless of the
surgical procedure or anesthetic technique.
• Perioperative seizures occur most commonly during induction and emergence. They often
resolve without treatment. However, it is important to discern treatable causes; for example,
hypoxia, metabolic derangements, non-therapeutic AEDs. Consider supportive care and
injury prevention.
PERIOPERATIVE STATINS
BASICS
DESCRIPTION
• Statins are competitive inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
reductase; they are primarily indicated for the treatment of hypercholesterolemia and
reducing low-density lipoprotein-cholesterol (LDL-C).
• Statins have also been shown to possess several pleiotropic effects:
– Improved vascular endothelial function
– Immunomodulation
– Stabilization of atheromatous plaques
– Protection against thrombosis
• In future investigations, indications for perioperative statin use are likely to be expanded
and further delineated.
• Pharmacology: Primary role is the reduction of cholesterol synthesis. Statins competitively
inhibit HMG-CoA reductase in the liver. HMG-CoA reductase catalyzes the synthesis of
mevalonate, the rate-limiting step in cholesterol biosynthesis.
• Decreases in hepatic intracellular cholesterol synthesis and release result in extrahepatic
upregulation of LDL receptor expression on their cell surfaces, thereby increasing clearance
of LDL and VLDL.
• Pleiotropic effects
– Improved endothelial function; impairments are closely associated with adverse outcomes.
Hypercholesterolemia and atherosclerosis impair endothelium-dependent vasodilation
and nitric oxide (NO) production.
NO has several anti-inflammatory and anti-thrombotic effects that protect against
chemokine expression, left ventricular remodeling and dysfunction, and thrombogenesis.
– Immunomodulation: Statins decrease systemic inflammation and stabilize atheromatous
plaques by reducing:
LDL levels: Normal oxidative modification of LDL-C elicits an antigenic response by
macrophages, strongly promoting inflammation.
Interleukins (IL): The inflammatory process in atherosclerotic plaques produce
inflammatory mediators (e.g., interleukin-6 [IL-6])
Tumor necrosis factor (TNF): A pro-inflammatory cytokine produced from atherosclerotic
plaque-related inflammatory processes.
C-reactive Protein (CRP): Produced by hepatocytes in response to IL-6 and TNF. CRP is a
universal marker for inflammation, and is prognostic for coronary heart disease.
– Protection against thrombosis: Statin therapy reduces platelet adhesion and inhibits
thrombogenesis. Venous thrombosis increases the risk of MI and stroke.
• Adverse effects are rare and dose dependent.
– Muscle damage: Rhabdomyolysis and myopathy (rare). More common when combined
with fibrate therapy or used jointly with amiodarone or verapamil.
– Mild transient proteinuria: There is no associated pattern of renal failure or injury.
– Mild hepatotoxicity:
Hepatic transaminase levels are elevated in 0.5–2.0% of patients; this is a dose-
dependent response (1)[A].
Abnormal liver function is typically clinically insignificant and progression to liver
failure due to statin therapy is rare, if existent.
Despite this evidence, cholestasis and acute liver disease are contraindications to statin
therapy.
– Teratogenicity has been described and therefore statins should not be used during
pregnancy.
– Diabetes mellitus: Slightly increases the risk of development.
• Evidence of adverse effects due to perioperative statin exposure (muscle cramps or myalgias,
jaundice, or hepatic tenderness) should be followed by testing for creatine kinase or liver
function tests, and statins should be discontinued (2)[A].
• Cardiac protection
– Perioperative MI
Type I MI (coronary plaque rupture): Statin therapy has been shown to decrease the
incidence by stabilizing coronary plaques and protect against rupture, thus reducing
coronary thrombosis (2)[A].
Type II MI (due to oxygen supply/demand mismatch): Not affected by statin therapy.
– Arrhythmias: Decreased incidence, likely via an anti-inflammatory process. Statin therapy
has been shown to consistently and significantly protect against atrial fibrillation.
However, there is inconclusive evidence indicating protection against ventricular
fibrillation.
– Valvular effects: Active inflammatory processes can lead to valvulitis and calcification.
Inhibition of inflammation and stabilization of valvular endothelium is thought to inhibit
progression of stenosis.
Statin therapy is associated with a reduced incidence of both rheumatic aortic and mitral
valve stenosis.
There is conflicting evidence as to whether statin exposure influences postoperative
morbidity and mortality (as measured by EuroSCORE risk of mortality and long-term
survival rates) after valvular heart surgery (2).
– All-cause mortality following cardiac surgery: Significantly decreased with both long-term
treatment and immediate preoperative statin exposure.
• Vascular protection
– Thrombosis/venous adverse events are decreased.
– Atherosclerosis
Therapy with rosuvastatin or atorvastatin reduced LDL ≥40%, the amount necessary to
achieve atherosclerosis regression.
Reasonable target LDL-C levels in high-risk patients are <70 mg/dL (2)[A].
– Abdominal aortic aneurysm (AAA): A meta-analysis correlates statin exposure with
reduced expansion rates of small AAA, as well as improved outcomes in surgical and
endovascular AAA repair. Likely due to immunomodulatory effects.
– Carotid artery disease: Statins may slow progression or cause regression of intima-media
thickness and decrease the rate of microemboli. Outcome studies have shown a reduction
in stroke risk and cardiovascular events (1).
– Peripheral artery disease: Statins have been shown to decrease the incidence of cardiac
events, perioperative mortality, and renal dysfunction.
• Renal protection
– Percutaneous coronary interventions: Statin preloading has been shown to decrease
contrast-induced nephropathy (CIN).
– Major vascular surgery: Chronic use has been associated with decreased renal insufficiency
and improved recovery rates from renal injury (2)[A]. The role of preloading is unclear.
• Neuroprotection
– Stroke: Observational studies demonstrate reduced frequency of stroke following major
vascular surgery (3). When combined with beta-blockers, statin exposure reduced the
incidence of stroke during CABG.
– Encephalopathy: Evidence is currently inconclusive.
• Other effects
– Sepsis: Statins appear to play an adjuvant role via suppression of inflammation (reduced
IL-6 and TNF levels) and antithrombotic effects. Meta-analyses correlate therapy with
reduced infection and improved mortality rates during sepsis. Randomized trials are
needed to develop applicable recommendations for use in sepsis.
– Reactive airway disease: Statin exposure is linked with reduced bronchial hyperreactivity.
• Perioperative strategy of beginning statin therapy: While there is evidence suggesting the
beneficial effects of statin therapy in perioperative outcome, further evidence from
randomized clinical trials is needed to develop a comprehensive strategy. At this time, dose,
type, and duration of therapy need to be determined as well as differentiating between
indications for high-risk and average-risk patients.
– Indications: Currently only for treatment of high-risk cardiac patients. Should be combined
with aspirin and titrated with a beta-blocker regimen in patients with ischemic heart
disease (4)[A].
– Type:
A meta-analysis of literature determined rosuvastatin or atorvastatin ≥20 mg/dL
(potency: Rosuvastatin > atorvastatin > pravastatin > simvastatin) to be optimal
(achieved target LDL-C levels) (1)[A].
Rosuvastatin has a similar risk-benefit profile as other statins, but its increased potency is
advantageous due to the dose-dependent nature of adverse effects.
Fluvastatin is less potent than rosuvastatin or atorvastatin. However, its longer half-life
and extended release may make it preferable in patients unable to receive oral
medications in the immediate postoperative period. It is not hepatically metabolized, so
it may be preferred in cases of hepatic injury (2)[A],(1)[B].
– Duration of therapy:
Short-term therapy (≤7 days) initiated preoperatively in cardiac and vascular surgical
patients is associated with a reduced incidence of adverse events.
If possible, it has been suggested to administer the day of or the night before surgery to
maximize potential benefits.
A high loading dose immediately prior to percutaneous coronary intervention was also
shown to reduce myocardial injury and major cardiac adverse events (1)[A].
• Discontinuation of statin therapy
– Statin therapy should not be discontinued prior to open or endovascular procedures and
should be resumed postoperatively as soon as possible.
– Discontinuation after major vascular surgery has been shown to significantly increase
incidence risk for cardiac death or recurrent MI (5).
– A delay of >4 days in restarting therapy increased the risk of cardiac myonecrosis (related
to duration of hospitalization and death) in treatment of infrarenal aneurysms (5)[B].
– Effects of statin withdrawal are related to severity of coronary artery disease.
There is evidence that perioperative statin treatment has a greater effect on outcome in older,
high-risk patients than in younger patients.
REFERENCES
1. Paraskevas PI, Mikhailidis DP, Veith FJ. Optimal statin type and dosage for vascular
patients. J Vasc Surg. 2011;53(3):837–844.
2. Singh N, Patel P, Wyckoff T, et al. Progress in perioperative medicine: focus on statins. J
Cardiothorac Vasc Anes. 2010;24(5):892–896.
3. Liakopoulos OJ, Choi Y, Haldenwang PL, et al. Impact of preoperative statin therapy on
postoperative adverse outcomes in patients undergoing cardiac surgery: A meta analysis of
over 30000 patients. Eur Heart J. 2008;29(12):1548–1559.
4. Poldermans D, Bax JJ, Boersma E, et al. Guidelines for preoperative cardiac risk assessment
and perioperative cardiac management in non-cardiac surgery. Eur J Anaesthesiol.
2010;27:92–137.
5. Le Manach Y, Estevez CI, Bertrand M, et al. Impact of preoperative statin therapy on
adverse postoperative outcomes in patients undergoing vascular surgery. Anesthesiology.
2011:98–104.
ADDITIONAL READING
• Bouchard D, Carrier M, Demers P, et al. Statin in combination with beta-blocker therapy
reduces postoperative stroke after coronary artery bypass graft surgery. Ann Thorac Surg.
2011;91:654–660.
• Landmesser U, Drexler H. The clinical significance of endothelial dysfunction. Curr Opin
Cardiol. 2005;20:547–551.
• Quist-Paulsen P. Statins and inflammation: an update. Curr Opin Cardiol. 2010;25:399–405.
• Robinson JG, Smith B, Maheshwari N, et al. Pleiotropic effects of statins: Benefit beyond
cholesterol reduction? A meta-regression analysis. J Am Coll Cardiol. 2005;46:1855–1862.
• Liver function tests
• Aortic valve repair
• Septic shock
• Chronic angina
CLINICAL PEARLS
• Statins are associated with multiple beneficial pleiotropic effects, which improve outcomes
in both high-risk and average-risk patients during cardiovascular procedures.
• Postoperative statin withdrawal is associated with increased risk of adverse events and
death. Statin therapy should not be discontinued prior to open or endovascular procedures
and should be resumed postoperatively as soon as possible.
• Further randomized clinical studies are needed to define the role and efficacy of the
pleiotropic effects of statins in perioperative strategy.
PERIOPERATIVE STROKE
BASICS
DESCRIPTION
• Perioperative strokes are predominantly ischemic and embolic (less frequently
hemorrhagic). They result in formidable morbidity and unfortunately high mortality.
• The majority occur postoperatively (83% vs. 17% intraoperatively) and are usually
identified on postoperative Day 1 (45%).
• Similar to cardiac disease, the anaesthetist should risk stratify, optimize risk factors, and
consider preventive measures in order to reduce incidence and aid in management.
EPIDEMIOLOGY
Prevalence
• Perioperative stroke ranges from 0.1–5%.
• Incidence increases with intraoperative hypotension (1%), the presence of carotid stenosis
(3.6%), and cardiac surgery (5%) (1,2).
Morbidity/Mortality
Acute mortality: 16–50%. Early mortality may be due to further extension of cerebral
infarction with edema and increased ICP. Late mortality may be from aspiration, pneumonia,
sepsis, MI, or metabolic derangement.
• Patient-related risk factors: Prior stroke or TIA (particularly if within the prior 6 months);
advanced age (>70 years old); female gender; long bone fractures; hypertension
(particularly poorly controlled); diabetes mellitus; preeclampsia; peripheral vascular
disease; carotid disease; arrhythmias; systolic dysfunction (EF <40%); renal disease;
hypercoagulability; valvular disease.
• Intraoperative (procedure-related) risk factors: Type and nature of surgical procedure;
anesthetic choice (GA vs neuraxial vs local); duration of surgery, cardiopulmonary bypass
(CPB); aortic cross-clamp time; manipulations of neck or proximal aortic atherosclerotic
lesions; arrhythmias; hyperglycemia; hypotension or hypertension; controlled hypotension;
urgent surgery; air embolism after endoscopic procedures; intravascular interventions; fat
embolism after orthopedic procedures; paradoxical embolism from postoperative deep-vein
thrombosis in patients with patent foramen ovale (PFO).
• Postoperative risk factors: Heart failure; low ejection fraction; myocardial infarction (MI);
arrhythmias (particularly atrial fibrillation); dehydration; blood loss; hyperglycemia;
infection.
• Perioperative strokes are predominantly ischemic and embolic; they result from a
combination of patient risk factors, surgical stress and inflammation, as well as anesthetic-
related hemodynamic changes.
• Atrial fibrillation is a co-morbid disease present in 27.6% of all perioperative strokes. It can
cause cardioembolism (particularly when anticoagulants have been held for surgery) or
cerebral hypoperfusion (from rapid ventricular rate and hypotension). Perioperative
electrolyte abnormalities, sympathetic stimulation, and pulmonary complications may
predispose patients to new-onset atrial fibrillation after surgery.
• Valvular heart disease and prosthetic valves serve as a nidus for embolus formation,
particularly when anticoagulation must be held for surgery.
• PFO is present in up to 30% of the general population and provides a direct communication
from the right (venous) to the left (arterial) side of the heart. This allows air from IV or
other venous catheters to more easily gain access to the cerebral and cardiac arteries (the
pulmonary system has some capacity to absorb and exhale air from the venous circulation).
• Surgical trauma is associated with tissue injury and disrupted endothelial homeostasis.
Microvascular dysfunction, inflammation, and oxidative stress decrease nitric oxide,
promote hypercoagulability, and predispose vessels to vasoconstriction, leukocyte adhesion,
and thrombosis factors. Furthermore, there is evidence that the fibrinolytic systems are
impaired while hemostatic systems are activated postoperatively for up to 21 days:
Decreased tissue plasminogen activator (t-PA) and increased activity of plasminogen
activator inhibitor type 1 as well as levels of fibrinogen-degradation product, thrombin–
antithrombin complex, thrombus precursor protein, and D-dimer.
• Carotid endarterectomy: Causes include ischemia during carotid artery clamping,
postoperative thrombosis or embolization, and, to a lesser extent, intracerebral hemorrhage.
Thrombus and thromboembolization, due to technical error or imperfection at the
endarterectomy site, can cause up to 38% of all perioperative strokes. Re-operation and re-
exploration is often performed to assess for intraluminal thrombi or other causes (1).
• Cardiac surgery has multiple factors that increase the incidence of stroke or short- and long-
term cognitive changes (executive dysfunction, short-term memory loss, and psychomotor
slowing). Causes include intracardiac surgery, surgical trauma, pre-existing vascular
changes, temperature, postoperative atrial fibrillation, CPB, and hypoperfusion. Intracardiac
surgery introduces gaseous and particulate emboli. Atrial fibrillation occurs in 30–50% of
patients postoperatively (peaks on POD 2–4) and has been attributed to electrolyte
imbalance and intravascular volume shifts. CPB introduces air, fat, platelet, and fibrin
aggregates into the systemic circulation and can lead to stroke. This most frequently occurs
during placement and removal of aortic cross-clamps and cannulae (2).
• Anesthetic causes stem from hemodynamic changes such as hypotension and hypoxemia;
there is some evidence of exacerbating hypercoagulability. Patients with chronic
hypertension have a right shift in their cerebral autoregulation curve, making them less
capable of handling abrupt drops in BP compared to normotensives.
• Dehydration can accelerate thrombus formation due to decreased levels of antithrombin III
and increased venous hemostasis.
• Risk stratification includes an assessment of risk factors and optimization of co-morbid
conditions. Those at high risk should be considered for minimization or avoidance of
surgery if and when possible.
• Carotid disease, particularly symptomatic stenosis, should be evaluated by means of Doppler
ultrasound. Patients with >60% stenosis should be evaluated or assessed for correction
prior to scheduled surgery; risks of delaying surgery versus the benefits must be weighed.
Carotid revascularization prior to, or at the same time as cardiac surgery remains
controversial. Opponents state that it exposes patients to the risks of perioperative stroke
and MI twice and that the benefits may not exceed the risks. However, the risk of
hemodynamically significant, high-grade, asymptomatic carotid stenosis, particularly
bilateral stenosis, may exceed that of carotid revascularization. Antiplatelet and aspirin
reduces the incidence without increasing the odds of bleeding complications (1).
• Recent stroke: Outcome studies suggest delaying surgery for 2–6 weeks; this allows for a
stable post-infarction neurologic status to be achieved and for brain vascular reserve to
return to normal. However, the urgency of surgery and extent of stroke and co-morbid
diseases must be weighed.
• Avoid perioperative hyperglycemia, fever, and dehydration. Hyperglycemia should be
treated aggressively with insulin.
• Infections should be prevented and treated perioperatively (pulmonary, urinary, wound,
central lines). High white cell counts correlate with an increased incidence of stroke as well
as atrial fibrillation.
• Cerebral protection prophylaxis involves measures that reduce oxygen consumption and
includes the use of barbiturates or attainment of burst suppression, general anesthesia, and
hypothermia.
• Neuromonitoring techniques (particularly during CEA or cerebral aneurysm clipping)
include functional, flow, and pressure monitors. They help to identify ischemic events.
However, they are also indirect and have the potential for false positives and negatives.
• Choice of anesthetic: MAC with local infiltration has been associated with a reduced
incidence of stroke. Epidural anesthetics have been associated with a reduced incidence of
emboli, likely due to the increase in blood flow and reduction in venous stasis in the lower
extremities. However, hypotension from sympatholysis should be anticipated, avoided, and
aggressively treated.
• Cardiac surgery: Consider minimally invasive procedures; minimize duration of CPB,
hypotensive episodes, aortic trauma in patients with severe calcification; implement higher
MAPs during CPB (especially in patients with carotid disease), de-airing maneuvers of
chambers, pulsatile perfusion bypass, hypothermic measures, and alpha-stat pH
management. Separately, risk reduction of atrial fibrillation via adequate hydration,
maintenance of electrolytes, and possibly prophylaxis with amiodarone, beta-blockers, and
statins. Consideration for IV heparin therapy in patients who are high risk (history of CVA
or TIA) and develop atrial fibrillation; this should be continued for 30 days after the return
of normal sinus rhythm.
• Bridging anticoagulation and antiplatelet therapy with medications such as heparin or
argatroban may be implemented in order to minimize the period of time where the patient
is at risk; consider for high-risk patients.
• Resumption of anticoagulants or antiplatelets should be coordinated with the surgical and
primary teams. This involves an assessment of active bleeding (drains, wound sites, stable
hemoglobin).
• Continuing blood thinners in certain procedures and surgeries such as dental procedures,
arthrocentesis, cataract surgery, and endoscopy or colonoscopy with biopsies have minimal
risk for major bleeding. Some studies have shown that continuing warfarin for knee or hip
replacements with an INR of 1.8–2.1 may be safe and effective. However, blood thinners
should be withheld in more invasive procedures.
• Statins may reduce the incidence of stroke following major vascular and cardiac surgeries
(3% absolute reduction); their role in non-cardiac surgery is not well-defined at this time.
The mechanism is believed to be due to pleiotropic effects: Stabilization of atheromatous
plaques at risk for rupture, vasodilation by stimulating nitric oxide, reduction of C-reactive
protein, and inhibition of thrombosis and platelet aggregation. Although it is clear that
patients on chronic statin therapy should be continued perioperatively, the debate exists
over initiating statin therapy (which statin, how long, what dose, which patients).
• Aspirin therapy is associated with up to 7% absolute reduction in early stroke.
• Beta-blockers, although shown to reduce adverse cardiac events and mortality, may increase
stroke and mortality perioperatively possibly due to hypotension and bradycardia. However,
this is controversial as the key study did not control for BP, timing, type and heart rate
parameters.
• History of sudden loss of focal brain function or mental status.
• Delayed anesthetic awakening should first rule out medication (neuromuscular blocking
drugs, narcotics, benzodiazepines, and other sedatives) and metabolic (hypothermia,
hypoglycemia, acidosis, alkalosis, hyponatremia, hypercarbia, hypoxia) causes (2).
• Non-contrast head CT or MRI
• Transesophageal or transthoracic echocardiogram may help detect microemboli and
macroemboli, as well as the presence of a PFO.
• Neurology consultation.
• Delayed anesthetic awakening due to medications or metabolic causes
• Delirium
• Postoperative toxic metabolic disturbances including hypoglycemia, acute renal failure, drug
intoxication, hepatic insufficiency
• Seizures
• Increased intracranial pressure and edema
TREATMENT
• Prevention and prophylactic measures are key, given the poor morbidity and mortality.
• Dependent upon cause: In the event of aspiration risk, intubation should be performed.
• Thrombolytic therapy for embolic causes may be considered within 48 hours of symptom
onset and after weighing the risks for bleeding. It is contraindicated after major surgery;
alternatively, intraarterial administration and endovascular mechanical disruption may be
considered. Consult and coordinate with neurology and stroke teams.
• Increased intracranial pressure may be treated with ventriculostomy to reduce further
injury.
• Reduction of cerebral oxygen consumption may be performed via hypothermic measures or
barbiturate coma or burst suppression.
• Normoglycemia should be maintained. Hyperglycemia has been associated with worsened
outcomes as well as increased atrial fibrillation.
• BP management remains controversial. Most consensus guidelines recommend that BP NOT
be treated acutely in patients with ischemic stroke unless SBP >220 mm Hg or DBP >110
mm Hg or the patient has active CAD, heart failure, or aortic dissection. In addition to
arterial line BP monitoring, potential IV choices include labetalol, nicardipine, nitroglycerin,
and nitroprusside.
• Antihypertensive medications may be restarted approximately 24 hours after stroke in
patients with preexisting hypertension who are neurologically stable.
• Anticipate and prevent medical complications of stroke. Common conditions associated with
stroke are MI, heart failure, dysphasia, aspiration, pneumonia, urinary tract infection, DVT,
PE, dehydration, malnutrition, and pressure sores.
FOLLOW-UP
• Neurology consult
• Physical and occupational therapy
CLOSED CLAIMS DATA
• Stroke comprises 3% of all claims (N = 6446)
REFERENCES
1. alm EA, Tuhrim S, Wang JJ, et al. Risk factors for perioperative death and stroke after
carotid endarterectomy: Results of the New York carotid artery surgery study. Stroke.
2009;40(1):221–229.
2. ouglas JM, Spaniol SE. A multimodal approach to the prevention of postoperative stroke in
patients undergoing coronary artery bypass surgery. Am J Surg. 2009;197(5):587–590.
3. Selim M. Current concepts perioperative stroke. NEJM. 2007;356:706–713
4. anders RD, Grocott HP. Perioperative stroke: Time to redefine the impact of age? Stroke.
2012;43:3–5.
5. ashour G, Shanks A, Kheterpal S. Perioperative stroke and associated mortality after
noncardiac, nonneurologic surgery. Anesthesiology. 2011;114(6):1289–1296.
6. arik S, Cohen JR. Perioperative stroke after general surgical procedures. NY State J Med.
1993;93(3):162–165.
7. cDonagh D, Mathew J. Perioperative stroke: Where do we go from here? Anesthesiology.
2011;114(6):1263–1264.
8. ateman B, Schumacher H, Wang S, et al. Perioperative acute ischemic stroke in noncardiac
and nonvascular surgery: Incidence, risk factors, and outcomes. Anesthesiology.
2009;110(2):231–238.
ADDITIONAL READING
• American Society of Anesthesiologists Closed Claims Study
• Poldermans D, Schouten O, van Lier, et al. Perioperative stroke and beta-blockade.
Anesthesiology. 2009;111(5):940–945.
CODES
ICD9
997.02 Iatrogenic cerebrovascular infarction or hemorrhage
ICD10
I97.811 Intraoperative cerebrovascular infarction during oth surgery
CLINICAL PEARLS
• Perioperative stroke is a grave complication that increases with certain patient, surgical, and
anesthetic factors.
• The majority of perioperative strokes are secondary to thromboembolic phenomenon.
PERIPHERAL VASCULAR DISEASE
Eric W. Nelson, MD
BASICS
DESCRIPTION
• Organic peripheral vascular disease (PVD) is atherosclerosis of blood vessels outside of the
heart and brain.
– It results from hardening and narrowing of blood vessels and causes insufficient tissue
perfusion, similar to coronary or carotid artery disease.
– It is a systemic disease that affects many circulatory networks including the kidneys,
extremities, and stomach.
• Patients with PVD frequently present for vascular as well as non-related procedures (1,2).
– Peripheral vascular surgery is classified as a “high-risk” surgical procedure by the
American Heart Association Perioperative Guidelines.
– Even in non-vascular procedures, patients present with significant comorbidities that can
result in “high” or “intermediate” patient risk stratification.
EPIDEMIOLOGY
Prevalence
• 12–14% of individuals in the general population (3).
• 20% of individuals over the age of 70 years (3).
• 1 in 3 diabetics over the age of 50 years (3).
• Endovascular procedures are increasing in frequency; approximately 1,300 endovascular
abdominal aortic aneurysm (AAA) repairs are performed each year in the US.
Morbidity
50% of affected patients had a major event or surgery in a 6-year time span.
Mortality
33.2% death rate over 5 years
• Diabetes (2,3)
• Hypercholesterolemia
• Hypertension
• Renal failure
• Smoking
• PVD can be classified as either organic (the result of atherosclerosis) or functional
(thrombosis, emboli, acute trauma, vasculitis, autoimmune disease). The focus of this
chapter is organic PVD (3).
• Atherosclerosis can be described as a ubiquitous process of chronic low-grade inflammation
and plaque formation with the possibility of superimposed acute thrombotic events.
• PVD affects the venous and arterial systems and impairs perfusion. This can result in chronic
distal ischemia and increases the potential for acute complete occlusion and infarction.
Myocardial dysfunction is the most important cause of morbidity in patients with PVD;
therefore, cardioprotective strategies should not only be maintained during anesthesia, but
also perioperatively.
SYMPTOMS
• Intermittent claudication is typically an early symptom.
• Pain at rest is a more worrisome symptom as it typically signifies ischemia in the affected
extremity.
• Patients also typically notice skin changes on the affected extremity.
History
• Duration and progression of PVD, activity level, pain.
• A complete history of the patient’s PVD must be supplemented by a thorough investigation
of other vascular diseases (cardiovascular, cerebrovascular, renovascular) to help determine
the best type of anesthetic, monitoring, and if further workup is necessary.
Signs/Physical Exam
• 5 P’s of PVD: Pain, pallor, paresthesia, paralysis, pulselessness
• Auscultate for bruits and palpate for thrills
• Skin examination: Atrophic and shiny, alopecia, dry, scaly, erythema, brittle nails
MEDICATIONS
• Cardioprotective drugs: Beta-blockers, statins, aspirin, ACE inhibitors
• Cilostazol and pentoxifylline help to decrease claudication in patients with PVD but have
not been found to decrease mortality.
• Oral hypoglycemics and insulin are commonly seen; patients should hold long-acting oral
drugs on the morning of surgery to avoid perioperative hypoglycemia. Metformin is
commonly held perioperatively due to its potential for fatal metabolic acidosis.
• Anticoagulation: Potent platelet inhibitors, heparin infusions, or thrombolytic therapy may
need to be started or continued perioperatively; this decision should be discussed with the
surgeon and the cardiologist.
Labs/Studies
• Electrolytes to assess renal function
• CBC to assess for anemia, quantitative platelet abnormalities
• ECG to check for dysrhythmias, ischemia, infarction
• A cardiac stress test may be indicated to assess function and the potential for ischemia. If
the patient has good exercise tolerance, >4 METS, cardiac workup is typically not
necessary (however, their PVD may affect activity levels independent of coronary disease
and preclude the ability to assess this).
• Pulmonary function testing may be indicated in patients with lung dysfunction, particularly
in surgical procedures with the potential for postoperative impairment (thoracic, upper
abdominal procedures).
• Renal dysfunction
• Non-vascular procedures: If there is worsening of claudication or pain at rest, this may
signal progression of disease and the need to address/treat a priori.
• Absence of cardiac workup or management in patients with coronary disease or with
myocardium that appears at risk for ischemia
CLASSIFICATIONS
Fontaine stages for ischemia
• Mild claudication
• Intermittent claudication (pain with walking about 150 m)
• Rest pain
• Gangrene
TREATMENT
Premedications
• Anxiolytics can allay increases in BP and heart rate.
• Beta-blockers should be continued and titrated to goal heart rates (3).
• Supplemental oxygen may be appropriate.
• Blood sugar control with IV or SQ insulin as appropriate (3).
• Bronchodilators and steroids may be considered in patients with pulmonary disease.
• Gastric medications such as antacids, prokinetics, and acid reducers should be considered in
patients with gastroparesis or delayed gastric emptying.
• If the patient has a history of neurovascular disease, and is deemed not competent, informed
consent may have to be obtained from a power of attorney.
• Discuss smoking cessation
INTRAOPERATIVE CARE
• Outcome studies on anesthetic choice for PVD procedures and patients have yielded varying
results and conclusions. At this time, recommendations or guidelines applicable to all
patients, procedures, and situations do not exist. Rather, risks versus benefits and
practicality need to be weighed.
• Epidural and spinal
– Benefits include the ability to block the endocrine stress response seen with surgery;
avoids the need for airway manipulation and controlled ventilation; reduces the potential
for blood loss, hemodynamic swings associated with general anesthesia and
hypercoagulability; increases blood flow and perfusion to lower extremities and decreases
time to ambulation; diminishes need for systematic opioids and their side effects
(respiratory complications).
– Drawbacks include risks associated with neuraxial techniques (infections, hematomas,
difficult placement, high spinals, inadvertent intravascular injection) and
contraindications with common anticoagulants.
• Peripheral nerve blocks
– Benefits include the ability to block the endocrine stress response seen with surgery as
well as avoid the need for airway manipulation, controlled ventilation, and systemic
opioids.
– Drawbacks include failed or incomplete surgical blocks, local anesthetic systemic toxicity,
complications of sedation (hypoxia, hypercarbia), and concerns with anticoagulants
(brachial plexus blocks in the thorax).
– Benefits include the potential for a still surgical field, controlled ventilation, and patient
preference to not be awake.
• MAC with local anesthetic infiltration should be considered when appropriate as it avoids
many of the drawbacks seen with the above mentioned techniques
Monitors
• ECG and ST segment monitoring will help to detect perioperative myocardial ischemia in
this high-risk patient population.
• Arterial line placement should be considered in patients with concurrent coronary artery
disease, decreased left ventricular function, or for procedures with the potential for large
swings in BP and/or require beat-to-beat BP monitoring. Consider pre-induction placement.
PVD may make line placement difficult.
Slow and controlled to ensure steady hemodynamics and organ perfusion as well as provide
an adequate depth of anesthesia. Heart rate, EKG, and arterial line/NIBP should be carefully
monitored and abnormalities treated to optimize myocardial oxygen supply and perfusion.
Maintenance
• The myocardial oxygen supply and demand ratio needs to be optimized. It may be necessary
to place more invasive monitors as needed intraoperatively.
• In patients with chronic hypertension, the cerebral perfusion pressure curve may be shifted
to the right. A good rule of thumb is to maintain BP within 20% of the patient’s baseline.
• Normothermia should be maintained to avoid shivering and increased myocardial oxygen
consumption.
• Glycemic control should be considered in long or brittle diabetics.
• Avoid or treat shifts in BP and heart rate.
• Consider “deep” extubation in patients with COPD to avoid bronchospasm.
FOLLOW-UP
BED ACUITY
• Patients should typically be monitored on telemetry as most have CAD.
• Monitoring of pulses and color of the affected extremity is useful in determining worsening
of disease.
• Restart cardioprotective medications as soon as appropriate. Discontinuation of statin
therapy has been affiliated with increased cardiac morbidity and mortality (4).
• Tight glycemic control can improve wound healing and reduce the incidence of infection
• Consider BMP and replace electrolytes; CBC if there was blood loss during the surgery.
Transfusion may be necessary to maintain adequate oxygen carrying capacity in the blood
(however, it carries intrinsic risks).
COMPLICATIONS
• MI is the major source of morbidity in this population.
• Extremity ischemia may occur.
• Worsening renal disease
• Cerebrovascular accidents
REFERENCES
1. Fleisher LA, et al. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation
and care for noncardiac surgery: Executive summary: A report of the American College of
Cardiology/American Heart Association Task Force on practice guidelines. Anesth Analg.
2008;106(3):685–712.
2. Kheterpal S, O’Reilly M, Englesbe MJ, et al. Preoperative and intraoperative predictors of
cardiac adverse events after general, vascular, and urological surgery. Anesthesiology. 2009;
110:58–66.
3. Shammas NW. Epidemiology, classification, and modifiable risk factors of peripheral
arterial disease. Vasc Health Risk Manag. 2007;3(2):229–234.
4. Schouten O, Hoeks SE, Welten GM, et al. Effect of statin withdrawal on frequency of
cardiac events after vascular surgery. Am J Cardiol. 2007; 100(2):316–320.
5. Hallet JW. Peripheral Arterial Disease. The Merck Manuals Online Medical Library. 2008.
• www.americanheart.org
• Lower extremity bypass
CODES
ICD9
443.9 Peripheral vascular disease unspecified
ICD10
I73.9 Peripheral vascular disease, unspecified
CLINICAL PEARLS
• Peripheral vascular surgery is considered a high-risk surgical procedure. Patients presenting
for peripheral vascular surgery often do so after failed medical or endovascular
management.
• In addition, patients often have intermediate or high-risk cardiac comorbidities that increase
the possibility for perioperative morbidity or mortality. Common comorbidities include
hypertension, coronary artery disease, cerebrovascular disease, diabetes mellitus, and
pulmonary disease from smoking.
• It is important to obtain a detailed cardiac history to decrease the risk of perioperative MI as
much as possible.
PH MEASUREMENTS
Sara Miller, MD
BASICS
DESCRIPTION
pH measurements are most commonly measured by blood gas analyzers. They are comprised
of a:
• pH sensor: Contains a measuring and reference electrode.
• PCO2 electrode: A pH sensitive glass probe that is surrounded by a bicarbonate solution and
is enclosed by a CO2 permeable membrane.
• PO2 electrode: A platinum probe bathed in an electrolyte solution and separated from the
blood sample by an O2 permeable membrane (1)[A].
• pH is a measure of the hydrogen ion (H+) concentration in a liquid. pH is defined as the
negative logarithm to the base 10 of H+. For example, if H+ equals 0.000001, then pH is
equal to the negative log10[0.000001], or 6.0.
• Modern blood gas analyzers directly measure:
– pH: Sensing (or measuring) electrodes produce an electrical signal or potential (voltage)
that is directly related to the [H+]. Reference electrodes produce a stable potential by
which the potential difference is measured and converted into a pH value.
– CO2 tension: CO2 is relatively soluble in blood, and exists in other forms: HCO3-, CO2,
H2CO3 (CO2 + H2O←→H2CO3 ←→H+ + HCO3-). It is attached to hemoglobin as
carbaminohemoglobin. These dissolved and bound forms exist in equilibrium with CO2
in its gas form, but do not exert partial pressure and are not included in the PaCO2
measurement.
– Arterial oxygen tension: O2 is poorly soluble in blood; the solubility coefficient is 0.003.
Most of the O2 is carried in blood attached to hemoglobin. Dissolve and bound forms exist
in equilibrium with O2 in its gas form, but do not exert partial pressure and are not
included in the PaO2 measurement.
– Current equipment may also have the capability of measuring hemoglobin, electrolytes,
glucose, and lactate.
– Samples are warmed to 37%C prior to measurement.
• Modern blood gas analyzers calculate:
– Arterial oxyhemoglobin saturation
– Base excess: A reflection of the amount of strong acid necessary to bring the pH to 7.4
– Bicarbonate concentration. This value is derived from the pH and PCO2 measured values.
• Factors that can affect the accuracy of pH measurements:
– Gas solubility: Changes in temperature affect the kinetic energy of O2 and CO2 and
consequently the solubility of gases in blood (partial pressures). For example, decreased
temperature will consequently decrease the kinetic energy of O2 and CO2; this increases
their solubility and decreases their partial pressures (less in gas form). In addition, there is
an increase in O2 and CO2 binding affinity to hemoglobin which further decreases the
amount of oxygen and carbon dioxide in its gas form.
– Water dissociation constant (pKw): Changes in temperature affect water’s self-ionization
(proton from one water molecule is transferred to another to form hydronium and
hydroxide ions). H2O + H2O ←→ H3O+ + OH−. Water is the primary source of
hydrogen ions. Thus, decreased temperature will decrease [H+] and hence increase the
pH (alkalosis).
– Electroneutrality: Maintained due to the compensatory pK adjustment of histidine’s
imidazole moieties (alpha residues) that parallel pKw. Imidazole retains its buffering
capacity at all temperatures.
– Storage time: A sample that is stored longer than 20 minutes before analyzing it can
artificially change measured and calculated values, due to environmental cooling and
cellular metabolism. Blood samples are warmer than the ambient temperature, and
cooling can cause increased oxygen solubility, thereby reducing PO2. In addition, as
cellular metabolism ensues, PCO2 increases and PO2 and pH decrease.
– Number of cells in the sample: Increases in the WBC, platelet, or hemoglobin levels result
in increased metabolism. To reduce this effect, samples are normally placed on ice after
they are obtained to maintain their stability and the addition of sodium fluoride or
cyanide can reduce cellular oxygen consumption.
• Cardiopulmonary bypass (CPB) management presents a unique dilemma due to the
implementation of significant hypothermia. To that extent, two techniques of management
are utilized. Controversy exists regarding the most optimal methods. Blood gas samples
need to be warmed to 37°C prior to measurement. Whether these values are then inserted
into a table or nomogram in order to temperature “correct” for partial pressures and pH to
the patient’s actual temperature is what is referred to as alpha stat and pH stat
measurements.
– pH stat utilizes a nomogram or table to adjust to the patient’s current hypothermic
temperature. The readings, therefore, will reflect in vivo partial pressures and pH (reduced
partial pressures, increased pH). Management based upon these values will result in the
addition of CO2 to the CPB pump in order to increase PaCO2 and reduce pH.
– Alpha stat pH management does not utilize a nomogram or table to adjust to the patient’s
hypothermic temperature. This is referred to as an “uncorrected” temperature system.
Thus, although in vivo partial pressures may be lower and pH higher than measured
values, management using this technique focuses on “total” content and does not add CO2
to the CPB pump or affect electroneutrality.
• Transcutaneous blood gas analysis is a continuous, non-invasive method to monitor blood
gas levels. The device induces hyperperfusion by local heating and PtcO2 and PtCO2 are
measured electrochemically; these values are used to estimate PaO2 and PaCO2. This
technique may be inaccurate in hypoperfused states and when vasoactive drugs are used.
ANATOMY
• pH measurements can be drawn commonly from the radial artery located on the distal
lateral wrist or from the femoral artery which is lateral to the femoral vein and medial to
the femoral nerve in the crease of the groin.
• Venous pH can be measured from any of the veins, commonly from the antecubital vein.
• “Arterialized” samples may be considered from an extremity vein that has minimal tissue
extraction (cold extremity).
CPB:
• pH stat management usually requires adding CO2 to the oxygenated gas inflow. This
increases total blood CO2 content and increases cerebral blood flow (results in cerebral
autoregulation uncoupling). This “luxuriant” flow may result in an increased embolic load
(including air), thus potentially increasing the risk of cerebral injury (2)[B]. In ischemic
stroke, pH stat management has been shown to imply better cerebral blood flow to injured
brain, but it may be dangerous by elevating intracranial pressure in subacute stages (3)[B].
• Alpha stat management preserves cerebral autoregulation. There is no CO2 added to the
oxygenator; thus total CO2 content stays constant. Normally, cerebral blood vessels are able
to adjust the flow of blood by vasoconstriction when arterial BP is raised and vasodilation
when arterial BP is lowered; thus if the PaCO2 doubles, the CBF doubles. Since alpha stat
management maintains CO2 at normal levels, cerebral autoregulation in response to BP
remains intact. As a result, it may have less adverse effects on enzyme function and cerebral
autoregulation, and is more commonly utilized during CPB.
• Arterial blood gas measurements are useful perioperatively and on the floor when acid–base
or oxygenation abnormalities are suspected.
– Preoperatively, baseline values can be attained to assess a patient’s normal respiratory
status. Abnormalities can aid with risk stratification, the need for preoperative
optimization, as well as ventilatory settings, invasive monitors, and bed acuity.
– Intraoperatively, arterial blood gas measurements are used to identify respiratory and
metabolic derangements. Hypoxia and alveolar–arterial oxygen gradients can aid with
discerning between ventilation/perfusion mismatching, shunting or diffusion barriers.
Extubation criteria are often based upon clinical signs and examination; however, in some
patients, arterial blood gas measures are useful in identifying patients who may fail
extubation.
– Intensive care unit: Intubated patients are carefully assessed for the return of adequate
mechanical functions as well as PO2 and PCO2 levels during spontaneous ventilation.
• pH stat versus alpha stat approaches during CPB: Patients managed by the pH stat approach
are considered hypercarbic and have a lower pH (respiratory acidosis). Patients managed by
the alpha stat approach are considered hypocarbic and have an increased pH (respiratory
alkalosis). The two techniques may have different cerebral and cardiac outcomes, and
controversy exists as to which approach yields a better patient outcome Comp Please
change this to a single sentence.
– Adults: Several studies have shown that during moderate hypothermia, alpha stat
management produces better neurologic outcomes, and is thus more widely used.
– Pediatrics: Several studies have shown that pH stat management produces better
neurologic outcomes secondary to decreased oxygen consumption, more homogenous
brain cooling, and better cerebral metabolic recovery. Data also shows that pH stat
management results in better outcomes with shorter ventilation times and shorter
intensive care unit stays after pediatric cardiac surgery (4)[B]. Thus, pH stat is more
commonly used; it may also be combined with alpha stat (pH stat used during cooling and
alpha stat used during rewarming) (5)[B].
EQUATIONS
pH = 6.1 + log [HCO3-]/ 0.03 × PaCO2
GRAPHS/FIGURES
See Table
REFERENCE
1. everinghaus JW. First electrodes for blood PO2 and PCO2 determination. J Appl Physiol.
2004;97:1599–1600.
2. Hoover LR, Dinavahi R. Jugular venous oxygenation during hypothermic cardiopulmonary
bypass in patients at risk for abnormal cerebral autoregulation. Influence of alpha stat
versus pH-stat blood gas management. Anesthesia and Analgesia. 2009;108:1389–1292.
3. Kollmar R, Georgiadus D, Schwab S. Alpha stat vs. pH stat guided ventilation in patients
with large ischemic stroke treated by hypothermia. Neurocritical Care. 2009;2:173–180.
4. Griffin DA. Blood gas strategies and management during pediatric cardiopulmonary bypass.
ASAIO Journal. 2005;5:657–658.
5. Groom RC, Froebe S, Martin J, et al. Update on pediatric perfusion practice in North
America: 2005 survey. J Extra Corpor Technol. 2005;37:343–350.
6. Yao F, Malhotra V, Fontes M. Yao and Artusio’s anesthesiology: Problem oriented patient
management, 2007.
• Extubation and intubation criteria
CLINICAL PEARLS
• pH measurements aid with diagnosing cardiorespiratory system function and derangements
as well as managing acid–base disorders.
• Arterial blood gas measurements may have flaws due to cooling of the sample and cellular
metabolism that can affect accuracy.
• pH stat:
• Is temperature corrected
• Aims to keep PaCO2 normal
• Requires adding CO2 to inspired gases
• Increases cerebral blood flow
• Uncouples cerebral autoregulation.
• Alpha stat:
• Is temperature uncorrected
• Does not add CO2 to inspired gases
• Maintains electrochemical neutrality
• Preserves cerebral autoregulation
• More commonly used in adult CPB.
PHEOCHROMOCYTOMA
Joe C. Hong, MD
BASICS
DESCRIPTION
• Pheochromocytoma is a rare endocrine disorder characterized by catecholamine-secreting
tumors of chromaffin tissue. The hallmark of pheochromocytoma is the excess production of
catecholamines.
• 10% of pheochromocytomas are extra-adrenal; they can occur wherever chromaffin tissue is
located. These sites include the celiac, mesenteric, renal, hypogastric, testicular, and
paravertebral sympathetic nerve plexus.
EPIDEMIOLOGY
Prevalence
In the US: ∼800 new cases/year
Prevalence
• ∼1:5,000 patients with hypertension have pheochromocytoma.
• Prevalence equal in men and women.
Morbidity/Mortality
• Patients with pheochromocytoma are at increased risk of multisystem morbidity and
mortality, particularly of the cardiovascular system. Comorbidities are the result of high
catecholamine levels on the end organs.
• Intraoperative diagnosis of a previously unknown pheochromocytoma is associated with
morbidity and mortality approaching 50% (primarily from myocardial infarctions or
cerebrovascular accidents) (1).
• Preoperative diagnosis with appropriate medical and anesthetic management significantly
decreases perioperative mortality and morbidity.
Positive family history of pheochromocytoma, multiple endocrine neoplasia (MEN) syndrome,
or von Hippel–Lindau disease.
• The vast majority of pheochromocytomas arise spontaneously; however, some are associated
with familial syndromes such as simple familial pheochromocytoma, MEN types IIa and IIb,
neurofibromatosis, tuberous sclerosis, von Hippel–Lindau disease, and Sturge–Weber
syndrome.
• Rule of 10: Approximately 10% familial, 10% bilateral, 10% extra-adrenal, and 10%
malignant.
• Pheochromocytomas are capable of manufacturing, storing, and secreting catecholamines
(norepinephrine, epinephrine, and dopamine). The vast majority (90%) secrete
predominately norepinephrine (2).
• Prior to surgery, patients must be adequately alpha-blocked followed by beta-blocked,
volume resuscitated, and concomitant organ dysfunctions identified and optimized prior to
surgery (3).
• Careful intraoperative communication between the surgeon and the anaesthetist must take
place to help anticipate periods of hemodynamic fluctuation.
SYMPTOMS
• Manifestations of supraphysiologic activity of catecholamines. Headaches, palpitations, and
diaphoresis are the most common symptoms.
• Other symptoms include anxiety, flushing, flank pain, abdominal pain, dizziness, syncope,
nausea, vomiting, weight loss, and constipation.
History
• In patients with undiagnosed pheochromocytoma, clinical suspicion is warranted when the
patient exhibits a history of difficult to control hypertension despite multiple drug therapy
or paroxysmal spells of sudden increases in BP, headaches, diaphoresis, palpitation, and
pallor.
• In patients with known diagnosis, a careful review of a BP diary, antihypertensive regimen,
duration of therapy, and timing of last dose will help establish adequacy of alpha-blockade.
• History taking should also identify other signs of adequate alpha-blockade such as nasal
congestion and orthostasis.
• A focused, relevant review of systems should include neurologic, cardiovascular,
hematologic, gastrointestinal, metabolic, pulmonary, and musculoskeletal systems.
Signs/Physical Exam
• Manifestations of supraphysiologic activity of catecholamines. Hypertension is the most
common sign and can be either sustained or paroxysmal.
• Other signs and examination findings include fever, tachycardia, orthostatic hypotension,
and palpable flank mass.
MEDICATIONS
• Preoperative alpha-blockade is vital in controlling BP and reversing catecholamine-induced
vasoconstriction and hypovolemia.
• Oral phenoxybenzamine, a non-competitive alpha-1 and alpha-2 antagonist, is the drug of
choice for alpha-blockade. It should be started and titrated upward, ideally, several weeks
prior to surgery (4).
• Oral prazosin and doxazosin are alpha-1 antagonists with fast onset and short half-lives
making them easier to titrate. Competitive antagonism puts them at a disadvantage as they
can be overcome by a large catecholamine surge.
• Phentolamine is an intravenous competitive alpha-1 and alpha-2 antagonist. The
competitive nature of antagonism also means that it can be overcome by a large
catecholamine surge.
• Beta-blockade should be used only after achieving adequate alpha-blockade (if not, can
cause a relatively unopposed alpha-adrenergic tone, resulting in CHF). Beta-blockade is
important for the control of tachycardia, arrhythmias, and myocardial ischemia. Metoprolol
is the agent of choice after adequate alpha-blockade. Labetalol with a beta:alpha ratio of 3:1
is a good alternative.
Labs/Studies
• Elevated free catecholamine or catecholamine metabolites in a 24-hour urinary sample has
the highest sensitivity for making a laboratory diagnosis.
• Imaging studies utilizing CT and MRI offer accurate and consistent identification of adrenal
pheochromocytomas.
• 131I-meta-iodobenzyl guanidine (MIBG) scan is useful in detecting recurrent tumors,
metastases, and extra-adrenal tumors.
• Hgb in unblocked patients will show polycythemia due to hemoconcentration. Adequate
alpha-blockade will result in blood volume re-expansion and a decrease of Hgb back to
normal values.
• Chemistry panel should be ordered to assess hyperglycemia and renal function.
• EKG should be examined for evidence of arrhythmias, ischemia, and left ventricular
hypertrophy.
• Chest x-ray should be examined for evidence of CHF.
• Echocardiogram to assess for cardiomyopathy should be considered if there is a decrease in
exercise tolerance.
• Cardiovascular: Increased risk of arrhythmias, particularly ventricular tachycardia and
fibrillation; dilated and hypertrophic cardiomyopathy in chronic high catecholamine states;
and congestive heart failure, myocarditis, and myocardial infarction.
• Pulmonary: Cardiogenic pulmonary edema from dilated cardiomyopathy as well as
noncardiogenic pulmonary edema.
• Gastrointestinal: High catecholamine state may decrease peristalsis leading to ileus and
obstipation.
• Renal: Renal artery stenosis from mass effect and renal infarction from hypertensive crisis
leading to acute renal failure.
• Hematologic: Polycythemia from intravascular volume depletion secondary to high systemic
vascular resistance.
• Metabolic: Glucose intolerance leading to diabetes. Lactic acidosis.
Recently diagnosed pheochromocytoma without adequate alpha-blockade.
TREATMENT
Premedications
Benzodiazepine and opioids are helpful for awake arterial line placement.
INTRAOPERATIVE CARE
• The vast majority of adrenalectomies for resection of pheochromocytoma are performed via
the laparoscopic approach. Deep general endotracheal anesthesia is the technique of choice.
• Neuraxial anesthesia to provide analgesia for incisional pain should be considered when
open adrenalectomy is planned. It does not, however, prevent catecholamine surges; and
hypotension after ligation of venous drainage may be more difficult to treat with
sympatholysis.
Monitors
• Arterial line
• Central venous catheter; pulmonary artery catheter if evidence of catecholamine-induced
cardiomyopathy or CHF
• Urinary catheter
• Induction should only proceed after arterial BP monitoring is established and emergency
drugs to treat acute hypertension and tachycardia are immediately available.
• Propofol can be used safely for induction. Patients need to be deeply anesthetized prior to
laryngoscopy and intubation. Drugs that increase sympathetic activity such as ketamine
should be avoided.
• Succinylcholine should be used with caution due to the theoretical concern that
fasciculations will increase intraabdominal pressure leading to tumor compression and
release of catecholamines.
• Nondepolarizing muscle relaxants (mivacurium, atracurium) that liberate histamine, which
can stimulate catecholamine release, should be avoided. Pancuronium, with
sympathomimetic activity, should also be avoided.
Maintenance
• Patients should be maintained at a deep level of general anesthesia. Opioids and volatile
anesthetics that do not sensitize the heart to catecholamines should be used.
• Anticipate marked increases in BP and heart rate during the establishment of
pneumoperitoneum and tumor manipulation. Mechanical compressive forces during these
two critical stages of surgery may cause release of catecholamines.
• Nitroprusside infusion via a central venous catheter provides a quick on, quick off method of
BP control that is easy to titrate. Other medications used successfully to temporize surges in
catecholamine include nitroglycerine, phentolamine, nicardipine, and esmolol.
• Anticipate marked decrease in BP and heart rate during ligation of the tumor’s venous
drainage. The sudden removal of the catecholamine source can precipitate hypotension in a
well alpha-blocked patient.
– Intravascular volume loading prior to ligation of venous drainage can temporize the
hypotensive effect of acute catecholamine withdrawal.
– Vasopressin infusion via a central venous catheter provides an effective method to treat
hypotension as it does not rely on the availability of alpha-adrenergic receptors (which
may still exhibit a significant degree of antagonism from preoperative alpha-blockade).
– Phenylephrine, norepinephrine, and epinephrine can be used to treat hypotension.
However, a larger than anticipated dose may be necessary due to preoperative alpha-
blockade.
• Glucose should be checked at regular intervals after ligation; the sudden withdrawal of
catecholamines may cause acute hypoglycemia.
General extubation criterion can be used.
FOLLOW-UP
BED ACUITY
Patients with persistent labile BP requiring a postoperative infusion of vasoactive medications
should be monitored in the ICU.
COMPLICATIONS
• The majority of intraoperative complications are related to catecholamine-induced extremes
of BP and heart rate. These may manifest as stroke, cerebral hemorrhage, myocardial
ischemia and infarct, other major end-organ damage, and death.
• Common postoperative complications include hypotension, hypertension, and
hypoglycemia.
– Hypotension is most common and is likely due to a combination of residual preoperative
alpha-blockade, insufficient volume resuscitation, adrenoreceptor down-regulation, and
lack of catecholamine output from the contralateral adrenal gland that had been
chronically suppressed.
– Most common cause of residual hypertension is due to elevated catecholamine stores in
adrenergic nerve endings. This may persist for up to 1 week after resection. Other causes
of residual hypertension include volume overload, inadvertent ligation of a renal artery,
or presence of residual tumor.
REFERENCES
1. Pacak K. Preoperative management of the pheochromocytoma patient. J Clin Endocrinol
Metab. 2007;92(11):4069–4079.
2. Connery LE, Coursin DB. Assessment and therapy of selected endocrine disorders.
Anesthesiol Clin North America. 2004;22(1):93–123.
3. Kinney MA, Warner ME, vanHeerden JA, et al. Perianesthetic risks and outcomes of
pheochromocytoma and paraganglioma resection. Anesth Analg. 2000;91(5):1118–1123.
4. Witteles RM, Kaplan EL, Roizen MF. Safe and cost-effective preoperative preparation of
patients with pheochromocytoma. Anesth Analg. 2000;91(2):302–304.
ADDITIONAL READING
• Kinney MA, Narr BJ, Warner MA. Perioperative management of pheochromocytoma. J
Cardiothorac Vasc Anesth. 2002;16(3):359–369.
• Prys-Roberts C. Phaeochromocytoma – recent progress in its management. Br J Anaesth.
2000; 85(1):44–57.
• Adrenalectomy
• Laparoscopy
CODES
ICD9
227.0 Benign neoplasm of adrenal gland
ICD10
• D35.00 Benign neoplasm of unspecified adrenal gland
• D35.01 Benign neoplasm of right adrenal gland
• D35.02 Benign neoplasm of left adrenal gland
CLINICAL PEARLS
• Pheochromocytoma may present with paroxysmal spells known as the “5 P’s”
– Pressure: Sudden increase in BP
– Pain: Headache, abdominal and flank pain
– Perspiration
– Palpitation
– Pallor
• Patients with pheochromocytoma must be adequately alpha-blockade followed by beta-
blocked (if tachycardic), volume resuscitated, and concomitant organ dysfunctions
identified and optimized prior to surgery. Phenoxybenzamine is the alpha-blocker of choice
as it mediates antagonism in a non-competitive fashion.
• Signs of adequate alpha-blockade include re-expansion of intravascular volume as measured
by the normalization of Hgb concentration, normalization of BP, and nasal congestion.
• Intraoperative hemodynamic fluctuations are most prominent during induction/intubation,
establishment of pneumoperitoneum, tumor manipulation, and ligation of the tumor’s
venous drainage.
• Arterial line is needed to monitor for hemodynamic fluctuations. Central venous catheter is
useful for assessing volume status and for vasoactive drug infusions. Pulmonary artery
catheter is utilized if there is any evidence of catecholamine-induced cardiomyopathy or
CHF.
• Intraoperative hypertension is best managed with titration of nitroprusside and esmolol.
• Intraoperative hypotension occurs after ligation of venous drainage and is best managed by
intravascular volume resuscitation and temporized by an infusion of vasopressin.
• Common postoperative complications include hypotension, hypertension, and
hypoglycemia.
PHOSPHATE
BASICS
DESCRIPTION
• Phosphate is an abundant intracellular anion and required for cell membrane structure,
cellular energy, cell transport, and oxygen release from hemoglobin.
• Normally, phosphate is maintained at 3–4.5 mg/dL in adults and 4–5 mg/dL in children.
• Abnormalities of phosphate homeostasis are seen in many common perioperative conditions
such as malnutrition, alcoholism, sepsis, trauma, hyperparathyroidism, patients with
metastases, major surgery, diabetic ketoacidosis, refeeding syndrome, and pathophysiologic
states associated with high serum catecholamine levels.
• Phosphate is required for many key cellular functions:
– Adenosine triphosphate (ATP) and creatinine phosphate as an energy store via high-
energy phosphate bonds
– DNA and RNA in genetic translation
– 2,3-diphosphoglycerate (2,3-DPG) as a key component in oxygen transport and release of
oxygen to tissues
– Cellular metabolism with uptake of phosphate increased by ingestion of glucose, fructose,
insulin levels, beta-adrenergic stimulation and anabolism
– Phospholipids and cell membrane structure
– Hydroxyapatite in bone makes up 90% of total body phosphate (the remaining 10% is
intracellular and <1% is extracellular)
– Inorganic phosphate provides an acid–base buffering system
• Absorption: Phosphate is normally ingested in excess of daily requirement
– It is absorbed passively in the small intestine (duodenum and jejunum); however, it
becomes an active sodium-dependent transport process in hypophosphatemia.
– Calcium, magnesium, aluminum and other cations can decrease absorption by
binding/chelating phosphate.
– Absorption is also regulated by 1,25-dihydroxyvitamin D3.
– Decreased phosphate absorption leads to the pathology of hypophosphatemia in
postoperative and/or physiologically stressed patients
• Production: When the body requires extra calcium, bone (hydroxyapatite) is broken down
and phosphate (in addition to calcium) is liberated.
• Excretion: Excess phosphate is excreted via the kidneys and the gastrointestinal system.
– In the glomerulus, phosphate is filtered freely with a glomerular concentration similar to
plasma.
– In co-transport with sodium, phosphate is reabsorbed in the proximal tubule. This co-
transport is regulated by plasma levels and the parathyroid hormone (PTH).
PTH normally inhibits phosphate reabsorption and increases excretion renally; thus, in
patients with hyperparathyroidism and increased PTH, plasma phosphate may be low.
On the other hand, patients lacking proper parathyroid function may suffer from
hyperphosphatemia.
– Increased renal loss can be seen in the postoperative or trauma patient, as well as
hypomagnesemia and volume expansion.
• Hyperphosphatemia occurs with either increased absorption, increased release of skeletal
phosphate, and/or decreased excretion.
– Renal failure with a GFR <25 mL/min impairs normal excretion.
– Hypoparathyroidism is often associated with hypocalcemia.
– Tissue damage or cell death from hematologic malignancies with high cell turnover, cell
destruction, and/or tumor lysis syndrome.
– Other causes include iatrogenic hyperphosphatemia (i.e., parenteral administration in
total parenteral nutrition [TPN], cathartics, medications with vitamin D), hypothermia,
malignant hyperthermia, rhabdomyolysis, and massive liver failure.
• Hypophosphatemia is severe when levels decrease to <1 mg/dL, respiratory or
cardiovascular symptoms manifest, and/or cellular dysfunction is present.
– Increased cellular uptake of phosphate from the extracellular compartment across the cell
membrane is the most common cause in hospitalized and critically ill patients.
– Etiologies of phosphate redistribution include carbohydrate-induced hypophosphatemia,
refeeding syndrome or TPN therapy, treatment of diabetic ketoacidosis, diuretics or
steroid therapy, osmotic diuresis, acidosis, tetany, and catabolic states.
– Septic, trauma, and other patients with high catecholamine states (endogenous and/or
exogenous epinephrine and norepinephrine) are prone to decreases in serum phosphate.
– Prolonged respiratory alkalosis can cause cellular uptake of phosphate due to imbalances
in intracellular pH and increased glycolysis. Phosphate continues to decrease even after
hyperventilation ceases. Furthermore, the respiratory alkalosis associated with sepsis in
gram-negative bacteremia and salicylate poisoning may explain the hypophosphatemia
seen in these patients.
– Hyperthermia and recovery from exhaustive exercise.
– Poor dietary uptake and malnutrition such as in hospitalized alcoholic patients (50%)
results in total body deficiency.
– Depletion of phosphate in the form of 2,3-DPG shifts the oxygen dissociation curve to the
left, leading to decreased tissue delivery of oxygen.
– Decreased phosphate in the form of ATP leads to a lack of energy. This can exacerbate
respiratory failure due to muscle weakness and diminish energy available for myocardial
tissue.
– Hypophosphatemic syndrome includes phosphate trapping, rhabdomyolysis,
cardiomyopathy, respiratory insufficiency from profound muscle weakness, erythrocyte
and leukocyte dysfunction, skeletal demineralization, metabolic acidosis, and nervous
system dysfunction.
• Manifestations of hyperphosphatemia are primarily related to the formation of calcium
phosphate salts and the subsequent development of hypocalcemia. Treatment includes the
following:
– Correcting the underlying etiology.
– Reducing dietary intake, decreasing iatrogenic/parenteral supply, and augmenting dietary
loss with enteric dietary phosphate binders (i.e., calcium acetate, calcium carbonate,
aluminum hydroxide, or sevelamer) may be beneficial.
– Increasing renal excretion by saline volume expansion and/or diuresis. If appropriate
indication exists, renal replacement therapy may be needed or adjusted.
• Hypophosphatemia is more commonly seen in the perioperative period. In critically ill
patients, incidence ranges from 44–68% and is associated with increased mortality.
– Pulmonary complications include respiratory muscle dysfunction, which leads to acute
respiratory muscle failure and difficulty liberating patients from mechanical ventilation.
– Myocardial dysfunction is not uncommon with manifestations of arrhythmias, decreased
contractility, and acute heart failure.
– Neurologic manifestations include paresthesia, myopathy, encephalopathy, delirium,
seizures, and coma.
– Muscle weakness and malaise is also common with rhabdomyolysis resulting from severe
hypophosphatemia.
– Hematologic abnormalities include dysfunction of all cell lines (erythrocytes, platelets,
and leukocytes).
– Immune dysfunction may occur as a result of impaired chemotactic, phagocytic, and
bactericidal activity of granulocytes.
• Cardiac surgery: In patients undergoing elective cardiac surgery, 34.3% of patients suffered
from postoperative hypophosphatemia (1).
– Hypophosphatemia was associated with prolonged ventilation, increased requirement of
inotropic support, and prolonged hospital stay.
– Blood, plasma, and platelet transfusions were associated with decreased postoperative
phosphate levels.
• Hepatic surgery: In patients undergoing major hepatic surgery, the incidence of
hypophosphatemia was 67% in one series (2), while another series showed decreased
phosphate levels in all patients undergoing hepatic lobectomy (3).
– Postoperative complications were more prevalent in patients with hypophosphatemia.
– Proposed mechanisms include intracellular shifts into hepatocytes and renal phosphate
wasting.
– Antacids were associated with increased postoperative hypophosphatemia.
• Trauma
– The incidence of hypophosphatemia and other electrolyte abnormalities is higher in
patients with severe head injury than with patients without significant head injury (4).
– Hypothermic protocols for neuro-protection in patients with severe head injury further
exacerbate hypophosphatemia (5).
• Kidney transplant recipients are also prone to hypophosphatemia due to multiple
mechanisms that are not clearly understood.
• In patients with the potential for refeeding syndrome, it is best to initially avoid glucose-
containing fluids and then reintroduce them slowly.
– Since the electrolyte abnormalities (hypophosphatemia, hypokalemia) occur due to
increased cellular uptake–associated glucose and insulin, avoiding glucose-containing
substances can alleviate electrolyte derangements.
– If there is evidence of refeeding syndrome, nutrition should be started slowly and
advanced only after electrolytes are stabilized.
EQUATIONS
• Phosphate replacement can be made in the form of both sodium phosphate and potassium
phosphate, either orally or parenterally. The desired amount to be administered can be
achieved by multiplying the volume of distribution (400 mL/kg) by the desired change. The
rate of IV administration should not exceed 0.25 mmol/kg over 4–6 hours to avoid
hypocalcemia and tissue damage.
• In patients with hyperkalemia or risk factors for hyperkalemia, sodium phosphate may be
preferred over potassium phosphate.
REFERENCES
1. Cohen J, Kogan A, Sahar G, et al. Hypophosphatemia following open heart surgery:
Incidences and consequences. Eur J Cardiothorac Surg. 2004;26(2):306–310.
2. Buell JF, Berger AC, Plotkin JS, et al. The clinical implications of hypophosphatemia
following major hepatic resection or cryosurgery. Arch Surg. 1998;133(7):757–761.
3. George R, Shiu MH. Hypophosphatemia after major hepatic surgery. Surgery.
1992;111(3):281–286.
4. Polderman KH, Bloemers FW, Peerdeman SM, et al. Hypomagnesemia and
hypophosphatemia at admission in patients with severe head injury. Crit Care Med.
2000;28(6):2022–2025.
5. Polderman KH, Peerdeman SM, Girbes AR. Hypophosphatemia and hypomagnesemia
induced by cooling in patients with severe head injury. J Neurosurg. 2001;94(5):697–705.
6. Geerse DA, Bindels AJ, Kuiper MA, et al. Treatment of hypophosphatemia in the intensive
care unit: A review. Crit Care. 2010;14(4):R147.
• Trauma
• Renal transplant
• End stage renal disease
CLINICAL PEARLS
• Hypophosphatemia is prevalent in patients undergoing major surgery, including cardiac
surgery, hepatic surgery, abdominal aorta surgery, trauma, and burn victims.
• Identifying patients at risk for hypophosphatemia (i.e., post-surgical, malnourished) allows
for earlier detection and prompt treatment to prevent major complications, especially
respiratory failure, cardiac failure, and mortality.
• Correction of hypophosphatemia with large doses of intravenous phosphate can lead to
hypocalcemia by precipitation of calcium phosphate salts. Electrolytes should be monitored
either during or after replacement of phosphate.
PIERRE ROBIN SEQUENCE
Mohamad Iravani, MD
Swati Patel, MD
BASICS
DESCRIPTION
• Pierre Robin syndrome presents as a variable degree of micrognathia (resulting from
mandibular aplasia), glossoptosis, and cleft palate.
• The cardiovascular and neuromuscular systems may also be affected.
• Synonyms: Pierre Robin sequence; Pierre Robin malformation; Robin sequence; Pierre Robin
anomalad
EPIDEMIOLOGY
Prevalence
May occur in isolation or as part of a more complex syndrome (Stickler syndrome,
cerebrocostomandibular syndrome, velocardiofacial syndrome, fetal alcohol syndrome and
trisomy 18). Greater than 80% occur as part of a syndrome.
Prevalence
• Ranges from 1 in 8,500 to 1 in 20,000 children.
• The male to female ratio is one-to-one.
Morbidity
Airway obstruction and failure to thrive
Mortality
A mortality of 2.2–26% has been reported in the literature.
The etiology of Pierre Robin sequence is unclear but it may be associated with the deletion
2q32.2–33.2
• The term Pierre Robin sequence, in place of a syndrome, was introduced because a sequence
of events leads to the anomaly rather than a constellation of anomalies.
• Mandibular hypoplasia is the initial event that leads to the posterior placement of the
tongue (glossoptosis) and loss of support and coordination of the genioglossi muscles.
– Thus, on inspiration, the tongue is further displaced posteriorly, worsening airway
obstruction.
– Chronic obstruction can lead to failure to thrive, pulmonary hypertension, and cor
pulmonale.
• Cleft palate results from the failure of the tongue to descend during development, which
interferes with the midline fusion of palatal shelves.
• Severe airway obstruction may require immediate intervention at birth. Prone or lateral
position may assist in maintaining airway patency (these patients may necessitate induction
and intubation in the lateral or prone position).
• Subsequent growth of the mandible, development of voluntary tongue control, and
improved coordination of the parapharyngeal muscles occurring over the first years of life
leads to lessening of the airway obstruction.
Preservation of a patent airway is the main perioperative goal; the posterior positioning of the
tongue, combined with micrognathia requires special consideration.
• Induction: Maintenance of spontaneous ventilation with adequate ventilation and
oxygenation must be ensured until the airway is secured.
• Extubation: Patients must be fully awake and have full reversal of muscle relaxation. In
addition, tongue stitches, careful monitoring, and emergency airway equipment need to be
considered.
• Elective tracheostomy may be considered for patients with severe obstruction especially if
the patient will need multiple surgeries or to prevent chronic obstruction and development
of pulmonary hypertension.
SYMPTOMS
• May range from none to severe airway obstruction resulting in respiratory distress, hypoxia,
and hypercarbia.
• Severe disease may be associated with feeding difficulties and resultant failure to thrive.
History
• History of apnea and obstruction including the position required for airway patency.
• Need for supplemental oxygen.
• Full cardiac history to rule out associated congenital heart disease.
• Record of previous anesthetics should be obtained for relevant information regarding airway
management.
Signs/Physical Exam
• Vital signs
• Patient position necessary for airway patency
• Degree of airway obstruction and retractions
• Degree of mandibular hypoplasia and tongue position
• Assessment for cardiac murmur
• Presence of any other anomalies
TREATMENT HISTORY
• Nasopharyngeal airway, lip–tongue adhesions, or urgent tracheostomy may be necessary if
patient positioning fails to improve the obstruction.
• Mandibular distraction has been used successfully to alleviate airway obstruction and avoid
tracheostomy. Note that while distraction of the mandible can decrease the degree of
obstruction, it may not change the Cormack and Lehane grade classification for grading the
view of direct laryngoscopy.
Labs/Studies
As indicated by the severity of symptoms and co-morbidities
• Echocardiography
• CXR (hyperventilation, pneumonia, CHF)
• Arterial or venous blood gas
• Ocular diseases such as congenital glaucoma and retinal detachments
• Sensorineural hearing loss
• Pulmonary hypertension, cor pulmonale from chronic hypoxia
Any evidence of a recent URI such as rhinorrhea, abnormal lung sounds, or a cough might
justify a postponement of elective surgery.
TREATMENT
Premedications
• Due to the high incidence of airway obstruction, preoperative benzodiazepines should be
avoided or used with extreme caution depending on the index of suspicion.
• Peripheral access should be obtained and anti-cholinergics should be given to decrease oral
secretions and to counteract the vagal hyperreflexia present in these patients.
Airway management can be extremely difficult and parents should be accordingly informed of
the possible loss of airway and its consequences, including the need for emergent
tracheostomy.
INTRAOPERATIVE CARE
Consider regional anesthetic techniques whenever possible, so as to avoid airway
instrumentation.
Monitors
• Consider augmenting the ETCO2 waveform size on the monitor (slow rise to peak indicates
expiratory obstruction)
• Consider an arterial line in high-risk patients (for serial ABGs)
• Unless previous anesthetic records document the ability to mask ventilate and intubate or
the index of suspicion based on physical examination is reasonably low, fiberoptic
intubation with maintenance of spontaneous respirations is strongly recommended (consider
awake nasal or oral fiberoptic intubation).
• It is crucial to have a plan before induction; appropriate equipment including a
tracheostomy tray and adequate personnel must be available.
• The main goal is preservation of spontaneous ventilation; therefore muscle relaxants should
be avoided until the airway is secured.
• Topicalization of the airway with nebulized 4% lidocaine is beneficial for blunting airway
responses to intubation (care must be taken to avoid toxicity in small infants).
• The choice of anesthetic regimen for sedation during intubation is crucial. The key is to
maintain an adequate depth of anesthesia to prevent laryngospasm without loss of
spontaneous respiratory effort.
– Sevoflurane and propofol have been used successfully but caution must be used as both
may cause airway obstruction and/or apnea.
– Ketamine and/or dexmedetomidine have been used successfully in this setting. Ketamine
and dexmedetomidine both preserve spontaneous respiration while providing adequate
anesthesia. When used together, dexmedetomidine may offset the excess oral secretions
and sympathomimetic effects of ketamine.
• The narrowed pharyngeal space (secondary to small jaw and relatively large posteriorly
located tongue) can add an additional challenge for fiberoptic intubation. During
intubation, consider:
– Additional skilled personnel to provide jaw thrust
– Tongue “retraction” anteriorly using towel clamp, tongue stitch, or gauze. Care must be
taken to minimize trauma to the tongue.
• Fiberoptic endotracheal intubation through a laryngeal mask airway has been successfully
described.
• Indirect videolaryngoscopy can also be utilized, as it allows a more anterior view of the
airway.
• Once the airway is established and appropriate position is confirmed, consider suturing the
ETT in place for added security.
Maintenance
Consider steroid (dexamethasone) administration if airway edema is anticipated.
• Extubation should be carried out only when the patient is fully awake with regular
breathing and adequate tidal volumes.
• A tongue stitch may aid in maintaining a patent airway postoperatively.
FOLLOW-UP
BED ACUITY
• One-to-one nursing in an ICU setting is mandatory to allow for close monitoring of
respiratory issues.
• Emergency airway equipment should be immediately available.
• No particular medications are indicated for Pierre Robin.
• Arterial blood gas may provide guide to degree of airway obstruction.
• For patients with severe obstruction or known difficult airway, consider ENT consult or
standby in the operating room for potential urgent/emergent tracheostomy.
COMPLICATIONS
The main complications are associated with loss of airway and the subsequent
hypoxia/anoxia.
REFERENCES
1. Bush PG, Williams AJ. Incidence of the Robin Anomalad (Pierre Robin syndrome). Br J
Plast Surg. 1983;36:434–437.
2. Rintala A, Ranta T, Shears T. On the pathogenesis of cleft palate in the Pierre Robin
syndrome. Scand J Plast Reconstr Surg. 1984;18:237–240.
3. issonnette B. Syndromes: Rapid recognition and perioperative implications. McGraw-Hill
Companies, Inc. 2006.
4. Iravani M, Wald SH. Dexmedetomidine and ketamine for fiberoptic intubation in a child
with severe mandibular hypoplasia. J Clin Anesth. 2008;20(6):455–457.
5. Van den Elzen APM, Semmekrot BA, Bongers EMHF, et al. Diagnosis and treatment of the
Pierre Robin Sequence: Results of a retrospective clinical study and review of the
literature. Eur J Pediatr. 2001;160:47–53.
• Tracheostomy
• Cleft palate
CODES
ICD9
756.0 Anomalies of skull and face bones
ICD10
Q87.0 Congen malform syndromes predom affecting facial appearance
CLINICAL PEARLS
• Maintain spontaneous ventilation until the airway is secured or the ability to bag mask
ventilate is confirmed.
• Consider suturing the tube for the duration of the procedure.
• Consider a tongue stitch for the postoperative period to decrease obstruction.
• Always have equipment ready for re-intubation.
PLACENTA ACCRETA
Izabela M. Wasiluk, MD
BASICS
DESCRIPTION
• Placenta accreta refers to the abnormally deep and firm attachment of the placenta to the
uterine wall. This may lead to massive, life-threatening hemorrhage during manual
placental separation.
• The differential diagnosis of placenta accreta includes other causes of postpartum
hemorrhage:
– Uterine: Atony, rupture, inversion, retention of placental products
– Non-uterine: Vaginal tears, perineal hematoma, coagulopathy
• When discovered early, an elective Cesarean section/hysterectomy may be performed in a
more controlled situation:
– Can be scheduled at a facility capable of managing postpartum hemorrhage.
– A multidisciplinary team can be scheduled to be in the operating room (obstetrician,
anaesthetist, neonatologist, interventional radiologist).
– Uterine preservation may be considered.
– Type and crossed blood products can be in the room and ready for transfusion; a cell saver
can be set up and ready for use. The blood bank should be informed.
– Techniques to decrease blood loss may be implemented, including leaving the placenta in
situ.
– An epidural catheter may be considered as opposed to general anesthesia.
• However, when diagnosed at the time of, or after, placental separation, the delivery of care
becomes emergent and challenging to members of the health team. In addition, maternal
morbidity and mortality increase.
EPIDEMIOLOGY
Prevalence
• In the US: Occurs in 1 of 2,500 deliveries
• Increased association in women with placenta previa: Approaches 10% of cases (1)
• Increased 10-fold in the past 50 years due to the increased frequency of Cesarean sections.
– Unscarred uterus: 3% (2)
– ≥5 prior Cesarean sections: 67%
Prevalence
Cesarean sections have increased due to maternal obesity, multiple gestations (assisted
reproductive technology), concern about litigation, and decreases in the use of operative
vaginal delivery for cephalic and breech presentations (5)
Morbidity
• Hysterectomy, loss of fertility
• Coagulopathy, DIC
• Hypotension
Mortality
Maternal mortality rate is 7%
• Number of Cesarean sections (relative risk 11.32) (1).
• Advanced maternal age >35 years (relative risk 4.45)
• Placenta previa (relative risk 2.28).
• Previous myomectomy
• Normally, the layer of the decidua basalis prevents the attachment of placental villi through
the endometrium and into the myometrium. Thus, at delivery, the placenta can readily
detach from the uterine wall.
• In placenta accreta, deeper invasion by trophoblasts may occur in thin, poorly formed
decidua, as seen in the lower segment of the uterus or related to prior hysterotomy scars.
• This may lead to failure of the placenta to separate after delivery, or uncontrolled bleeding
when it does.
• Management and outcome depend upon when the placenta accreta is diagnosed. Common to
both scenarios is the need for a multidisciplinary team.
• When diagnosed early, or before placental separation, surgical management often involves
an elective Cesarean hysterectomy. Procedures or techniques to decrease blood loss include
intrauterine artery balloon catheterization for ligation and/or reversible embolization,
endouterine square hemostatic sutures, and leaving the placenta in the uterus during the
hysterectomy.
• There has been a recent trend toward conservative management/uterine preservation in an
attempt to preserve fertility. This involves implementing some of the above-mentioned
techniques that decrease blood flow to the uterus, thus allowing separation of the placenta.
• In both scenarios, the anaesthetist must be prepared to treat postpartum hemorrhage. This
can involve the transfusion of multiple units of blood products, as well as the use of a cell
saver, antifibrinolytics, or recombinant factors. Large-bore IV access is necessary.
• The decision to provide anesthesia via an epidural or general anesthesia is dependent upon
several factors: Elective versus emergent, volume status, altered mental status, development
of a coagulopathy, and comfort of the anaesthetist and patient.
SYMPTOMS
• Usually signs and symptoms are not detected until labor and delivery.
• Third trimester vaginal bleeding can be noted.
History
• Prior Cesarean section, placenta previa, myomectomy, or manual removal of the placenta
Signs/Physical Exam
• Profuse vaginal bleeding during manual separation of the placenta after delivery
• Non-delivery of the placenta in a half-hour post delivery.
TREATMENT HISTORY
See techniques for decreasing blood loss
MEDICATIONS
Not applicable
Labs/Studies
• 45% women with placenta accreta were found to have elevated serum alpha-fetoprotein
levels.
• Definitive diagnosis can be made only on histologic examination.
• Ultrasonography has a relatively high sensitivity (0.77) and specificity (0.96).
• MRI increases diagnostic accuracy in cases when ultrasonography is inconclusive (sensitivity
0.88, specificity 1.0) (3).
• Possible invasion into the myometrium or the serosa and surrounding structures.
• Disseminated intravascular coagulopathy (DIC)
• In elective cases, all members of the multidisciplinary team should be available. In addition,
cell salvage, blood products that are type and crossed, and possibly recombinant factors or
antifibrinolytics should be present before proceeding.
• In emergent cases, any delay should be avoided.
CLASSIFICATIONS
Three variants of the condition are recognized on the basis of the degree of placental
penetration of the myometrium:
• Placenta accreta: Chorionic villi abnormally adhere to the myometrium.
• Placenta increta: Villi invade the myometrium.
• Placenta percreta: Villi penetrate through the uterine serosa and may adhere to surrounding
structure.
TREATMENT
Premedications
• Gastric volume and acid reducing medications in elective cases.
• In emergent cases, fluid resuscitation (crystalloid, colloid, transfusion products) and
vasopressor therapy, should be started, as appropriate.
• In elective cases, a discussion about invasive monitoring, transfusion of blood products, and
choice of anesthesia should be discussed.
INTRAOPERATIVE CARE
• General anesthesia is usually administered, in particular, for emergent cases.
• If a laboring epidural is in place, continuous epidural anesthesia may be used for many cases
of elective Cesarean hysterectomy (4). Conversion to general anesthesia, however, may be
warranted in hemodynamically unstable patients secondary to massive peripartum
hemorrhage with cardiovascular decompensation
Monitors
• Two large-bore IVs
• Arterial line for BP monitoring and frequent lab draws. Consider noninvasive cardiac output
monitoring (NICOM) for monitoring CO, CI, PVR, and PVRI.
• Central line placement may be considered for large-bore access, pressure monitoring, and
the administration of medications (e.g., vasopressors).
• General anesthesia: A rapid sequence induction should be performed, after the abdomen is
prepped and the surgical team, blood products, and other personnel are in the room. The
goal is to minimize the time from induction to delivery and hence anesthetic drug exposure
to the fetus.
• Laboring epidural in place: Bolus with local anesthetic and confirm an adequate T6 level.
Maintenance
• If the accreta is found co-incidentally during a Cesarean section, the interventional
radiologist should be informed so that procedures to decrease blood loss before
hysterectomy/placental separation can be performed.
• Blood product transfusion may be guided by hematocrit/hemoglobin levels, platelet values,
coagulation profile, thromboelastogram, and/or clinical judgment.
• Cell saver allows for autologous blood to be returned to the patient after being suctioned
from the field, washed, and filtered. It requires a technician to set up and manage. When
large volumes of blood are auto-transfused, a coagulopathy may result from the loss of
clotting factors and platelets.
• Recombinant-activated factor VII is a potent procoagulant that bypasses parts of the
coagulation cascade. It is commonly used for hemophilia, but off-label uses include the
treatment of refractory bleeding. Studies suggest that there is a more favorable outcome
when it is administered early in the course of refractory hemorrhage, rather than as a last
resort. Risk may be prohibitive if the patient is at high risk for thromboembolic
complications or has developed disseminated intravascular coagulation.
• Tranexamic acid (TA) is a synthetic lysine analog that can be used prophylactically for
refractory bleeding. TA acts reversibly by inhibiting the binding of plasminogen to charged
lysine sites on the surface of fibrin molecules; thus it prevents the conversion of
plasminogen to plasmin.
• Extubation may be considered if the patient is:
– Hemodynamically stable
– Volume repleted
– Without airway edema from the large fluid shifts
– Other extubation criteria are met
• If an epidural catheter is in place, and a coagulopathy is suspected, it should not be removed
until fully resolved, and PT/PTT/INR are within normal limits.
FOLLOW-UP
BED ACUITY
Intensive care unit should be available for direct transfer.
• CCU bed with hemodynamic monitoring
• Maintain oxygenation, circulation, control of hemorrhage, and coagulopathy
COMPLICATIONS
• Hemorrhagic shock, cardiovascular collapse
• Uterine atony
• Coagulopathy/DIC
• Hysterectomy
REFERENCES
1. Miller DA, Chollet JA, Goodwin TM. Clinical risk factors for placenta previa – placenta
accreta. Am J Obstet Gynecol. 1997;177:210–214.
2. Silver RM, Landon MB, Rouse DJ, et al. Maternal morbidity associated with multiple repeat
cesarean deliveries. Obstet Gynecol. 2006;107(6):1226–1232.
3. Warshak CR, Eskander R, Hull AD, et al. Accuracy of ultrasonography and MRI in the
diagnosis of placenta accreta. Obstet Gynecol. 2006;108:573–581.
4. Chestnut DH, Dewan DM, Redick LF, et al. Anesthetic management for obstetric
hysterectomy: A multiinstitutional study. Anesthesiology. 1989;70:607–610.
5. Warshak CR, Ramos GA, Eskander R, et al. Effect of predelivery diagnosis in 99 consecutive
cases of placenta accreta. Obstet Gynecol. 2010;115(1):65–69.
6. Hull AD, Moore TR. Multiple repeat cesareans and the threat of placenta accrete:
Incidence, diagnosis, management. Clin Perinatol. 2011;38(2):285–296.
7. John J Sciarra. Gynecology and Obstetrics. Philadelphia, PA: Lippincott, Williams and
Wilkins, 2000.
• Robert Resnick. Diagnosis and Management of Placenta Accreta. UpToDate.
• Placenta previa
• Cell savage
• Recombinant-activated factor VII
• Hysterectomy
CODES
ICD9
667.00 Retained placenta without hemorrhage, unspecified as to episode of care or not
applicable
ICD10
• O43.211 Placenta accreta, first trimester
• O43.212 Placenta accreta, second trimester
• O43.219 Placenta accreta, unspecified trimester
CLINICAL PEARLS
• Placenta accreta may cause major postpartum bleeding.
• Women with placenta previa and/or a history of prior Cesarean deliveries are at increased
risk of placenta accreta.
• A Cesarean section combined with a hysterectomy (placenta left in situ) is frequently
necessary, although uterine conservation may be considered in select cases.
• A multidisciplinary approach and rapid resuscitation efforts are required in order to have a
desirable clinical outcome.
PLACENTA PREVIA
Peter H. Kim, MD
Mark Zakowski, MD
BASICS
DESCRIPTION
• Placenta previa is a condition in pregnancy where the placenta overlies all or part of the
internal os of the cervix.
– A total placenta previa completely covers the cervical os.
– A partial placenta previa covers only a portion of the cervical os.
– A marginal or a low-lying placenta previa only encroaches on the edge of the internal
cervical os.
EPIDEMIOLOGY
Prevalence
In the US: 2.8/1,000 live births (1)
Morbidity
• Complete or partial placenta previa is an absolute indication for Cesarean delivery. Cervical
dilation with labor will lead to spontaneous, life-threatening maternal hemorrhage.
• According to the World Health Organization (WHO), placenta previa is the number one risk
factor for blood transfusion in obstetrics.
• There is an increased risk of placenta accreta (where the placenta is attached too deep in the
uterine wall) in parturients with a placental previa. This causes difficulty with the placental
detachment. Hemorrhage can occur during manual attempts to detach the placenta,
resulting in the need for a hysterectomy. In parturients with placenta previa, placenta
accreta can occur in:
– ∼3% who have had an unscarred uterus
– ∼11% who have had a previous Cesarean section
– ∼40% who have had two previous Cesarean deliveries
Mortality
• Maternal mortality rate: 0.03% of all births in the US. The majority of deaths are attributed
to maternal hemorrhage and disseminated intravascular coagulation (DIC) (3).
• Neonatal mortality: 10.7/1000 births. The majority of deaths are attributed to prematurity
and/or fetal growth restriction (1).
• The etiology of placenta previa is unknown.
• Risk factors include: Previous placenta previa, presence of a uterine scar, multiparity,
multiple gestation, and advanced maternal age.
– Women >35 years old are ∼3 times more likely to have placenta previa than women
<25 years old (4).
No specific cause has been identified to date
• Evaluate maternal airway in the event that a general anesthetic must be performed
emergently.
• Regional anesthesia is preferred. General anesthesia carries a 1.7 times increased risk of
maternal mortality (5) due to airway complications. Parturients are more likely to have
airway edema and difficulty with mask ventilation and intubation; this is combined with a
decreased functional residual capacity (FRC) and increased oxygen demand.
• Prepare for maternal hemorrhage.
– Ensure adequate IV access.
– Type and cross for blood.
– In the operating room, O-negative or crossmatched (preferred) packed red blood cells, as
well as fresh frozen plasma, platelets, and possibly activated factor VII need to be
immediately available.
• Identify the position of the placenta to assess the risk of placenta accreta; there is an
increased risk if the placenta overlies a previous uterine scar.
SYMPTOMS
Lightheadedness or dizziness
History
• Timing of bleed: Vaginal bleeding from placenta previa generally occurs in the second or
third trimester.
• Painless vaginal bleeding: In contrast, placental abruption is characterized by vaginal
bleeding with painful contractions. Bleeding from a placenta previa may spontaneously stop
but it will recur.
• History of a prior uterine surgery and/or injury: There is an increased risk of placenta
accreta if a placenta previa occurs in the presence of a prior uterine scar.
Signs/Physical Exam
• Painless vaginal bleeding
• Hypotension
• Tachycardia
• Non-reassuring fetal heart tracing
MEDICATIONS
• If the diagnosis of placenta previa is made between 24 and 34 weeks gestation,
corticosteroids may be administered to accelerate fetal lung maturity. Patients with placenta
previa are prone to preterm labor.
Labs/Studies
• Assess the severity of hemorrhage: Hemoglobin/hematocrit. Values may be falsely elevated
if adequate fluid resuscitation has not occurred.
• Evaluate coagulation status: Platelets, PT/PTT, INR, fibrinogen.
• Type and cross
• Abdominal ultrasound: Confirms the presence and type of placenta previa. Evaluate the risk
of placenta accreta.
• No vaginal examinations should be performed if there is a suspected previa.
If the parturient is hemodynamically stable and vaginal bleeding is controlled. Cesarean
delivery should be delayed to allow for fetal lung maturity.
CLASSIFICATIONS
Marginal, partial, total
TREATMENT
• Cesarean delivery is indicated in the presence of complete or partial placenta previa.

– Timing of delivery is determined by the fetal and maternal status.
Premedications
• Anti-aspiration precautions: Sodium bicitrate, cimetidine, and/or metoclopramide.
• Avoid benzodiazepines and opioids; they can cross the placenta and contribute to neonatal
depression.
• Type and cross 4–6 pRBC units; may need to transfuse O-negative uncrossmatched blood in
an emergency. Consider rapid transfusion devices or cell saver.
• Conversion to general anesthesia if the patient is hemodynamically unstable.
• Possible need for transfusion of blood products.
• Possible need for placement of invasive monitors including arterial catheter and/or central
venous catheterization.
INTRAOPERATIVE CARE
• Neuraxial anesthesia preferred.
• General anesthesia indicated for actively bleeding, hemodynamically unstable patients.
Monitors
• Standard: Pulse oximetry, noninvasive BP, EKG, temperature, capnography.
• Invasive monitors (arterial catheter, CVP) if indicated.
• Regional anesthesia is preferred.
• Rapid-sequence intubation if general anesthesia is indicated.
– Etomidate (0.3 mg/kg) or ketamine (1.5 mg/kg) preferred for hemodynamically unstable
patients.
– Be prepared for difficult intubation. There is a 7-fold increase in failed intubation in the
parturient population.
– Succinylcholine, a depolarizing muscle relaxant, is preferred (1–1.5 mg/kg). The greater
blood volume is countered by the lower concentration of plasma pseudocholinesterase
(metabolizes succinylcholine) during pregnancy.
Maintenance
• The neonatal team should be in the room.
• General anesthesia is maintained with a combination of volatile anesthetic and nitrous
oxide. Following delivery of the fetus, decrease the volatile anesthetic to <0.5 MAC to
minimize decrease in uterine tone.
• Opioids: IV or epidural dosing can be given following clamping of the cord.
• Muscle relaxation: Non-depolarizing muscle relaxants may be used to facilitate closure;
dosage is not altered for the parturient.
• Volume status
– Aggressively titrate fluids to maintain hemodynamic stability (BP >100 mm Hg, HR
<120) and urine output (>0.5 mL/kg/hr). Consider early use of colloids (e.g., Hetastarch
6% or albumin 5%).
– Blood loss may be difficult to assess visually (typically underestimated by 33–50%) (6). All
blood loss should be quantitated, including weighing laparotomy sponges and bed
underpads.
– In the case of massive transfusion, the recommendation is that pRBCs and fresh frozen
plasma are given in a 1:1 ratio; one unit of platelets is given for every 4 units of pRBCs.
• Normothermia: Utilize fluid warmers as well as forced air warming blankets. There is an
increased tendency for hypothermia and shivering (increased metabolic demand) with
massive blood loss and fluid replacement.
• Uterotonics to reduce bleeding after delivery:
– Oxytocin; proceed with additional agents after 20 units
– Methylergonovine 0.25 mg IM (do not administer IV)
– 15-methyl prostaglandin F2-alpha 250 mcg IM or directly into the uterus
– Misoprostol 1000 mcg may be placed rectally (prostaglandin E1 derivative)
• Alternate techniques to control hemorrhage
– Arterial embolization in the radiology suite
– Intrauterine balloon tamponade
– Surgical ligation of uterine and hypogastric arteries may slow down the bleeding.
• Extubation criteria include adequate oxygenation, adequate ventilation, and ability to
protect the airway.
• Consider orogastric tube suctioning prior to extubation to reduce the gastric volume.
• Prophylactic antiemetics
FOLLOW-UP
BED ACUITY
• Monitor for continued or recurrent bleeding and DIC in the recovery room and postpartum
period.
• In the setting of moderate to severe hemorrhage, consider higher acuity care until
hemodynamically stable or no further bleeding for several hours.
Follow Hb/Hct and coagulation status.
COMPLICATIONS
• Maternal hemorrhage
– Poor contractility of the lower uterine segment following separation of the placenta previa
may lead to increased blood loss.
– Increased risk of entering the placenta with uterine incision at Cesarean delivery.
– Increased risk of placenta accreta in the setting of placenta previa.
– If bleeding is uncontrolled, may necessitate ligation of uterine vessels or hysterectomy.
• Disseminated intravascular coagulation (DIC)
REFERENCES
1. Ananth CV, Smulian JC, Vintzileos AM. The effect of placenta previa on neonatal mortality:
A population-based study in the United States, 1989 through 1997. Am J Obstet Gynecol.
2003;188(5):1299–1304.
2. Silver RM, Landon MB, Rouse DJ, et al. Maternal morbidity associated with multiple repeat
cesarean deliveries. Obstet Gynecol. 2006;107:1226–1232.
3. Crane S, Chun B, Acker D. Treatment of obstetrical hemorrhagic emergencies. Curr Opin
Obstet Gynecol. 1993;5(5):675–682.
4. Zhang J, Savitz DA. Maternal age and placenta previa: a population-based, case-control
study. Am J Obstet Gynecol. 1993;168(2):641–645.
5. Hawkins J, Chang J, Palmer S, et al. Anesthesia-related maternal mortality in the United
States: 1979–2002.
6. Obstet Gynecol. 2011;117:69–74.
7. Lyndon A, Miller S, Huwe V, et al. CMQCC.org, Blood Loss: Clinical techniques for ongoing
quantitative measurement. Available at : http://www.cmqcc.org/resources/916.
• Placenta accreta
CODES
ICD9
• 641.00 Placenta previa without hemorrhage, unspecified as to episode of care or not
applicable
• 641.10 Hemorrhage from placenta previa, unspecified as to episode of care or not applicable
ICD10
• O44.00 Placenta previa specified as w/o hemorrhage, unsp trimester
• O44.10 Placenta previa with hemorrhage, unspecified trimester
CLINICAL PEARLS
• The hallmark of placenta previa is painless vaginal bleeding. Placenta previa can be
classified as complete, partial, or low lying/marginal. In addition, it can be a risk factor for
placenta accreta.
• Bleeding typically stops, but may worsen with recurring episodes.
• Vaginal examinations are contraindicated in the setting of a placenta previa.
• Parturients with marginal or low-lying placenta previa may be considered for vaginal
delivery. However, those with a complete or partial placenta previa must be delivered by
Cesarean section.
• Placenta previa is a risk factor for maternal hemorrhage. Adequate intravascular access
should be attained and blood products should be immediately available.
PLACENTAL ABRUPTION
BASICS
DESCRIPTION
• Placental abruption is the premature, complete, or partial separation of the placenta from
the uterine wall prior to delivery of the fetus, after 20 weeks gestation.
• It may be revealed by vaginal bleeding or remains concealed.
EPIDEMIOLOGY
Prevalence
• Occurs in ∼0.5–1% of deliveries (1,2,3,4)
• Rate of clinically detected abruptions have increased in the US, with a disproportionate
increase seen in African-American women (1)
• Incidence peaks between 24–26 weeks gestation, and decreases with advancing gestational
age (2).
Morbidity
• Maternal morbidity depends on the severity of the abruption and results from DIC, renal
failure, transfusion reactions, ischemic necrosis of distal organs, hemorrhagic shock, uterine
rupture, and uncontrolled hemorrhage resulting in hysterectomy (1,2,3).
• Fetal morbidity depends on the location and severity of abruption, in addition to the
gestational age of the fetus. It results from hypoxia, anemia, CNS anomalies, IUGR, SGA,
preterm delivery or fetal death. Retroplacental abruptions have the worst prognosis (2).
Mortality
• Perinatal mortality has been reported as 11–12% (2,3).
• Maternal risk factors
– History of prior abruption
– History of smoking, cocaine, and substance abuse
– Alcohol consumption
– Hypertension or preeclampsia
– Elevated 2nd trimester maternal AFP
– Thrombophilias
– Folate deficiency or Anemia (11)
– Placenta previa or bleeding early in pregnancy
– Uterine fibromyomas/tumors
– Advanced maternal age
– Higher mean levels of homocysteine
– Hospitalizations for acute and chronic respiratory diseases during pregnancy (9)
• Procedural or situational risk factors
– Trauma or domestic violence
– Velamentous insertion of umbilical cord or short cord
• Fetal-related risk factors
– Multifetal gestation (or sudden decompression of the uterus)
– Oligohydramnios
– Preterm premature rupture of membrane
– Intrauterine infections or chorioamnionitis
– Male fetus
• Placental abruption most likely results from a cascade of underlying pathophysiological
processes, and the precise mechanism remains elusive in many cases. Furthermore different
mechanisms may be involved in preterm versus term abruptions . Inflammatory mediators
present in both acute and chronic inflammatory processes, may play a role in increased
premature production of matrix metalloproteinase-9, an enzyme that helps in the normal
placental detachment following delivery (5).
• Abnormal placental vasculature, thrombosis, and decreased placental perfusion may play a
role in abruption on the basis of pathologic studies (3). Acute vasospasm of small vessels,
coupled with thrombosis of decidual vessels may lead to necrosis and venous hemorrhage at
the decidual placental interface, leading to uteroplacental insufficiency (2). In some cases,
abnormal trophoblast invasion leading to rupture of spiral arteries and premature
separation of the placenta may be responsible for abruption (6).
• Cocaine is a vasoconstrictor and may cause vasospasm of uterine vessels leading to
uteroplacental insufficiency and abruption (7).
• Increased capillary frailty, changes in uteroplacental circulation, and arterial rupture may
cause abruption in smokers (4). Nicotine’s effects may result from vasoconstriction of
uterine and umbilical arteries, coupled with increased carboxyhemoglobin levels that
compromise oxygenation, leading to hypoxia, placental microinfarctions, necrotic foci, and
ultimately abruption (8).
• Acute shearing forces may affect the placenta–decidua interface, leading to abruption. This
occurs with rapid deceleration injuries or sudden decompression following membrane
rupture of an over-distended uterus (polyhydramnios or multiple gestations).
• Vaginal delivery may be considered if the mother is stable and the fetus is at term or near
term with a reassuring fetal status.
• In the absence of maternal hypotension, clotting abnormalities, or signs of fetal distress,
labor analgesia may be provided by an epidural for vaginal delivery (2).
• In cases of fetal death with severe abruption, vaginal delivery is possible, as long as the
mother is stable. However, potential coagulopathy should be evaluated if considering an
epidural.
SYMPTOMS
• Vaginal bleeding
• Abdominal or back pain
• Frequent uterine contractions
• Fetal distress or fetal death
History
Elicit associated risk factors and symptoms since diagnosis is based mostly on clinical
grounds.
TREATMENT HISTORY
• Administer continuous high-flow supplemental oxygen
• Maintain left uterine displacement
• Monitor for bleeding and if DIC is present, correct coagulopathy prior to surgery, if possible
• Monitor maternal vital signs and fetal heart tones continuously
• Insert large bore IV lines and begin LR or NS infusion.
Labs/Studies
• Hemoglobin, hematocrit—to assess bleeding
• Platelets, fibrinogen, FDP, PT, aPTT, D-dimer—to assess coagulopathy
• BUN, electrolytes—to assess volume status/renal dysfunction
• Blood type and cross match
• Abdominal and vaginal ultrasound. Ultrasound is not sensitive but has a high PPV (10).
DIC, Renal failure, Hemorrhagic shock, Uterine rupture, Uncontrolled hemorrhage, Ischemic
necrosis of distal organs.
• If the fetus is preterm, shows no signs of distress, and the abruption is minimal, then the
patient may be hospitalized with conservative management, allowing pregnancy to continue
in order to promote fetal lung maturity prior to delivery. The patient should be transferred
to a facility with a neonatal unit capable of caring for a preterm baby.
• If the mother is unstable, or the fetal status is non-reassuring, then delivery should be
undertaken via prompt C-section (2).
CLASSIFICATIONS
Premature, complete, or partial separation
TREATMENT
Premedications
Cross-matched blood, FFP, and platelets should be available if DIC is present.
• Blood consent
• Potential postoperative intubation
• Planned or potential invasive monitoring
INTRAOPERATIVE CARE
General anesthesia is usually the preferred option for emergency C-section due to the
potential underlying coagulopathy and hypovolemia from hemorrhage.
Monitors
• In addition to routine monitors, central venous pressure monitoring may be helpful for fluid
management.
• An arterial line may be useful for continuous BP monitoring.
• Foley catheter output may be useful to guide fluid status.
• Consider agents that maintain better hemodynamics such as ketamine or etomidate.
• RSI with cricoid pressure should be considered on induction to minimize chances of
aspiration.
• Friable and edematous laryngeal mucosa, combined with underlying coagulopathy may
result in uncontrolled hemorrhage during intubation.
• Preparation for a difficult airway should include difficult airway equipment such as LMAs,
intubating LMAs, flexible fiberoptic bronchoscope, and videolaryngoscopy, if available.
• An awake fiberoptic intubation may be considered for a difficult airway if time permits.
Maintenance
• 50% nitrous oxide may be used along with oxygen and a reduced dose of volatile anesthetic
prior to delivery.
• Following delivery, nitrous oxide may be increased and the dose of volatile anesthetic may
be lowered to promote uterine contractions. IV agents such as opioids and midazolam may
be used to supplement anesthesia.
• These patients are at increased risk for uterine atony, therefore oxytocin should be infused
promptly after delivery.
• Bleeding should be controlled, hypovolemia and any coagulopathy should be corrected prior
to extubation.
• If the patient has undergone massive blood/products transfusion or fluid administration, or
if there are signs of ongoing bleeding or coagulopathy, the patient should remain intubated
and transferred to the ICU.
FOLLOW-UP
BED ACUITY
Most parturients improve following delivery, but if hypotension or coagulopathy persists, the
patient should be admitted to a multidisciplinary ICU for continued observation and
management.
• Oxytocin infusion may be continued in the postoperative period.
• Fluid management and vigilant observation for further bleeding should be continued.
Hemoglobin, hematocrit, and vital signs should be monitored.
• Coagulation profile and D-dimer should be ordered if DIC is suspected.
COMPLICATIONS
• Uterus may be hypotonic following delivery and may necessitate an emergency
hysterectomy.
• Prolonged hypovolemia may result in ATN.
• Coagulation cascade products may lead to renal cortical necrosis resulting in chronic renal
failure.
• Severe preeclampsia may be masked by hypovolemia in cases of massive hemorrhage, and
therefore extra vigilance is required to avoid overlooking this diagnosis.
REFERENCES
1. nanth CV, Oyelese Y, Yeo L, et al. Placental abruption in the United States, 1979 through
2001: Temporal trends and potential determinants. Am J Obstet Gynecol. 2005;192:191–
198.
2. Oyelese Y, Ananth CV. Placental abruption. Obstet Gynecol. 2006;108(4):1005–1016.
3. Ananth CV, Wilcox AJ. Placental abruption and perinatal mortality in the United States.
Am J Epidemiol, 2001;153:332–337.
4. Ananth CV, Smulian JC, Vintzileos AM, et al. Incidence of placental abruption in relation
to cigarette smoking and hypertensive disorders during pregnancy: A meta-analysis of
observational studies. Obstet Gynecol. 1999;93(4):622–628.
5. Ananth CV, Getahun D, Peltier MR, et al. Placental abruption in term and preterm
gestations. Evidence for heterogeneity in clinical pathways. Am J Obstet Gynecol.
2006;107:785–792.
6. Elsasser DA, Ananth CV, Prasad V, et al. Diagnosis of placental abruption: Relationship
between clinical and histopathological findings. Eur J Obstet Gynecol Reprod Biol.
2010;148(2):125–130.
7. Hoskins IA, Friedman DM, Frieden FJ, et al. Relationship between antepartum cocaine
abuse, abnormal umbilical artery doppler velocimetry and placental abruption. Obstet
Gynecol. 1991;78(2):279–282.
8. Kaminsky LM, Ananth CV, Prasad V, et al. The influence of maternal cigarette smoking on
placental pathology in pregnancies complicated by abruption. Am J Obstet Gynecol.
2007;197:275.e1–275.e5.
9. etahun D, Ananth CV, Peltier MR, Smulian JC, Vintzileos AM. Acute and chronic
respiratory diseases in pregnancy: associations with placental abruption. Am J Obstet
Gynecol. 2006;195:1180–1184.
10. lanz C, Purnell L. Clinical utility of sonography in the diagnosis and treatment of
placental abruption. J Ultrasound Med. 2002;21:837–840.
11. nanth CV, Smulian JC, Demissie K, Vintzileos AM, Knuppel RA. Placental abruption
among singleton and twin births in the United States: Risk factor profiles. American
Journal of Epidemiology. 2001;153:771–778.
CODES
ICD9
• 641.20 Premature separation of placenta, unspecified as to episode of care or not applicable
• 641.23 Premature separation of placenta, antepartum condition or complication
ICD10
• O45.90 Premature separation of placenta, unsp, unsp trimester
• O45.91 Premature separation of placenta, unsp, first trimester
• O45.92 Premature separation of placenta, unsp, second trimester
CLINICAL PEARLS
• In the presence of abruption, rule out DIC as a source of coagulopathy and hypovolemia
from massive hemorrhage before performing spinal or epidural anesthesia.
• Aggressive fluid and product resuscitation is required in the setting of massive hemorrhage
or DIC to prevent long-term consequences.
PLASMA OSMOLALITY
Erik Olness, MD
Stephen O. Bader, MD
BASICS
DESCRIPTION
• Osmolarity and osmolality are similar terms and are often used interchangeably.
– Osmolarity is defined as the number of moles of solute in a liter of solution.
– Osmolality refers to the number of moles of solute in a kilogram of solution; it is generally
the preferred term
Water’s molecular mass represents the number of water molecules more accurately than
the volume (molecular mass does not change with temperature, whereas water volume
does, albeit only slightly).
1 kg of water occupies exactly 1 L at 4%C, allowing the interchangeability of osmolality
and osmolarity in most instances.
• Osmoles are the number of unique particles into which a given substance dissociates in
solution.
– 1 mole of NaCl in solution contains 2 osmoles, since NaCl dissociates into Na+ and Cl−
ions.
– 1 mole of glucose in solution contains one osmole as glucose does not dissociate.
• Freezing point depression osmometry is used to directly measure plasma osmolality.
• Tonicity, a related term referring to the effect of a solution on cell volume, is often equated
incorrectly with osmolarity or osmolality.
• An average adult male is ∼60% water by weight; females are 50% water.
• Total body water (TBW) is divided into 2 major fluid compartments separated by cellular
membranes: Intracellular fluid (ICF) and extracellular fluid (ECF). The ECF can be further
divided into:
– Intravascular fluid, contained within the vascular endothelium
– Interstitial fluid, which includes all fluid outside of cells
• The fluid volume contained in a given compartment is determined by the compartment’s
solute concentration and composition. Differences in solute concentrations are largely due
to the physical characteristics of the barriers separating compartments. The trapped solutes
within compartments create osmotic forces that govern the distribution of water and
ultimately compartment volume.
• The cell membrane–bound Na+/K+ ATPase ion pump exchanges sodium (Na+) for
potassium (K+) in a 3:2 ratio. 3 Na+ ions are transported extracellularly for 2 K+ ions
transported intracellularly.
– Cell membranes are relatively impermeable to Na+, and to a lesser extent K+, such that
Na+ is the most important determinant of extracellular osmotic pressure while K+ is the
most important determinant of intracellular osmotic pressure.
• Cells are impermeable to most proteins resulting in a high intracellular protein
concentration. The anionic proteins are nondiffusible, making the unequal Na+/K+
exchange crucial in preventing intracellular hyperosmolality.
• Fluid compartment exchange is primarily governed by diffusion through cell membranes
and capillary endothelium. A substance’s rate of diffusion across a membrane depends on:
– The substance’s permeability through a given membrane
– The hydrostatic pressure difference between the two sides
– The substance’s concentration difference
– The electrical potential across the membrane for charged substances
• The ECF’s osmolality is equal to the sum of the concentration of all dissolved solutes.
– Na+ and its paired anions account for nearly 90% of the dissolved solutes in the ECF.
– This makes the following approximation possible: Plasma osmolality ∼2 × Plasma Na+
concentration ([Na+]plasma). Measured plasma osmolality is normally 280–290 mOsm/L.
• TBW and Na+ balance are maintained in a tight range by the interaction of multiple
neurohumoral mechanisms, including the renin–angiotensin– aldosterone system, the
hypothalamic–pituitary axis, the atrial and brain natriuretic peptides, and the sympathetic
nervous system.
• The main regulatory mechanism for water metabolism is the pituitary secretion of
antidiuretic hormone (ADH), also known as arginine vasopressin.
ANATOMY
• Osmoreceptors in the hypothalamus closely regulate plasma osmolality by controlling the
secretion of ADH and the thirst mechanism.
– The osmoreceptors can detect changes in osmolality as small as 1–2%.
– When ECF osmolality increases, these hypothalamic cells shrink and trigger the release of
ADH from the posterior pituitary.
– ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus, before
being stored in the posterior pituitary. It acts on renal distal tubules and collecting ducts
to increase water reabsorption by inducing increased expression of aquaporin-2 channels.
• A decrease in osmolality causes the osmoreceptors to swell, suppressing ADH release, and
results in increased excretion of water.
– This diuresis peaks at about 90–120 minutes
– Complete suppression of ADH secretion can result in excretion of 10–20 L of water a day
• Non-osmotic triggers of ADH release are:
– A 5–10% decrease in blood volume via carotid and aortic arch baroreceptors and possibly
atrial stretch receptors
– Pain, emotional stress, and hypoxia
• Thirst mechanism. Osmoreceptors in the lateral preoptic area of the hypothalamus also
respond to changes in extracellular osmolality, triggering thirst when osmolality increases
and suppressing thirst when osmolality decreases. Thirst represents the major defense
mechanism against hyperosmolality and hypernatremia, as it is the only response that
increases water intake. However, the thirst mechanism is only functional in the conscious
patient.
• Hyperosmolality (refers to the plasma osmolality): Usually, but not always, associated with
hypernatremia. Water moves/shifts out of cells and into the vasculature in response. Clinical
signs are predominantly neurologic. Lethargy, restlessness, and hyperreflexia can progress
to coma, seizures, and death. Cerebral vein rupture leading to intracerebral or subarachnoid
hemorrhage can result from rapid decreases in brain volume. Hyperosmolality is generally
treated by correcting water deficits over a period of 48 hours with hypotonic solutions
intravenously or increased oral water intake.
• Diabetes insipidus (DI) is a defect in renal concentrating ability characterized by
inappropriately dilute urine (<200 mOsm/kg) in the setting of an elevated serum
osmolality (>295 mOsm/kg). Thus, polyuria, in the setting of hypernatremia or other
indications of hyperosmolality, is seen.
– Central DI results from a lack of ADH secretion from the hypothalamic–pituitary
apparatus. It can result from a myriad of brain lesions, but is rare: Neurosurgical
procedures such as transsphenoidal pituitary resection, traumatic or hypoxic brain injury,
ruptured cerebral aneurysm, tumors, or inflammatory/infiltrative processes. Central DI
can be diagnosed by an increase in urine osmolality after administering exogenous ADH in
the form of desmopressin, also known as DDAVP.
– Nephrogenic DI is characterized by normal ADH secretion, but failure of the kidneys to
respond appropriately. The diagnosis is confirmed by administering exogenous ADH and
subsequent production of dilute urine. Causes include congenital, drug-induced, and
idiopathic etiologies; it can also be caused by hypercalcemia and hypokalemia. Treatment
is geared towards correcting the underlying disorder and maintaining adequate water
intake. Paradoxically, administration of a thiazide diuretic can decrease urine output by
depleting total body Na+ and intravascular volume. More water is absorbed in the
proximal tubules, and water delivery to distal tubules and collecting ducts is reduced.
Protein and sodium restriction can also reduce urinary output.
• Hypoosmolality (serum osmolality <260 mOsm/kg) always indicates excess TBW relative to
body solutes or an excess water to solute ratio in the ECF. It is nearly always associated
with hyponatremia. As with hyperosmolality, clinical symptoms of hypoosmolality are
primarily neurologic with severity related to how quickly extracellular hypoosmolality
develops. Rapid decreases in osmolality result in increased intracellular water, leading to
brain edema and increased intracranial pressure.
• Hyponatremia is the most common electrolyte abnormality encountered in clinical
medicine. The majority of cases are chronic and asymptomatic. Patients with [Na+] >125
mEq/L are frequently asymptomatic. Early symptoms such as anorexia, nausea, and
weakness are nonspecific. Progression of cerebral edema results in confusion, lethargy,
seizures, coma, and ultimately death unless treated. Plasma sodium levels <120 mEq/L are
associated with serious manifestations.
• The syndrome of inappropriate ADH secretion (SIADH): The most common reason for
acquired hyponatremia in hospitalized patients. A large variety of causes, including brain
injury, critical illness, paraneoplastic syndromes, inflammation, pain, infections, and
medications (selective serotonin reuptake inhibitors, opiates, tricyclic antidepressants,
diuretics, antineoplastic agents, antihypertensives, proton pump inhibitors). Characterized
by excess ADH secretion, resulting in decreased plasma osmolality (<275 mOsm/kg) and
inappropriately concentrated urine (>100 mOsm/kg). Patients are euvolemic and have
normal acid–base balance. Typically, it is a diagnosis of exclusion.
• Adrenal insufficiency can lead to increased ADH secretion from both non-osmotic
stimulation secondary to decreased BP, and increased adrenocorticotropic hormone levels.
• Hyperglycemia can result in [Na+]plasma decreases of ∼1 mEq/L for every 62 mg/dL
increase in glucose concentration.
• An osmolal gap is the discrepancy between measured and calculated osmolality; it indicates
the presence of abnormal osmotically active substances). It can be seen in the following
conditions:
– Methanol, ethanol, isopropyl alcohol, or ethylene glycol intoxication
– IV mannitol therapy
– Chronic renal failure
– Ketoacidosis
– Patients absorbing large amounts of glycine or sorbitol containing irrigants
– Marked hyperlipidemia or hyperproteinemia
• Hypernatremia and anesthetics:
– If associated with hypovolemia, hypotension and tissue hypoperfusion can occur;
vasodilation and cardiac depressant effects of anesthetic agents are accentuated.
Decreased volume of distribution requires reducing most IV drug doses, whereas
decreased cardiac output speeds up the onset of inhalational agents.
– Increases MAC values of inhaled agents
– Significant hypernatremia ([Na+] >150 mEq/L) should result in postponement of elective
procedures until fluid deficits are corrected and underlying causes established.
• A classic triphasic response to surgical or traumatic injury to the neurohypophysis consists
of early central DI symptoms (<24 hours). This lasts for 3–5 days, followed by a period of
hyponatremia resulting from the release of stored pituitary ADH. A week or more after the
injury, the patient may experience permanent central DI, as the pituitary stores of ADH are
exhausted.
• Hyponatremia is frequently a sign of a serious underlying condition requiring careful
preoperative workup. [Na+] >130 mEq/L are generally considered safe for patients
undergoing general anesthesia and should be corrected to this level prior to all elective
procedures even if the patient is asymptomatic. Lower concentrations can result in clinically
significant cerebral edema that can manifest intraoperatively as a decrease in MAC or
postoperatively as somnolence, agitation, or confusion.
• Patients undergoing transurethral resection of the prostate, hysteroscopy, or other
procedures can absorb large amounts (up to 20 mL/min) of water from irrigating fluids,
placing them at risk of developing acute hypoosmolality.
• Hypoosmolality is treated by eliminating body water using diuretics or replacing the
patient’s sodium deficit with saline solutions. Except in severe brain edema or known acute
cases, serum [Na+] should not be corrected more than 10 mEq/L in the first 24 hours, and
not more than 18 mEq/L in 48 hours. Rapid correction has been associated with
demyelinating lesions in the pons known as central pontine myelinolysis (CPM) resulting in
irreversible neurologic injury.
EQUATIONS
• TBW in liters can be estimated:
– 0.5 × weight (kg) for women
– 0.6 × weight (kg) for men
• Plasma osmolality can be estimated:
Osmolality (mOsm/kg) ∼ 2 × [Na+]plasma(mEq/L)
– When elevated, glucose and urea contribute significantly to extracellular osmolality,
therefore:
• Saline solutions for the hyponatremic patient:
0.9% saline contains 154 mEq/L Na+
3% saline contains 513 mEq/L Na+
REFERENCES
1. Bagshaw SM, Townsend DR, McDermid RC. Disorders of sodium and water balance in
hospitalized patients. Can J Anesth. 2009; 56:151–167.
2. cAlister V, Burns KE, Znajda T, et al. Hypertonic saline for perioperative fluid management.
Cochrane Database Syst Rev. 2010;20(1): CD005576.
ADDITIONAL READING
• Barash, Paul G, Cullen, et al. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott
• Brenner. Brenner and Rector’s The Kidney, 8th ed. Saunders, 2007.
• McPherson RA, Pincus MR. Henry’s clinical diagnosis and management by laboratory
methods, 21st ed. Philadelphia, PA: W.B. Saunders, 2006
• Morgan GE, Mikhail MS, Maged S, et al. Clinical Anesthesiology. 4th ed. New York:
Lange/McGraw-Hill, 2006.
• Syndrome of inappropriate antidiuretic hormone
• Hyponatremia
• Hypernatremia
• Extracellular fluid
• TURP syndrome
CLINICAL PEARLS
• Serum [Na+] can be used as a quick estimate of plasma osmolality under normal conditions.
• While abnormal osmolality and [Na+] are common, they can be a sign of serious problems.
• Rapid changes in osmolality from administration of hyperosmolal or hypoosmolal fluids
should be avoided.
PLATELETS
Yun Rose Li, BS
BASICS
DESCRIPTION
• Platelets are small cellular fragments that function to promote hemostasis and coagulation
upon endothelial cell injury.
• Minor platelet deficiencies usually present as bleeding of mucous membranes, petechiae,
and epistaxis; large deficiencies can lead to life-threatening spontaneous hemorrhage.
• Preoperative platelet counts are not typically checked unless there are clinical signs of
coagulopathy.
• A low platelet count is a poor indicator of platelet function.
• Tests such as thromboelastograms measure clotting kinetics and aid with assessing function.
• Platelets are small, irregularly shaped cell fragments that lack nuclei. Following endothelial
cell injury, subendothelial collagen, von Willebrand factor (vWF), and tissue factor (TF) are
exposed and activate the circulating platelets that they contact. Platelet clumping occurs
and the coagulation cascade is activated to strengthen the clot.
• Normal values for endogenous platelets:
– Range: 150,000–400,000/μL
– Production: ∼1 × 1011 produced daily
– Survival: ∼9–10 days
• Platelet donation
– Pooled platelets: Centrifugation separates plasma and red blood cells from platelets. One
platelet concentrate is attained via a “hard spin,” followed by a “soft spin” (or vice versa)
of a whole blood unit (450 mL). The term “pooled” describes combining concentrates;
however, it increases recipient exposure to HLA and infection (usually 6 different donor
concentrates to comprise 1 jumbo unit).
– Plasmapheresis: Extracorporeal collection of blood followed by separation and removal of
platelets from red blood cells and plasma; the red blood cells and plasma are returned to
the donor. The process lasts ∼90 minutes, and yields a single or double plateletpheresis
unit (equivalent to 1 or 2 jumbo units of pooled platelets, respectively). The main benefit
is the decreased exposure to multiple donors. Today, ∼80% of the US platelet supply
comes in this manner.
• Platelet storage
– May be stored for up to ∼5 days at room temperature.
– Unlike other blood products, cannot be cooled to slow down metabolism or reduce
bacterial growth; platelet function is temperature sensitive. Temperatures <18°C damage
micro-canalicular structures, and induce clustering of platelet receptors. In the recipient’s
circulation, macrophages will rapidly remove these previously “chilled” platelets.
– Need to be continuously agitated to reduce bacterial growth
– Special plastic containers are used to increase the surface-to-volume ratio and allow
sufficient gas exchange between the internal volume and external ambient air (hypoxia is
detrimental to survival, and metabolism is not slowed as with other transfusion units that
can be cooled)
• Platelet transfusion (1,2)
– Cross-matching the recipient’s platelets with those of the donor is unnecessary; however,
incompatibility can reduce post-transfusion counts. Platelets possess ABO antigens on
their surface and RBCs are present in small amounts (<0.5 mL); when several units are
needed, incompatible RBCs may cause hemolysis. Conversely, Type A and B antibodies
from the donor’s plasma portion may react against the recipient’s RBCs when large
volumes are administered. If several units are needed, ABO matching is prudent.
– Rh antigens are not present on the platelet surface; however, RBCs (<0.5 mL) contained
in the concentrate may lead to Rh immunization. Avoid incompatibility in women of
childbearing years; if unavoidable, Rh Ig should be considered to prevent
alloimmunization.
• Normal values for transfused platelets
– Range:
“Platelet concentrate” is the term used for the platelets separated from 1 unit of WB. At
most institutions, 6 platelet concentrates = 1 jumbo pack, or ∼3 × 1011 platelets.
Plateletpheresis donors donate a “single” or “double” unit in a sitting. A single unit or 1
plateletpheresis unit = 3 × 1011 platelets; this is equivalent to 1 jumbo pack or 6 units
of platelet concentrate.
– Survival: ∼1–7 days post-transfusion. At day 5, intravascular recovery is ∼51%.
ANATOMY
• Platelets are produced by invaginations from the surface of megakaryocytes in the marrow
of trabecular bone.
• Inactive platelets circulate in the blood for ∼10 days as smooth, disk-shaped cells and are
degraded via phagocytosis in the spleen and by Kupffer cells in the liver
• Thrombocytopenia: A low platelet count can result from:
– Increased destruction
– Decreased production
– Dilutional effects
– Pseudothrombocytopenia
• Thrombocytosis (thrombocythemia): Elevated platelet counts are due to:
– Essential causes (e.g., myeloproliferative diseases)
– Reactive causes (e.g., hyposplenism, splenectomy, acute phase reactant)
– Iatrogenic causes
• Infections
– Storage of platelets at higher temperatures increases the risk of bacterial growth.
– Frequently, infection is introduced by a needle entering the vein through nonsterile skin; it
can also occur, albeit rarely, from donor bacteremia or occult colon cancer.
– Mortality from infection is high, particularly in immunocompromised patients with cancer
or blood disorders.
– Donor pathogens include HIV, HBV, HCV, CMV.
• Febrile transfusion reactions: Secondary to leukocytes and soluble cytokines; may be
avoided by transfusing leukocyte-reduced platelets.
• Acute hemolytic reactions: Type A and B antibodies from the donor’s plasma may react
against the recipient’s RBCs when large numbers of ABO-incompatible units are given.
• Transfusion-associated graft versus host disease (TA-GVHD): Describes the abnormal
immune response of T-lymphocytes attacking the host tissue; the risk is increased in
immunocompromised patients. It is uniformly fatal, and there are minimal to no proven
treatment options. Prevention consists of gamma-irradiating donor platelets prior to
transfusions.
• Transfusion related lung injury (TRALI): To reduce the incidence, storage may be performed
in additive solutions instead of plasma.
• Quantitative: For most patients, a minimum of 50,000–100,000/μL is adequate to avoid
bleeding during procedures and surgeries. See table for specific procedures and suggestions.
• Qualitative: Platelet dysfunction and microvascular bleeding can occur despite adequate
platelet counts. Uremia, aplastic anemia, chemotherapy, irradiation, ITP, and DIC can
impair proper platelet function. Functional tests include the thromboelastogram (increased
R time, decreased MA suggest platelet dysfunction).
• Transfusion parameters
– In a 70 kg patient, 1 × 1011 platelets increase platelet counts ∼10,000/μL.
– 1 unit of pooled platelets (∼5–10 concentrates) contains ∼3 × 1011 and can increase
recipient platelet counts by ∼30–60,000/μL. This is roughly equivalent to dosing 1
platelet concentrate/10kg
– 1 plateletpheresis unit contains ∼3 × 1011 platelets, and can increase counts ∼30–
60,000/μL (equivalent to a jumbo unit of pooled platelets)
• Transfusion considerations (2)
– In children, consider ordering specific amounts from the blood bank to decrease waste
(e.g., 20–25 mL).
– “Volume reduce” by removing plasma to decrease the volume load in children or fluid
overloaded patients (dialysis patients, congestive heart disease). However, this can result
in a loss of 15–55% of platelets; alternatively, a smaller dose (with smaller volume) may
be appropriate.
– Inpatients or chronic conditions: Frequent transfusions of a lower dose of platelets may
reduce the total amount of platelets needed, whereas larger doses extend the time needed
between transfusions and may be more convenient.
– Lack of response may be due to patient factors such as HLA antibodies, splenomegaly, DIC,
amphotericin administration, and fever, as well as long storage time. Consider HLA
matching, cross-matching, or “fresh platelets” (<48 hours after collection).
– If donor-incompatible platelets are administered, consider washing or removing plasma
and resuspension with saline. This serves to decrease donor plasma antibodies and
incompatible RBCs.
• Massive transfusion/“damage control resuscitation." 1:1:1 transfusion of pRBC:FFP:platelets
reduces risk of thrombocytopenia that can occur from the initial loss, followed by dilution
from component therapy (FFP, PRBC devoid of platelets).
• “Swirling” is a visual effect from diffraction when platelets are manually re-suspended and
held up to a strong light. This indicates that the platelets are high quality and discoid and
can be easily performed at bedside. Old platelets lack “swirling” and have a spherical
morphology that lacks diffraction.
GRAPHS/FIGURES
Recommended platelet levels for procedures and surgeries:
See Table
REFERENCES
1. McCullough J. Overview of platelet transfusion. Seminars in hematology. 2010;47(3):235–
242.
2. Stroncek DF, Rebulla P. Platelet transfusions. Lancet. 2007;370(9585):427–438.
ADDITIONAL READING
• Michelson AD. Platelets. 2nd ed. Academic Press, 2005.
• Slichter SJ. Evidence-based platelet transfusion guidelines. Hematology. 2007;172–178.
• Transfusion related lung injury (TRALI)
• Von Willebrand’s disease
• Transfusion infection
CLINICAL PEARLS
• Physiologic range = 150–400,000/μL; there are approximately 1 × 1011 newly produced
platelets/day. For most patients, a minimum of 50–100,000/μL is adequate to avoid
bleeding during procedures and surgeries.
• Platelets are stored at a higher temperature than other transfusion products; they cannot be
frozen, refrigerated, or infused through warmed tubing.
PNEUMONECTOMY
Daniel Castillo, MD
BASICS
DESCRIPTION
General
• Pneumonectomy describes the complete removal of the lung and can be performed for
ipsilateral lymph node metastasis or when a lobectomy and its modifications are not
sufficient to remove diseased tissue.
• For open procedures (thoracotomy), exposure and dissection involves either rib spreading or
removal of a portion of the rib. The pulmonary artery and veins are identified and stapled
first, followed by the main bronchus; removal of the lung from the chest cavity occurs
subsequently. An extrapleural pneumonectomy requires a more extensive resection of lymph
nodes, pericardium, diaphragm, parietal pleura, and the chest wall.
• The procedure may also be performed thoracoscopically (VATS). The smaller incision and
reduced surgical stress (inflammatory mediators) may decrease postoperative pain and
pulmonary dysfunction.
Position
• Lateral decubitus with the operative side up.
• A bean bag and axillary roll are often utilized.
Incision
• Posterior-lateral incision usually at the fifth or sixth intercostal space.
• Median sternotomy approach has been described but is rarely performed today.
Approximate Time
∼2–3 hours
EBL Expected
<500 mL; re-do or extrapleural pneumonectomies can be significantly higher
Hospital Stay
An average of 5–12 days
Arm boards and arm rest for lateral positioning
EPIDEMIOLOGY
Prevalence
Most commonly performed for lung carcinoma
Prevalence
The prevalence of lung cancer is second to that of prostate cancer in men and breast cancer in
women.
Morbidity
• Postoperative pulmonary complications range from 11 to 49% (1)[B].
• Right pneumonectomy is associated with cardiac herniation.
• Age > 65 years, right-sided procedures, and dysrhythmias were associated with an
increased risk of a major complication (p < 0.05) (2)[B].
• Dysrhythmias increased the median length of stay from 8 to 11 days (p < 0.05). Age > 65
years, intrapericardial or extrapleural pneumonectomy, right-sided procedure, and any
major complication are factors associated with an increased risk of dysrhythmias (p < 0.05)
(2)[B].
• Others: Pulmonary embolism, myocardial infarction (MI), bronchopleural fistulas,
chylothorax, subcutaneous emphysema, phrenic and recurrent laryngeal nerve injury.
Mortality
• Overall 30-day mortality ranges from 5–13% (5)[B].
• Increased with low predicted postoperative FEV1 (ppo-FEV1), high perfusion fraction of the
resected lung (3)[B], and postoperative acute lung injury (30–50%) (4)[B].
• Preoperative evaluation of lung and cardiac function along with discussion with the surgeon
can help decrease factors leading to pulmonary complications.
• One lung ventilation physiology and management
• Judicious intraoperative fluid management can decrease acute lung injury (ALI).
SYMPTOMS
Dyspnea, cough, hemoptysis
History
• Extensive evaluation of pulmonary disease and cardiac status; exercise tolerance, cigarette
smoking
• Myasthenic syndrome (Eaton–Lambert)
Signs/Physical Exam
• Cyanosis, clubbing
• Auscultation: Crackles, wheezes, distant sounds.
• Pulmonary hypertension: Split or increased second sound
• Heart failure: Peripheral edema, jugular venous distention, hepatomegaly
MEDICATIONS
• Radiation therapy and chemotherapy
• Inhaled beta agonists, anticholinergics, or steroids
• Antibiotics
• Diuretics
• Home oxygen
• Antiarrhythmics
Labs/Studies
• EKG
– COPD: Right atrial and ventricular hypertrophy, low voltage QRS, and poor R wave
progression across the precordial leads
– Cor pulmonale: Enlarged P waves in lead II.
• Arterial blood gas: Baseline hypoxia or CO2 retention
• Imaging: Chest x-ray (CXR), CT scan, MRI to identify airway anatomy, masses, obstruction
to flow and narrowing of airway, lung lesions/disease, lung hyperinflation, effusions,
abscesses and hematomas
• Pulmonary function tests: Performed to establish a baseline, to determine the ability to
tolerate lung resection, and to risk stratify.
• Split-lung function tests: Predicts the function of the lung tissue that will remain after
resection
• Cardiac failure due to pulmonary disease
• Right ventricular straining and hypertrophy
• Arrhythmias
• Hepatic congestion
TREATMENT
Premedications
• Minimize use of benzodiazepines and narcotics (may worsen hypercarbia). Benzodiazepines
may contribute to postoperative delirium, especially in elderly patients.
• Nebulizers: Beta agonists and anticholinergics.
• Possibility of prolonged postoperative intubation and mechanical ventilation
• Blood and blood product transfusion
• Invasive monitoring: Central line, arterial line, transesophageal echocardiography (TEE)
• Regional anesthesia: Epidural, paravertebral blocks(6)[B]
Third generation cephalosporin for skin organisms
INTRAOPERATIVE CARE
General anesthesia with thoracic epidural placement or ipsilateral paravertebral blocks with
catheter placement for continuous infusion (6,7)[B]
Monitors
• Arterial line
• Central line for CVP tracing and SvO2 monitoring
• TEE
• Induction agent (often based on cardiac status) along with IV lidocaine, narcotics, and
muscle relaxation are most commonly used. Introduction of volatile agent during bag mask
ventilation will bronchodilate prior to laryngoscopy and intubation.
• Double lumen tube (DLT), bronchial blocker, or main-stemmed single lumen tube. A
fiberoptic scope is used to confirm proper placement.
Maintenance
• Ventilation
– During OLV, implement an FiO2 of 1.0, low tidal volumes 5–6 mL/kg, and limit peak and
plateau pressures to <35 and 25 cm H2O, respectively (8)[A].
– In the event of hypoxia, reassess tube position with FOB, if surgically possible proceed
with brief manual bilateral lung ventilation, if not possible implement CPAP to the
nondependent lung, followed by PEEP to the dependent lung, and consider pulmonary
artery clamping.
– ABGs should be performed intermittently or for intraoperative events to assess PaO2,
PaCO2
• Fluids: A fluid restrictive technique has been shown to decrease the risk of ALI; however, it
must be balanced with preserving renal funciton. It may be necessary to implement
inotropes and vasoactive drugs to maintain adequate perfusion pressure and hemodynamic
stability. Blood products should be administered in accordance with blood loss.
• Renal: Maintain adequate perfusion pressures and a urine output of 0.5 mL/kg/hr.
• Hemodynamics: Monitor cardiac function through TEE, CVP for right ventricle straining and
failure, especially after pulmonary artery occlusion.
• Analgesia: IV narcotics should be limited if a regional epidural catheter has been placed.
Medication administration through the epidural catheter is usually initiated toward the end
of the procedure once the chance of acute blood loss and unexpected hypotension is low.
• Following repositioning, the heart can herniate into the empty right chest causing severe
hemodynamic changes. The patient should be immediately repositioned in the left lateral
decubitus and the surgeon should evaluate. A CXR can reveal if there is rapid filling of the
empty chest and if drainage is necessary to balance the mediastinum.
• If the patient is left intubated, the DLT needs to be exchanged for a single lumen. Sedation
with propofol, dexmedetomidine, midazolam, or fentanyl should be started for transport to
the ICU.
FOLLOW-UP
BED ACUITY
ICU for a few days, followed by a step-down unit or floor.
ANALGESIA
• Analgesia through a paravertebral or epidural catheter should be started or continued (6)
[B], (7)[B]. Aids with deep inspiratory maneuvers and tolerance of respiratory
rehabilitation. Studies have shown decreased postoperative complications. (7)[B].
• IV narcotics can be used if regional analgesia is not in place.
COMPLICATIONS
• Postoperative bleeding
• Mediastinal shifting
• Reintubation after inadvertent extubation can be catastrophic if the ETT is pushed through
the bronchial stump
• Arrhythmias usually after 48–72 hours postoperatively
• Injuries related to the lateral decubitus position
• Pulmonary edema, pulmonary embolism
PROGNOSIS
• High risk patients (9,10,11)[B]:
– PaCO2 >46 mm Hg
– PaO2 <60 mm Hg (FiO2 of 21%)
– FVC <50% or <1.5 mL/kg
– FEV1 <50%
– Vital capacity <2 L
– MVV <50% or 50 L/minute
– RV/TLC <50%
– DLCO <50%
– Predicted post-resection FEV1 <800 mL
– Blood flow to the resected lung >70%
– VO2max <10 mL/kg/min
• Pulmonary complications increase the morbidity and mortality rate by 35% (1)[B].
REFERENCES
1. lgar F, Alvarez A, Salvatierra A, et al. Predicting pulmonary complications after
pneumonectomy for lung cancer. Eur J Cardiothorac Surg. 2003;23:201–208.
2. Harpole DH, Liptay MJ, DeCamp MM Jr, et al. Prospective analysis of pneumonectomy:
Risk factors for major morbidity and cardiac dysrhythmias. Ann Thorac Surg.
1996;61:977–982.
3. Kim JB, Lee SW, Park SI, et al. Risk factor analysis for postoperative acute respiratory
distress syndrome and early mortality after pneumonectomy: The predictive value of
preoperative lung perfusion distribution. J Thorac Cardiovasc Surg. 2010;140:26–31.
4. icker M, de Perrot M, Spiliopoulos A, et al. Risk factors for acute lung injury after thoracic
surgery for lung cancer. Anesth Analg. 2003;97:1558–1565.
5. Ramnath N, Demmy TL, Antun A, et al. Pneumonectomy for bronchogenic carcinoma:
Analysis of factors predicting survival. Ann Thorac Surg. 2007;83(5):1831–1836.
6. Richardson J, Sabanathan S, Jones J, et al. A prospective, randomized comparison of
preoperative and continuous balanced epidural or paravertebral bupivacaine on post-
thoracotomy pain, pulmonary function and stress responses. Br J Anaesth. 1999;83(3):387–
392.
7. Powell ES, Cook D, Pearce AC, et al. A prospective, multicentre, observational cohort study
of analgesia and outcome after pneumonectomy. Br J Anaesth. 2011;106(3):364–370.
8. Schilling T, Kozian A, Huth C, et al. The pulmonary immune effect of mechanical
ventilation in patients undergoing thoracic surgery. Anesth Analg. 2005;101:957–965.
9. Smetanta GW.Preoperative pulmonary evaluation: Identifying and reducing risks for
pulmonary complications. Cleve Clin J Med. 2006;73(Suppl 1):S36–S41.Slinger P, et
al.Preoperative evaluation of the thoracic surgery patient. Semin Anesth. 2002;21:168.
10. Nakahara K, Ohno K, Hashimoto J, et al. Prediction of postoperative respiratory failure in
patients undergoing lung resection for cancer. Ann Thorac Surg. 1988;46:549–552.
• Bronchoscopy
• Myasthenic syndrome
CLINICAL PEARLS
• Optimal analgesia is key in postoperative management and outcome of thoracic surgery (6)
[B], (7)[B].
• Pulmonary complications carry a significantly increased risk of mortality in post-
pneumonectomy patients.
PNEUMOTHORAX
Moustafa Ahmed, MD
BASICS
DESCRIPTION
• Pneumothorax describes the leaking and trapping of air or gas in the pleural space between
the visceral and parietal pleura. The abolishment of the negative pleural pressure can result
in intrapulmonary shunting, lung collapse, and hemodynamic embarrassment.
• Definitions (1,2):
– Non-communicating: The chest wall is intact or closed.
– Communicating: The chest wall is open and air from the atmosphere directly enters the
pleural space.
– Tension: Results from the presence of a one-way valve where air enters and cannot leave,
causing compression and displacement of mediastinal structures.
– Primary spontaneous: Occurs without underlying disease.
– Secondary spontaneous: Occurs as a result of underlying lung disease.
– Traumatic: Accidents or iatrogenic
• Perioperatively, patients with pneumothorax most often present:
– Following a trauma
– Iatrogenically from central line placement, brachial plexus blocks, barotrauma, or the
surgical procedure
– With a pre-existing diagnosis and a chest tube in situ
EPIDEMIOLOGY
Prevalence
• More than 20,000 new cases of spontaneous pneumothorax each year in the US (3).
– Primary spontaneous pneumothorax (PSP) comprises ∼55% of cases
– Secondary spontaneous pneumothorax (SSP) comprises ∼45% of cases
• Of brachial plexus blocks, the supraclavicular approach has the highest incidence and ranges
from 0.5–6% and diminishes with using ultrasound-guided nerve block.
Prevalence
• The recurrence rate of PSP is 28% and SSP is 43%. It typically occurs within 6 months–3
years (3).
• Male > female
Morbidity
New cases cost the health system around $130,000,000.00 annually
Mortality
• SSP is associated with a higher morbidity and mortality than PSP.
• Death is secondary to respiratory and/or cardiac arrest.
• PSP occurs without underlying lung disease.
– Tall, thin males, 10–30 years old
– Smokers
– Congenital disorders such as Marfan’s syndrome and familial pneumothorax
– Change in atmospheric pressure or emotional changes
– Pregnancy
• SSP occurs in patients with underlying lung disease (1).
– Airway disease: Chronic obstructive pulmonary disease, asthma, cystic fibrosis
– Infectious lung disease: Tuberculosis, pneumoconioses, necrotizing pneumonia,
pneumocystis carinii pneumonia
– Idiopathic pulmonary fibrosis: Sarcoidosis, histiocytosis X
– Connective-tissue disease: Rheumatoid arthritis, ankylosing spondylitis,
polymyositis/dermatomyositis, scleroderma, Marfan’s syndrome, Ehlers–Danlos syndrome
– Cancer: Lung cancer, sarcoma
• Traumatic pneumothorax
– Accidental: Penetrating, non-penetrating, rib fracture, diving, flying
– Iatrogenic: During invasive diagnostic and supportive modalities like transbronchial
biopsies, thoracentesis, mechanical ventilation, pleural biopsy, central venous access,
brachial plexus blocks
• The thoracic space is comprised of (going from out to in):
– Chest wall: Rigid, with outward expanding properties
– Parietal pleura: Layer of tissue that is attached to the inner surface of the rib cage and
moves in conjunction with the ribs.
– Intrapleural space: A potential space that is under negative pressure and contains a small
amount of fluid (provides lubrication and aids with movement). Maintains a “connection”
between the chest wall and lungs (via the pleura), allowing them to move in conjunction
with one another
– Visceral pleura: Layer of tissue that covers the lungs, blood vessels, and bronchi
– Lungs: Soft tissue without rigidity, and a tendency to collapse inward.
• Leaking or trapping of air in the pleural sac can lead to a loss of negative intrapleural
pressure with resultant lung collapse and outward chest wall movement. This can result in:
– Intrapulmonary shunting secondary to atelectasis (perfusion without ventilation)
– Decreased pulmonary compliance from decreased lung volumes. Manifests as increased
peak and mean pressures
– Tension pneumothorax if a one-way valve traps air within the intrapleural space with each
inspiration. Pressure develops and accumulates without a means to escape and can cause
compression and displacement of mediastinal structures (heart, great vessels). Severe
hypotension or cardiac arrest as well as hypoxia and respiratory arrest can occur.
• Ventilator settings should be adjusted to decrease peak and mean pressures
• For subclavian line placement
– Consider ultrasound guidance
– In mechanically ventilated patients, decrease tidal volumes; in awake, spontaneously
ventilated patients, ask the patient to hold their breath after exhaling.
– Utilize a shallow angle for needle insertion
– Minimize the number of attempts and consider alternate sites, if appropriate
• For brachial plexus blocks, consider ultrasound guidance, in particular with supraclavicular
blocks
• Prior to sternotomy, hold inspiration
• Intraoperatively
– History: Trauma patients; recent central line placement or brachial plexus block; high
peak or mean pressures needed to mechanically ventilate the patient; recent surgical
events; smokers; tall thin males; and underlying pulmonary disease
– Symptoms: Dependent upon the size and speed by which it occurs. In awake patients,
sudden onset of chest pain associated with shortness of breath, coughing.
– Physical examination
General: Hypoxia, cyanosis, tachycardia, hypotension
Chest: Rapid shallow breathing, dyspnea, deviation of the trachea, limited chest wall
motion, distended neck veins; asymmetry of chest wall expansion; hyper-resonance;
diminished or absent breath sounds on the side of the pneumothorax, absent egophony
and bronchophony
Beck’s triad: Hypotension, jugular venous distention, and muffled heart tones
– Arterial blood gas: PaO2 decreased, Alveolar- arterial (A-a) gradient increased (a/A ratio
decreased).
– Chest radiography can confirm the diagnosis as well as provide information on the size
and location. It should be performed during inspiration to yield the best results. However,
in the event of hemodynamic instability and high suspicion of a pneumothorax, it should
not delay needle decompression (1).
Non-tension: The visceral pleura is separated from the parietal pleura and appears as a
white line with no lung or vascular markings adjacent to the chest wall.
Tension: Lung tissue has collapsed and “hugs" the heart; there is a “black-out" of a large
portion of the affected lung site (air); and mediastinal structures are shifted away from
the affected lung.
– Ultrasound scan: May be more readily available to perform. This technique is commonly
used in trauma bays with the benefit of being fast and effective, and improving earlier
detection. It has a sensitivity of 95–100% (superior to CXR and comparable with CT scan)
(4).
• Esophageal spasm
• Acute pericarditis
• Pleural effusion
• Pneumonia
• Foreign body and airway obstruction
• Esophageal perforation
TREATMENT
• Management strategy is based on the degree of clinical compromise, and not necessarily the
size of the pneumothorax. A chest tube, or tube thoracostomy, is performed to drain the air
collection and allow for re-expansion of the lung. It is attached to a drainage system with
three compartments (collection, water seal, and suction control chamber). A chest
radiograph is performed to verify placement (2).
• Tension pneumothorax management is a clinical emergency and requires (2):
– Immediate needle decompression, by placing a 14 gauge angio-catheter in the second
intercostal space at the midclavicular line. If the angio-catheter is not long enough or the
patient has a thick chest wall, it is possible to use the fourth or the fifth interspace as an
alternative site (the chest wall is not as deep at this space)
– Placement of a chest tube.
FOLLOW-UP
• Persistent air leak requires a thoracic surgery consult. Surgical management may be
indicated for:
– Persistent air leak more than 5–7 days with chest tube drainage or failure of lung re-
expansion
– Spontaneous hemothorax
– Professions at risk (pilot, divers)
– Pregnancy
– Synchronous bilateral spontaneous pneumothorax
– First contralateral pneumothorax
– Second ipsilateral pneumothorax
• Chemical pleurodesis may be indicated when the patient is not a candidate for surgery, or
refuses surgical intervention (high rate of recurrence). It involves the insulation of
sclerosant into the pleural space that induces aseptic inflammation with resultant adhesion
of the parietal and visceral pleura. Agents include tetracycline, minocycline, talc, and
doxycycline.
• Air travel should be avoided until full resolution.
• Diving should be permanently avoided unless instructed to do so.
CLOSED CLAIMS DATA
Not available
REFERENCES
1. acDuff A, Arnold A, Harvey J. Management of spontaneous pneumothorax: British Thoracic
Society Pleural Disease Guideline 2010. Thorax. 2010;65(Suppl 2):ii18–ii31. Warakaulle
DR, Trail ZC. Imaging of pleural disease. Imaging. 2004;16(4):10–21.
2. Wakai A, O’Sullivan RG, McCabe G. Simple aspiration versus intercostals tube drainage for
primary spontaneous pneumothorax in adults. Cochrane Database Syst Rev.
2007:CD004479.
3. Lyon M, Walton P, Bhalla V, et al. Ultrasound detection of the sliding lung sign by
prehospital critical care providers. Am Emerg Med. 2012; 30(3):485–488.
4. Baumann MH, Strange C, Heffner JE, et al. AACP Pneumothorax Consensus Group.
Management of spontaneous pneumothorax: An American College of Chest Physicians
Delphi consensus statement. Chest. 2001;119(2):590–602.
• Chest tubes
• Trauma
CODES
ICD9
• 512.0 Spontaneous tension pneumothorax
• 512.81 Primary spontaneous pneumothorax
• 512.89 Other pneumothorax
ICD10
• J93.0 Spontaneous tension pneumothorax
• J93.9 Pneumothorax, unspecified
• J93.11 Primary spontaneous pneumothorax
CLINICAL PEARLS
• Patients with chest tubes in situ may present for surgical procedures. The anaesthetist should
identify the cause, size of the pneumothorax, and current chest tube management.
• Avoid nitrous oxide in trauma patients, as a pneumothorax may be present but not
identified. In addition, maintain a high degree of suspicion for the development of Beck’s
triad, or increases in peak and mean pressures in this patient population.
POLYCYTHEMIA
Keyuri Popat, MD
BASICS
DESCRIPTION
• Polycythemia is Greek for “too many cells in the blood.” Also known as erythrocytosis, it
describes the elevation of the hematocrit either from an increase in red blood cell mass
(absolute) or decrease in plasma volume (relative).
• Polycythemia vera (PCV) is a myeloproliferative disorder that is often accompanied by
dysfunctional platelets and an increase in white blood cells.
• Secondary polycythemia is the body’s compensatory or physiologic response to chronic
hypoxia.
• Polycythemia can increased blood viscosity and the risk of thrombosis.
EPIDEMIOLOGY
Prevalence
Polycythemia vera: 1.9/100,000 people
Prevalence
Higher in males aged 70–79 years
Morbidity
Arterial ischemic complications occur in 24–43% of patients
Mortality
Median survival of patients with untreated PCV is 6–18 months from the time of diagnosis.
The main causes of death are thrombosis and disease transformation into myelofibrosis with
myeloid metaplasia (MMM) and/or acute myeloid leukemia. Survival of treated patients
exceeds 10 years.
• Primary polycythemia results from increased sensitivity of erythroid progenitors to
regulatory growth factors; most commonly PCV.
• Secondary polycythemia or physiologic polycythemia
– Chronic hypoxia from chronic obstructive pulmonary disease, obstructive sleep apnea
(OSA), or Pickwickian syndrome
– Elevated altitude
– Cyanotic heart disease
– Increased erythropoiesis from exogenous erythropoietin or erythropoietin-secreting tumors
– Endocrine disorders such as Cushing’s syndrome
• Relative polycythemia can result from a decrease in plasma volume. Causes include
insensible fluid losses, diarrhea, sweating, fever, or phlebotomy
• PCV is a chronic myeloproliferative disorder that is characterized by erythroid proliferation
and secondary platelet proliferation. PCV can progress from a proliferative stage to a
metastatic phase and develop into a malignant phase. Treatment revolves around
controlling excessive production of erythrocytes or platelets. However, the clinical course of
PCV can be complicated by a variety of events, such as:
– Bleeding due to poor quality of platelets despite normal or high numbers, as well as
acquired von Willebrand’s disease (likely due to increased binding of large vWF multimers
to the platelets and their removal from the plasma). Cytoreduction with drugs such as
hydroxyurea corrects the clinical and lab value. Desmopressin can also be used for
treatment.
– Thrombosis can result from the increased viscosity of blood. Fatal thrombotic
complications include myocardial infarction. Low dose aspirin is helpful
• Secondary polycythemia is a physiologic, compensatory response to chronic hypoxia by
stimulating erythropoietin. In turn, erythropoietin stimulates red blood cell production to
increase the oxygen carrying capacity and delivery to tissues.
– Smoking: Carbon monoxide (CO) results in decreased levels of oxyhemoglobin; CO has a
300-fold increased affinity to hemoglobin compared to oxygen. In addition,
carboxyhemoglobin has impaired oxygen offloading at peripheral tissues.
– OSA
– High altitude
– Endocrine disorders: Patients with JAK2 mutation also have hypercortisolism
– Congenital heart disease: Cyanotic heart disease results in increased pulmonary vascular
resistance as well as sustained hypoxia. The body may respond with increased
erythropoietin levels.
• Increased blood viscosity can result in:
– Increased myocardial wall tension. LaPlace’s law states that tension is directly
proportional to myocardial chamber radius and intraventricular pressures, and indirectly
related to myocardial wall thickness. Viscosity is a determinant of intraventricular
pressure (e.g., a bag filled with air would require less tension to empty than if filled with
water or a thick, gel-like substance).
– Decreased blood flow secondary to thrombosis
– Decreased blood flow secondary to increased vessel wall resistance
• For PCV, the severity of disease needs to be assessed; consider a hematology consult to
determine the need for phlebotomy, hemodilution, thromboprophylaxis, and prevention of
hemorrhage.
• Since secondary polycythemia is an indicator of chronic hypoxic disease, the underlying
pathology should be assessed. In patients with COPD, a careful history and examination
should be made to identify exacerbations or infection.
SYMPTOMS
• Headache
• Weakness
• Pruritus due to mast cell degranulation, with release of histamine
• Burning pain in hands and feet due to microvascular thrombotic
• Epistaxis
History
• Headaches
• Excessive sweating
• Exposure to, or residence in, high altitudes
Signs/Physical Exam
• Thrombosis
• Splenomegaly due to platelet sequestration
• Hepatomegaly
• Gouty arthritis increased uric acid due to cell breakdown
TREATMENT HISTORY
• Phlebotomy involves bleeding the patient down to a decreased hematocrit. This is usually
done in conjunction with aspirin and maybe chlorambucil or hydroxyurea
• Oxygen therapy may aid with decreasing erythrocytosis in patients with secondary
polycythemia (e.g., chronic obstructive pulmonary disease).
MEDICATIONS
• Hydroxyurea
• Aspirin
• Chlorambucil
• Interferon alpha
• Secondary polycythemia from pulmonary disease. Patients may be on bronchodilators,
inhaled or oral steroids, or antibiotics.
Labs/Studies
• Red blood cell volume
• White blood cell count
• Platelets: Patients can have concurrent thrombocytosis.
• Coagulation profile; abnormalities should prompt testing for von Willebrand’s disease.
• Urinalysis: Hematuria may be the only clue to the presence of erythropoietin-secreting renal
cell carcinoma
• JAK2 mutation on blood work
• Bone marrow biopsy will show an increased number of megakaryocytes in a moderately to
markedly hypercellular marrow.
• Peptic ulcer disease
• Renal failure
• Organ dysfunction due to thrombosis (myocardial infarction, cerebrovascular accident, deep
venous thrombosis, pulmonary embolism)
• Acute thrombosis as evidenced by acute myocardial ischemia or acute ischemic stroke
• Pulmonary disease exacerbation (e.g., COPD)
CLASSIFICATIONS
• Primary polycythemia
• Secondary polycythemia
• Relative polycythemia
TREATMENT
Premedications
• Hydration
• Phlebotomy and hemodilution
• Thromboprophylaxis with sequential compression devices, antiplatelets, anticoagulants
INTRAOPERATIVE CARE
• Depends upon the surgical procedure and patient preference
• Neuraxial blocks may be contraindicated depending upon the thromboprophylaxis chosen,
as well as platelet dysfunction.
Monitors
• Consider an arterial line for frequent intraoperative labs
• Foley catheters may be placed when hemodilution needs to be performed, or in cases that
are long or have large fluid shifts
• Airway instrumentation should be performed with care, as platelet dysfunction can result in
bleeding
• In patients with pulmonary disease, avoid bronchospasm by ensuring an adequate depth of
anesthetic and muscle relaxation prior to airway instrumentation
Maintenance
• Fluid hydration: Maintain adequate hemodynamics and urine output. The monitors would
depend on the type of surgery and any other co-morbidities.
• In patients with pulmonary disease, maintain an adequate depth of anesthesia to avoid
bronchospasm.
• Acquired von Willebrand’s disease can result in increased intraoperative bleeding.
• Avoid airway trauma
• In patients with pulmonary disease, consider deep extubation or other maneuvers to avoid
coughing, bucking, or bronchospasm
FOLLOW-UP
BED ACUITY
Standard postoperative care
Hematology consult may be considered as appropriate
COMPLICATIONS
• Thrombosis including myocardial infarction, cerebrovascular thrombosis, deep vein
thrombosis, pulmonary embolism
• Bleeding from dysfunctional platelets or disseminated intravascular coagulation
REFERENCES
1. Logan MS, Watson CM, Nottingham JM. Symptomatic splenomegaly in polycythemia vera:
A review of the indications for splenectomy and perioperative considerations. Am Surg.
2009;75(5):363–368.
2. Landolfi R, Di Gennaro L. Thrombosis in myeloproliferative and myelodysplastic
syndromes. Hematology. 2012;17(Suppl 1):S174–176.
3. Barosi G, Lupo L, Rosti V. Management of myeloproliferative neoplasms: From academic
guidelines to clinical practice. Curr Hematol Malig Rep. 2012;7(1):50–56.
4. Passamonti F. How to manage polycythemia vera. Leukemia. 2012;26(5):870–874.
5. Kent BD, Mitchell PD. McNicholas WT. Hypoxemia in patients with COPD: Cause, effects,
and disease progression. Int J Chron Obstruct Pulmon Dis. 2011;6:199–208.
• Obesity hypoventilation syndrome
• Chronic bronchitis
• Smoking
CODES
ICD9
• 238.4 Polycythemia vera
• 289.0 Polycythemia, secondary
• 289.6 Familial polycythemia
ICD10
• D45 Polycythemia vera
• D75.0 Familial erythrocytosis
• D75.1 Secondary polycythemia
CLINICAL PEARLS
• Spurious polycythemia should be assessed in light of overall volume status;
hemoconcentration should first be ruled out.
POSITIVE END EXPIRATORY PRESSURE (PEEP)
Justin C. Shields, MD
BASICS
DESCRIPTION
• Positive end expiratory pressure (PEEP) is the supra-atmospheric pressure present in the
alveoli at the end of expiration.
• During mechanical ventilation, PEEP is generated by valves incorporated into the ventilator
or externally applied to the expiratory side of the respiratory circuit.
• PEEP has effects on the pulmonary and cardiovascular systems.
– Pulmonary: Increases functional residual capacity (FRC) by preventing collapse and
contributes to the re-opening of distal airways and alveoli; optimizes ventilation and
hence V/Q matching.
– Cardiac: Decreases venous return to the heart, and diminishes cardiac output. This effect is
more pronounced in patients with normal lung compliance and/or hypovolemia.
– “Best PEEP” is the level of end expiratory pressure required to produce maximal oxygen
transport, while maintaining an adequate cardiac output necessary to deliver the arterial
oxygen to the peripheral tissues. It represents the point of equilibrium between the effects
on the respiratory and cardio-circulatory system.
• “Physiologic PEEP” is present in all spontaneously breathing subjects and is produced by
narrowing of the glottis during exhalation. Physiologic PEEP is estimated to be around 3–5
cm H2O.
• “Extrinsic PEEP” is applied to the airways of patients on ventilator support with the goal of
improving oxygenation and respiratory mechanics. Clinicians may select different levels of
PEEP depending on a patient’s clinical condition, and the respiratory and hemodynamic
response to the initial setting.
• PEEP’s effects on respiratory function:
– Stabilizes lung parenchyma by maintaining the patency of distal airways and alveoli
especially in the dependent areas of the lung that tend to collapse in patients under
general anesthesia. Patent alveoli can be ventilated and participate in oxygenation of
pulmonary blood (V/Q matching). This is manifested as an increase in SpO2, PaO2, and
decrease in intrapulmonary shunt fraction.
– Increases FRC by contributing to the re-opening of collapsed alveoli
– Prevents cyclic opening and closing of alveoli during the respiratory cycle. This repeated
opening and closing has been associated with alveolar damage and the systemic release of
inflammatory mediators. Theoretically, they can contribute to the development of multi-
organ failure.
– Extrinsic PEEP may decrease work of breathing in patients with airway flow limitation on
partial respiratory support.
– Overdistension is associated with decreased lung compliance and increased dead space
ventilation.
• PEEP’s effects on cardiovascular function:
– Increases mean airway pressure that gets partially transmitted to the heart and increases
the transmural pressure. As a result, this can compromise venous return to the right
atrium, and reduce cardiac output. On the contrary, in patients with reduced left ventricle
function, PEEP decreases the relative afterload of the LV. LV dysfunction can result in
decreased pulmonary volume and compliance. As a result, greater (more negative)
inspiratory pressures, and hence transmural pressures, are required to maintain tidal
volumes. The addition of PEEP can partially offset this.
– Alveolar overdistension results in compression of alveolar capillaries and increased
pulmonary vascular resistance; this results in increased right ventricular afterload and can
impair right ventricular output.
• PEEP’s effects on neurologic function:
– Levels >10 cm H2O may increase intracranial pressure (ICP) by impeding venous
drainage from the brain. Thus, in patients with increased ICP, judicious PEEP titration is
recommended, taking into consideration both changes in oxygen delivery to the brain and
intracranial compliance.
– PEEP use with the intent of maintaining positive pressure in the intracranial venous
sinuses is a frequently reported practice. However, there is no conclusive evidence to
suggest that PEEP alone is sufficient to prevent venous air embolism (VAE) in
neurosurgical procedures. In addition, in patients with a patent foramen ovale, it can
increase the mean intrathoracic pressures and theoretically favor the entry of an embolus
into the left heart.
• PEEP’s effects on renal function:
– If PEEP compromises cardiac output, it can decrease renal perfusion and activate the
renin–angiotensin–aldosterone system (RAAS). The RAAS causes an increase in solute and
water reabsorption at the glomerular level, and reduced urinary output.
ANATOMY
PEEP exerts most of its direct effects at the level of the alveoli and distal bronchi. Atelectasis,
however, occurs mostly in the dependent portions of the lungs during general anesthesia or
with the use of neuromuscular blockade.
• Atelectasis is considered a pre-inflammatory state, and can serve as a nidus for infection and
contribute to pulmonary complications.
• “Intrinsic PEEP”: Although the therapeutic effects of physiologic and extrinsic PEEP are
often discussed, “intrinsic” PEEP (or auto-PEEP) should also be considered. Intrinsic PEEP is
caused by alveolar air trapping secondary to incomplete breath exhalation. This incomplete
expiration results in supra-atmospheric alveolar pressure and increased lung volume. There
are 3 possible mechanisms leading to the development of intrinsic PEEP:
– Dynamic hyperinflation, caused by large tidal volumes and high respiratory rate, which
does not allow full lung exhalation before the next breath starts.
– Airway flow limitation, caused by `premature’ small airway collapse that is typical of
patients with increased closing volumes (e.g., COPD).
– Increased expiratory resistance, as seen with a kinked endotracheal tube, small diameter
endotracheal tube, or airway obstruction by bronchial secretions.
• Extrinsic and intrinsic PEEP can both contribute to barotrauma.
• Obesity: A greater degree of atelectasis occurs during general anesthesia in obese patients.
Application of PEEP/CPAP by a face mask should begin prior to induction with the patient
in reverse Trendelenburg position. During the case, PEEP at a level of 10 cm H2O combined
with frequent recruitment maneuvers (40–60 cm H2O for 6–8 seconds) has been shown to
be effective. Continue PEEP until extubation and consider CPAP in the PACU.
• Laparoscopic surgery decreases FRC and respiratory compliance by moving the diaphragm
cephalad, and causing atelectasis. PEEP alone (at a level of 10 cm H2O) does not improve
oxygenation; however, in combination with frequent recruitment maneuvers and beach
chair positioning, PEEP has been shown to improve oxygenation, end expiratory lung
volume, and respiratory compliance (3)[B].
• FRC decreases under general anesthesia and paralysis. In infants, who typically have very
compliant chest walls, PEEP helps in maintaining the FRC, because it compensates for the
prevailing tendency toward alveolar collapse that results from the interaction between the
uneven and opposing forces generated by lung elastic recoil (favoring collapse) and by the
smaller forces generated by the chest wall (promoting lung expansion). PEEP at levels of 3–
6 cm H2O has been shown to increase FRC in ventilated children without respiratory
disease. Its effects on increasing FRC is more pronounced in children receiving 100% FiO2
(prevention of reabsorption atelectasis is the likely mechanism). Optimal intraoperative
PEEP settings have not been clearly established for children, but likely vary depending on
age, comorbidities, and body size.
• One lung ventilation: Application of low to moderate levels of PEEP to the dependent lung
can improve arterial oxygenation depending upon individual amounts of atelectasis,
presence of intrinsic PEEP, and TV settings (4)[A]. PEEP usually improves oxygenation in
patients who respond to recruitment maneuvers. Conversely, by increasing mean pressure in
the dependent lung, it can shunt blood to the non-dependent and non-ventilated lung,
worsening V/Q mismatch.
• Prone positioning: Benefits are probably less pronounced, and optimal levels are likely lower
than in the same subjects in the supine position. This is due to the different effects on the
distribution of ventilation and perfusion as compared to supine subjects, leading to greater
V/Q mismatch in prone patients (2)[B].
• COPD: These patients are prone to develop intrinsic PEEP and require personalized
ventilator management; the I:E ratio should be adjusted to provide a longer expiratory time.
A low respiratory rate is also recommended. The application of low levels of extrinsic PEEP
(less than intrinsic PEEP) in supported ventilator modes can help alleviate intrinsic PEEP by
maintaining the peripheral bronchi open. In particular, during one lung ventilation, these
patients tend to develop intrinsic PEEP. The application of extrinsic PEEP may worsen air
trapping.
• Asthma: Flow limitation and airway inflammation can result in intrinsic PEEP. Thus, as in
COPD patients, low respiratory rates and adequate expiratory time should be established.
PEEP in controlled, mechanical ventilation may lead to hyperinflation. Conversely,
spontaneously breathing patients will have a reduced work of breathing with modest
amounts of PEEP.
• Acute respiratory distress syndrome (ARDS): PEEP increases oxygenation and improves
respiratory mechanics by minimizing the amount of cyclic opening and closing of alveoli
(associated with the systemic release of inflammatory markers and multiple organ
dysfunction). Current evidence recommends the use of higher levels of PEEP for PaO2:FiO2
levels ≤200 mm Hg and lower levels of PEEP for PaO2:FiO2 between 201–300 mm Hg. It is
recommended that PEEP be increased with FiO2 in a stepwise fashion to maintain end
expiratory transpulmonary pressure (Ttp) between 0–10 cm H2O. Ttp can be calculated by
subtracting the esophageal pressure (a surrogate of pleural pressure) from airway pressure.
Esophageal balloon catheters can be used to measure esophageal pressure (6)[B]. In patients
with ARDS, an initial higher level of PEEP (>12 cm H2O) may confer a survival benefit
with respect to lower levels (7)[A].
• The typical initial setting of PEEP is 5 cm H2O; titration is usually up or down by 2–3 cm
H2O while monitoring for changes in:
– Hemodynamics: Heart rate, BP, and urine output
– Arterial line (if present): Changes in pulse pressure or stroke volume variation, possibly
reversed by volume loading.
– Oxygenation: Increases in SpO2 saturation and PaO2 on arterial blood gases.
– ETCO2: Increased values may suggest decreased intrapulmonary shunt or increased cardiac
output (improved CO2 delivery for exhalation).
– Respiration mechanics: A reduced gradient between plateau pressure and end expiratory
pressure suggests a PEEP-induced increase in lung recruitment shown by an increase in
respiratory compliance. However, high PEEP can cause barotrauma such as pneumothorax
or subcutaneous emphysema. Peak and airway pressures must be constantly monitored.
– FiO2 titration: High FiO2 can result in absorption atelectasis; if possible, titrate FiO2
downward.
– Intrinsic PEEP is suspected when the expiratory flow waveform fails to return to 0 at the
end of expiration.
– “Best PEEP”: Requires concurrent measurements of the cardiac output and PaO2.
• Outcome studies of PEEP during anesthesia: There is no sufficiently powered study to
indicate any improvement in mortality or in pulmonary complications following the use of
PEEP. There is, however, data indicating higher PaO2/FiO2 ratios on postoperative day 1
and less atelectasis by CT scan in patients who received PEEP during anesthesia (5)[A].
• Contraindications: PEEP should be avoided or used cautiously in patients with the following
conditions:
– Hypotension/hypovolemia
– Increased ICP
– Focal pneumonias: PEEP may cause overdistension of alveoli in the healthy lung, causing
compression of their capillaries and leading to diversion of blood flow to the affected lung
segments, causing hypoxemia.
– Bronchopleural fistulas: PEEP may lead to overpressurization of the pleural cavity causing
a tension pneumothorax. PEEP can also delay healing of a bronchopleural fistula (1)[A].
EQUATIONS
Lung compliance = Vt/(Ppl − PEEP); Vt = Tidal volume, Ppl = Plateau pressure
REFERENCES
1. Acosta P, Santisbon E, Varon J. The use of positive end-expiratory pressure in mechanical
ventilation. Crit Care Clin. 2007;23:251–261. (A)
2. Petersson J, Ax M, Frey J, et al. Positive end-expiratory pressure redistributes regional
blood flow and ventilation differently in supine and prone humans. Anesthesiology.
2010;113:1361–1369. (B)
3. Futier E, et al. Intraoperative recruitment maneuver reverses detrimental
pneumoperitoneum-induced respiratory effects in healthy weight and obese patients
undergoing laparoscopy. Anesthesiology. 2010;113:1310–1319. (B)
4. Karzai W, Schwarzkopf K. Hypoxemia during one-lung ventilation. Anesthesiology.
2009;110:1402–1411. (A)
5. Imberger G, McIlroy D, Pace NL, et al. Positive end-expiratory pressure (PEEP) during
anesthesia for the prevention of mortality and postoperative pulmonary complications.
Cochrane Database of Syst Rev. 2010;9. (A)
6. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal
pressure in acute lung injury. NEJM. 2008;359:2095–2104. (B)
7. Briel M, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung
injury and acute respiratory distress syndrome: Systematic review and meta-analysis.
JAMA. 2010;303(9):865–873. (A)
• Laparoscopy
CLINICAL PEARLS
• In patients under general anesthesia, PEEP contributes to preventing end expiratory closure
of airways and alveoli, which is the primary mechanism leading to shunt and hypoxemia in
anesthetized and mechanically ventilated subjects.
• The application of PEEP must be carefully titrated while weighing the benefits of improved
respiratory mechanics and arterial oxygenation against the risk of barotrauma and
decreased cardiac output.
• Intrinsic PEEP may increase inspiratory work of breathing in patients either breathing
spontaneously, or on CPAP and PS modalities. The application of extrinsic PEEP at values
less than the intrinsic PEEP (50–70% of intrinsic PEEP) may reduce the work of breathing.
POST-HEART TRANSPLANT
BASICS
DESCRIPTION
• Heart transplantation has become an established therapeutic modality for patients with end-
stage heart disease.
• Refined transplantation techniques, improved patient selection, cyclosporine
immunosuppression, improved monitoring and anesthetic management techniques as well
as appropriate postoperative care have enhanced the survival rate of recipients.
• Consequently, many more of these patients present for elective or emergency operations.
EPIDEMIOLOGY
Prevalence
• US population: ∼2,000–2,500 heart transplants are performed annually.
• The number of transplant surgeries is primarily limited by the availability of donors.
Prevalence
Familial idiopathic dilated cardiomyopathy: ∼20–40%
Morbidity
See Concomitant Organ Dysfunction
Mortality
Overall survival rate: 1 year 81%, 3 years 75%, 10 years 70%
The two most common indications for transplantation are ischemic cardiomyopathy and
idiopathic dilated cardiomyopathy. Together, they comprise 90% of all transplant recipients.
• Denervated heart: The post-transplant heart retains normal Frank–Starling mechanisms,
impulse formation and conductivity, as well as intact α and β receptors that respond to
circulating catecholamines. However, it lacks normal responses and variations to
respiration, carotid massage, and Valsalva maneuvers. The denervated heart has a faster
basal resting heart rate, increased incidence of cardiac dysrhythmias, and a preload-
dependent cardiac output.
• Allograft rejection: Most episodes occur within the first 3 months with a peak at about 4–6
weeks. The pathogenesis involves cellular (lymphocyte infiltration) and/or humoral
(antibody) mechanisms. The clinical spectrum of rejection includes fatigue, ventricular
dysrhythmias, congestive heart failure, silent myocardial infarction, and sudden death.
Early diagnosis is by endocardial biopsy. The time course involves a hyperacute stage (first
24 hours after transplant), an acute stage (within 6–8 weeks), and a chronic stage (months
to years after transplant). Treatment involves augmented steroid therapy.
• Infection: Immunosuppressive agents should be continued indefinitely, making infection an
ever-present risk. The leading cause is direct contact with contaminated material. Infections
are most prevalent in the first few weeks after transplantation, and include mediastinitis
and opportunistic infections (CMV, Pneumocystis carinii, toxoplasma, and Legionella).
• Effects of immunosuppressive agents on anesthetic management: Cyclosporine enhances the
effects of muscle relaxants. Thus, a prolonged blockade may be seen after vecuronium or
pancuronium.
• Effects of anesthetic management on immunosuppressive agents: Cyclosporine or tacrolimus
levels must be kept within indicated therapeutic range.
– Dilution with massive fluid infusion and cardiopulmonary bypass can result in significant
reductions in levels.
– Drugs that decrease blood levels: Phenobarbital, phenytoin, carbamazepine, and
ticlopidine
– Drugs that increase blood levels: Many antibiotics, antifungal agents, metoclopramide,
verapamil, and diltiazem
– Propofol does not appear to affect cyclosporine blood levels
– Data on the effects of general anesthesia and cyclosporine pharmacokinetics are limited.
• Allograft coronary artery disease (CAD): Present in ∼21% of patients 5 years post-
transplant; it is the leading cause of death 3–5 years post-transplant. The coronary arteries
undergo an accelerated process of coronary atherosclerosis (CAV). The etiology appears to
be multifactorial; risk factors include pre-existing CAD, female donors, female recipients,
and congenital cardiac disease.
• Post-transplant hypertension: Present in ∼67% of patients at 5 years post-transplant.
Cyclosporine therapy appears to be an important etiologic factor. Treatment with nifedipine
is poorly tolerated because of vasodilation, and beta-blockers are best avoided. Diltiazem
and ACE inhibitors are the drugs of choice (note that diltiazem can increase cyclosporine
levels and dose needs to be adjusted accordingly).
• Renal dysfunction: Present in ∼13% of patients at 5 years post-transplant. Cyclosporine
therapy appears to be an important etiologic factor. In addition, it may be worsened by the
simultaneous administration of NSAIDs or trimethoprim/sulfamethoxazole. Erythromycin
and diltiazem elevate cyclosporine blood concentrations and can further deteriorate renal
function.
• The physiology of the denervated heart needs to be understood and appropriate medications
should be chosen to treat bradycardia and hypotension.
• Heart transplant patients may be undergoing rejection and manifesting myocardial
dysfunction; additionally, they have increased CAV and cardiac dysrhythmias. A thorough
evaluation of the cardiovascular system is mandated.
• Strict aseptic precautions need to be followed and maintained; all intravascular and airway
equipment should be handled with sterile gloves.
SYMPTOMS
• Angina, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, limited functional capacity,
syncope.
• Fever, cough, or any other symptoms of systemic infection
History
• Medication compliance
• Episodes of rejection
Signs/Physical Exam
• Evaluate for infection
• Jugular venous distention, pitting edema
• Check for hypertension, arrhythmias.
• Airway examination: Potential difficult airway because of lymphoproliferative disease and
soft tissue hyperplasia because of corticosteroids.
TREATMENT HISTORY
About 5–10% of transplanted patients require a permanent pacemaker because of persistent
dysrhythmias.
MEDICATIONS
• Immunosuppressive agents: Cyclosporine, tacrolimus
• Steroids
• Anti-hypertensive: Diltiazem and ACE inhibitors
Labs/Studies
• Serum creatinine, liver function tests: Organ dysfunction secondary to immunosuppressive
therapy.
• Anti-rejection drug levels
• Chest radiography: To rule out congestive heart failure and pneumonia.
• EKG: Often two “p” waves are seen; first degree AV block is common. Incomplete and
complete heart blocks are seen in 5–10% of patients. Dysrhythmias are common.
• Echocardiogram: To evaluate LV function and myocardial ischemia.
• Results of the annual follow-up and angiography should be followed
• External pacemaker and defibrillator should be properly evaluated, if present.
• Cardiac: Accelerated CAD, arrhythmias, hypertension
• Renal dysfunction
• Hepatobiliary disease: Neoplasm
• Pancreatic disease: Relatively common in a transplanted patient.
Acute rejection, congestive heart failure, and persistent untreated arrhythmias may warrant
delaying elective surgery in post-cardiac transplant patients.
TREATMENT
Premedications
• Continue preoperative anti-rejection medications and steroids
• Appropriate antibiotic prophylaxis should be administered (and repeated appropriately in
the perioperative period)
• Intravascular volume status should be addressed and optimized; consider fluid bolusing
prior to induction (cardiac output is preload dependent).
The need for invasive monitoring, telemetry, or ICU care
INTRAOPERATIVE CARE
• Dependent upon the procedure; deep sedation, general, and regional anesthesia have all
been performed safely.
• Neuraxial anesthesia may be poorly tolerated because of the denervated heart. To minimize
hypotension, slow, titrated dosing with local anesthetics should be administered, while
maintaining the preload with IV fluids and pressors such as epinephrine or ephedrine.
Monitors
• EKG will have two P waves, one from the native SA node and another from the donor SA
node
• Invasive monitoring depends upon the preoperative cardiac functional status and
invasiveness of the surgery
• Transesophageal echocardiogram may be an alternative to invasive hemodynamic
monitoring
• Large bore IV access should be secured to assure the ability to administer volume
• Orotracheal intubation is preferred to nasotracheal intubation because of the risk of
infection.
• Sympathetic response to direct laryngoscopy and intubation are typically absent. The post-
transplant heart is denervated and associated with a loss of sympathetic and
parasympathetic innervation. Sympathetic responses are delayed, blunted, and occur in
response to circulating catecholamines.
Maintenance
• Effects of volatile inhalational agents are well tolerated because most of the transplanted
hearts have near-normal contractility.
• Nitrous oxide may be used, as needed.
• Depth of anesthesia: Tachyardia is an unreliable indicator.
• Ventilator settings: Hyperventilation should be avoided because cyclosporine and tacrolimus
can lower the seizure threshold.
• Hemodynamics
– Bradycardia: Positive chronotropic drugs such as isoproterenol may be needed. Vagolytic
drugs such as atropine and glycopyrrolate are ineffective because of parasympathetic
denervation.
– Hypotension: Epinephrine and indirect acting vasopressors like ephedrine need to be used
to restore BP. Glucagon is also useful as a positive inotropic and chronotropic agent.
– Cardiac output is augmented by increasing the stroke volume; thus fluid boluses to
increase preload are administered to restore the BP
• In patients with renal dysfunction, choose drugs that do not rely heavily upon renal
clearance and avoid nephrotoxic drugs. When muscle relaxation is given, consider the use of
cisatracurium.
• Ventricular dysrhythmias: Lidocaine should be used cautiously as it may have negative
inotropic effects.
• Reversal agents: Neostigmine will not have any effect on the heart rate, but will produce
effects at other muscarinic receptors. Reversal agents should be used concomitantly with
anticholinergics to counteract the peripheral muscarinic effects.
• Re-innervation of the transplanted heart may occur and has a more effective response to
sympathetic nervous system output. However, this is highly variable and of uncertain
functional significance.
FOLLOW-UP
BED ACUITY
Depends upon the procedure, preoperative status, and intraoperative events.
• Continue immunosuppressive drugs
• Proper functioning of the pacemaker needs to be ascertained.
• Appropriate hemodynamic monitoring, including invasive monitors, needs to be continued.
COMPLICATIONS
Infection, worsening renal function, arrhythmias, hypertension, drug interactions.
REFERENCES
1. Kostopanagiotou G, et al. Anaesthetic and perioperative management of adult transplant
recipients in nontransplant surgery. Anesth Analg. 1999;89(3):613–622.
2. Cheng DCH, Ong DD. Anaesthesia for non-cardiac surgery in heart-transplanted patients.
Can J Anaesth. 1993;40(10):981–986.
ADDITIONAL READING
• Bready L, Dillman D, Noorily SH. Decision Making in Anesthesiology: an algorithmic
approach: Chapter 165
• Hensley F, Martin ME, Gravlee GP. A Practical Approach to Cardiac Anesthesia: Chapter 15.
• Laparoscopy
• Trauma
• Pacemaker dependent
CODES
ICD9
V42.1 Heart replaced by transplant
ICD10
Z94.1 Heart transplant status
CLINICAL PEARLS
• Laparoscopic cases are being increasingly performed in these patients. There is a slightly
higher rate of conversion to open procedures (27% in transplant recipients compared to
11% in general population). Advantages include a shorter hospital stay, maintenance of oral
immunosuppression, low morbidity, and early return to preoperative routine.
• Trauma: Patients may be more susceptible to soft tissue damage and poor bone healing due
to immunosuppressive therapy. Graft dysfunction secondary to injury should be ruled out.
Initial resuscitation is similar to any other trauma patient.
• Maternal effects during pregnancy: Little effect on allograft survival; may have a higher risk
of preeclampsia, preterm labor, and acute rejection. Immunosuppressive drugs can cause
hepatorenal toxicity. Fetal effects: Low birth weight; abnormal function of the pancreas,
liver and lymphocytes; immunosuppressive drugs are able to cross the placenta. In the
second and third trimesters, these drugs affect the fetus’ immune system; however, they do
not appear to be strongly associated with congenital anomalies in the first trimester.
POST-TONSILLAR BLEED
Ranu Jain, MD
BASICS
DESCRIPTION
General
• Adenoidectomy and tonsillectomy are the most common operations performed in pediatric
patients. Post-tonsillar bleeding that requires return to the operating room poses several
challenges to the anaesthetist (e.g., full stomach, difficulty securing the airway,
dehydration).
• Blood supply to the tonsils
– Arterial blood supply to the tonsils is via the right and left external carotid arteries and
their branches. The superior pole is supplied by bilateral lesser palatine arteries and the
inferior pole is supplied by bilateral branches of the dorsal lingual arteries and the
ascending palatine arteries.
– Venous return is to the plexus around the tonsillar capsule, the pharyngeal plexus, and
bilateral lingual veins.
– Post-tonsillectomy bleeding is usually venous in origin.
• Classifications
– Primary bleeds occur within 24 hours of surgery. Approximately 75% of bleeds occur
within 6 hours.
– Secondary bleeds occur up to 28 days post-surgery and are associated with sloughing of
the eschar (dead tissue) overlying the tonsillar bed, loosened vessel ties, or infection from
underlying chronic tonsillitis.
– Primary bleeding is more profuse and brisk than secondary.
– 77% of the bleeding originates in the tonsillar fossa, 27% in the nasopharynx, and 7% in
both.
• Increasing age
• Male gender
• Increased surgical time
• Bleeding disorders
• Use of NSAIDs
• Surgical technique (blunt and sharp dissection have a 2.15% incidence compared to
electrocautery with 0.9%).
Position
Supine, with a shoulder roll
Incision
None
Approximate Time
30–40 minutes
EBL Expected
Depends on the time taken to find and stop the bleeding. The amount can range from
minimal to significant.
Hospital Stay
Typically an overnight stay
Mouth gag
EPIDEMIOLOGY
Prevalence
• Post-tonsillar bleeding can occur in ∼9% of all tonsillectomies.
• Increases significantly with age; in 30–34 year olds it occurs in ∼18–20% of patients
Morbidity
Serious hemorrhage (need for blood transfusion or return to the operating room) is ∼1.4%
and appears to increase with age
• Consider full stomach precautions and the increased risk of pulmonary aspiration from
swallowed blood
• Be prepared for a potentially difficult intubation due to blood in the airway, or airway
edema from a previous intubation.
• The post-tonsillectomy patient can be hypovolemic from several factors including emesis,
ongoing blood loss, potential decreased oral intake due to postoperative pain. Thus,
although tonsillar bleeds are emergencies, the patient must be resuscitated before the
induction of anesthesia to avoid cardiovascular collapse.
SYMPTOMS
• May present with altered mental status if severely hypovolemic.
• It is very difficult to estimate the blood loss since large amounts of blood may be swallowed.
History
• Time of the original surgery
• Time since last ingestion of food
• Examine the previous anesthesia record, if available, to identify endotracheal tube size, ease
of intubation, and opioid dosages. Opioids administered during the original operation must
be taken into account if treating a primary bleed, particularly when redosing morphine.
Signs/Physical Exam
• Mental status: Irritability and lethargy are late signs of hypovolemia.
• Heart rate: Increases are seen in response to catecholamine release in order to maintain
cardiac output. Bradycardia may result from metabolic acidosis and hypoxia and is a
preterminal sign
• BP: Hypotension is a late sign of hypovolemic shock in children. An acute blood loss of 30%
may occur before the changes of BP are seen.
• Perfusion: Capillary refill >2 seconds, mottling, pallor, cyanosis, and cold clammy skin are
due to peripheral vasoconstriction thus poor perfusion.
• Tachypnea: Develops as a compensatory response to metabolic acidosis (from severe anemia
and poor perfusion).
• Urine output may be decreased
MEDICATIONS
• IV fluids
Labs/Studies
• Coagulation studies (PT/PTT, INR)
• Blood gas analysis may reveal metabolic acidosis secondary to poor tissue perfusion.
TREATMENT
Premedications
• Volume resuscitation should be performed with isotonic crystalloid or with blood, as
appropriate. IV boluses of fluid, 20 mL/kg, should be administered and repeated if
necessary after reassessment of the cardiovascular system. Large volumes of crystalloids
may be required (40–60 mL/kg)
• The patient may be very apprehensive. If premedication is necessary, benzodiazepines may
be considered in certain scenarios with very close monitoring
• Possible need for blood transfusion
• Possible postoperative intubation
Not typically indicated, but may be considered based on surgeon preference.
INTRAOPERATIVE CARE
Monitors
• Intravenous access may be placed preoperatively to provide fluid resuscitation prior to
induction as well as allow for a rapid sequence induction. In hemodynamically stable
patients, it may be acceptable to insert after mask induction.
• An arterial line may be needed for closer monitoring of the BP, depending on co-morbidities
• Patients are considered to have a full stomach from the swallowed blood and the following
should be available before starting the case.
– Two suction devices with wide bore tubing, turned on, and available for immediate use.
– Laryngoscope with different blades
– Endotracheal tube, with smaller diameter size available in case of laryngeal edema
– Weight appropriate LMA (backup rescue device)
– The surgeon should be scrubbed and ready to operate.
• There is some debate about the safest technique of anesthesia for a bleeding tonsil. The two
common choices are:
– Modified rapid sequence induction with cricoid pressure (requires an IV). Adequate
preoxygenation in an anxious, bleeding child may be difficult; thus, facemask ventilation
will be required. The doses of the induction agents are reduced (e.g., propofol 1–2 mg/kg,
ketamine 1–2 mg/kg, etomidate 0.2 mg/kg) followed by the administration of
succinylcholine (1.2–2 mg/kg) or rocuronium (1–1.2 mg/kg). Care must be taken not to
inflate the stomach during facemask ventilation, as this can result in regurgitation and
aspiration.
– Inhalational induction in the head down, lateral position may be performed if the child
has no IV access (and is hemodynamically stable). This technique helps drain blood from
the airway by means of gravity and clots can be gently suctioned from the airway once an
adequate depth of anesthesia is achieved. Oxygenation is well maintained during
spontaneous ventilation. An IV line should be started once the patient is deep enough;
muscle relaxant can be administered followed by intubation.
Maintenance
• A balanced anesthetic technique is typically used, with inhalational agents and careful
titration of IV opioids.
• Additional paralytic is not usually needed.
• During the operation, warm fluid and blood should be administered on the basis of clinical
assessment. The hematocrit should be checked after rehydration to have a better estimate of
the blood loss.
• Prophylactic anti-emetics (ondansetron, dexamethasone) should be given.
• Prior to extubation, the stomach should be suctioned and decompressed with an orogastric
tube. The endotracheal tube should be suctioned to eliminate secretions.
• If there is any doubt of aspiration, direct visualization of the airway is recommended with
the bronchoscope.
• Reversal should be administered if a non-depolarizing agent is used.
• The patient should be extubated when fully awake and with a normal gag and cough reflex.
FOLLOW-UP
BED ACUITY
• Observe closely in an intermediate monitoring or intensive care unit.
• Check hematocrit levels every 6–8 hours, until stable.
• The ability to tolerate oral intake is usually a criteria for discharge.
ANALGESIA
• NSAIDs are not given.
• Pain can be initially controlled by IV narcotics (e.g., fentanyl, morphine).
• When the patient is able to eat, transition the patient to PO medications
COMPLICATIONS
• Laryngospasm/bronchospasm
• Aspiration
• Nausea/vomiting secondary to blood in the stomach (functions as a cathartic)
• Infection
• Anemia
• Delayed emergence due to hypothermia, anemia, or multiple anesthetics
REFERENCES
1. Alexander Hons RJ, Kukreja R, Ford GR. Secondary post-tonsillectomy haemorrhage and
informed consent. J Laryngol Otol. 2004;118:937–940.
2. Ozkiris M. Comparison of three techniques in pediatric tonsillectomy. Eur Arch
Otorhinolaryngol. 2011;269(5):1497–1501.
3. Kim YS, Hong SJ, Choi J, et al. Spontaneous tonsillar hemorrhage and post-tonsillectomy
hemorrhage. Clin Exp Otorhinolaryngol. 2010;3(1):56–58.
ADDITIONAL READING
• Alatas N, San I, Cengiz M. A mean red blood cell volume in tonsillectomy, adenoidectomy
and adenotonsillectomy. Int J Pediatr Otorhinolaryngol. 2006;70(5):835–841.
• Tonsillectomy and adenoidectomy
CODES
ICD9
998.11 Hemorrhage complicating a procedure
ICD10
J95.830 Postproc hemor/hemtom of a resp sys org fol a resp sys proc
CLINICAL PEARLS
• The patient may be hypotensive and anemic, and may require resuscitation with fluids and
blood products prior to anesthesia induction and/or perioperatively.
• Most anaesthetists feel more comfortable with the IV rapid sequence induction in the supine
position with the application of cricoid pressure to reduce the risk of aspiration. The use of
muscle relaxants helps produce ideal conditions for intubation.
• Always use full stomach precautions.
• Anticipate difficulty visualizing the airway if there is ongoing active bleeding.
• A smaller endotracheal tube may be necessary.
POST-DURAL PUNCTURE HEADACHE
BASICS
DESCRIPTION
• Post-dural puncture headache (PDPH) usually manifests as a severe, incapacitating frontal or
occipital headache following the introduction of a spinal or epidural needle into the dura
with subsequent loss of CSF through the puncture site
• It can occur following a diagnostic lumbar puncture, spinal, combined spinal/epidural or
epidural anesthesia procedure.
EPIDEMIOLOGY
Prevalence
• All epidural procedures: Ranges from 0.19–4.4% (1,2)
• Inadvertent dural puncture following labor epidurals: Ranges from 0.04–6% (3,4,5)
• Incidence of PDPH following accidental dural puncture with epidural placement: Ranges
from 50–85% (1,6)
• Following spinal anesthesia (1): 40% with a 20 GA, 25% with a 25 GA, 2–10% with a 26
GA, and <2% with a 29 GA needle.
• Following lumbar puncture: Ranges from 12–38% (7)
Morbidity
• Usually a self-limiting condition, with most headaches resolving within a week with
conservative management. However, it can vary in intensity from mild to severe, and may
be associated with photophobia, nausea, vomiting, neck stiffness, tinnitus, diplopia, and
dizziness (1,6).
• Symptoms following labor epidural placement may be so severe as to interfere with the
patient’s ability to care for herself or her newborn and to interact with other family
members (2).
• Severe symptoms may delay hospital discharge and result in increased cost (1).
• In one study, 17.8% of patients who developed a PDPH still complained of a headache 2–7
years following the procedure. 46.7% of patients complained of backache 1 year later (8).
• Cranial nerve palsies, unmasking of pre-existing cerebral pathology, seizures, persistent CSF
epidural fistulas, cranial subdural hematomas, intracerebral bleeding, and aneurysm rupture
have been reported following dural puncture (9,10,11).
Mortality
Uncommon: Rare cases of fatal subdural hematomas have been reported.
• Female gender: Almost twice as likely compared to males
• Young age: Rare over the age of 60 years; most commonly seen in 20–30 year olds
• Pregnancy
• Lower BMI
• Larger gauge needle
• Cutting versus pencil point needle
• Greater number of attempts
• Repeated dural punctures (12)
• Perpendicular as opposed to parallel direction of needle bevel with respect to dural fibers
• Previous history of PDPH
• Inexperienced operator
• Sleep deprivation, operator fatigue and effect of night work in junior personnel
• Loss of resistance to air
• Several mechanisms have been postulated. The most commonly accepted thought is that the
loss of CSF from the intrathecal space leads to a decrease in CSF volume and pressure,
which in turn causes painful traction on the meninges and intracranial pain sensitive
structures. Compensatory cerebral venous dilation may also occur, further giving rise to
PDPH symptoms.
• The loss of CSF volume may also lead to activation of adenosine receptors resulting in
venous and arterial vasodilation (1).
• Smaller, non-cutting needles should be used whenever possible.
• If inadvertent dural puncture occurs with an epidural needle, strategies include:
– Threading a catheter into the intrathecal space and leaving it in place for at least 24
hours; this may cause immediate plugging of the dural hole and promotion of an
inflammatory reaction that helps to seal the hole (9).
– 5-step strategy (1,2): Injecting the CSF back into the intrathecal space; advancing a
catheter into the intrathecal space; injecting 3–5 mL of preservative-free saline through
the catheter; using the catheter for labor analgesia with a bolus, followed by an infusion;
and leaving the catheter in place for 12–20 hours.
– Prophylactic epidural blood patch (injecting 15–20 mL of sterile venous blood into the
epidural space) may not reduce the incidence of development, but may shorten the length
and severity of symptoms (8,13).
– Epidural morphine: May decrease PDPH incidence, need for EBP, and onset to PDPH (4)
• Cosyntropin: Synthetic ACTH analog; associated with a significant reduction in the
incidence of PDPH and need for EBP, along with significant prolongation of the time from
accidental dural puncture to occurrence of PDPH (3).
• History of dural puncture
• Clinical symptoms: Incapacitating, dull or throbbing, frontal headache with radiation to the
occiput
• Positional component: There is an exacerbation of the headache and symptoms when
upright (usually within 20 seconds) and amelioration of symptoms when supine (usually
within 20 seconds) (14).
• Onset and duration: Usually develops within 7 days (typically within 48 hours) and resolves
within 14 days of the procedure (9).
• Migraine
• Caffeine-withdrawal headache
• Meningitis
• Sinus headache
• Preeclampsia
• Drugs (amphetamine, cocaine)
• Brain tumor
• Cerebral vein thrombosis
• Cervical facet syndrome
• Pneumocephalus-related headache
• Lactation headache
• Posterior leukoencephalopathy
• Stroke (ischemic and hemorrhagic)
• Subarachnoid/subdural hematoma
TREATMENT
• Conservative management. Shown to provide varying degrees of symptom relief, but none
have been shown to cure PDPH
– Supine position: Ameliorates symptoms but may not provide therapeutic benefit
– Hydration: May help to offset the decrease in CSF pressure. There is no evidence for
therapeutic effect (1)
– Caffeine: Causes cerebral vasoconstriction and thus may ameliorate symptoms, but the
effect may be transient. Caffeine is a CNS stimulant and rare side effects include dizziness,
jitteriness, flushing, and palpitations. Insomnia occurs in one-third of the patients and
caffeine may lower the seizure threshold, unmasking seizures (15).
– Theophylline: Causes potent cerebral vasoconstriction and may be used as an alternative
to caffeine (1).
– Sumatriptan: Serotonin agonist that causes cerebral vasoconstriction. It is expensive and
must be administered subcutaneously (1).
– Cosyntropin: Multiple doses may be effective after spinal anesthesia. Symptomatic relief is
associated with increased beta endorphin levels and increased intravascular volume (16).
– Hydrocortisone: May decrease the intensity in women who develop PDPH following spinal
anesthesia for C-section (16).
– Gabapentin: May be effective for prophylaxis and treatment of PDPH (16)
– Abdominal binder: May reduce symptoms due to increased CSF pressure caused by
increased intra-abdominal pressure. It is rarely used due to patient discomfort (6).
– Epidural dextran: Although postulated to remain in the epidural space longer due to the
high viscosity and MW of dextran, there is no clear evidence for this, or for accelerated
dural healing via an inflammatory process (1,2). It may be associated with anaphylaxis
(10).
• Although the above conservative, expectant measures may be carried out supportively,
aggressive management should be considered in symptomatic patients to decrease patient
discomfort, costs of extended stay, and return ER visits (5,9).
– EBP remains the gold standard for treating patients with symptomatic PDPH, despite
conservative measures (1,2,17). Its immediate effect is likely due to compression of the
dura caused by injection of blood into the epidural space, which leads to increased CSF
pressure and reduced traction on the pain sensitive structures. Its delayed effect likely
involves formation of a clot at the site of the dural tear. The injected blood forms a plug at
the dural hole and reduces further leakage of CSF. In one study, relief of symptoms has
been reported as high as 93% after one EBP and 97% after a second EBP (17). If the
headache persists after a second attempt, imaging studies should be considered, as well as
other etiologies for headache (16). Efficacy appears to be improved when EBP is
performed later as opposed to earlier, unknown reason.
Level. Should be performed at or below the level of the dural tear due to the preferential
cephalad spread of blood (10).
Volume. Most effective amount has not been determined; 15–20 cc of sterile blood is
generally injected and discontinued if and when the patient complains of back pain (9).
Contraindications include any potential contraindications for epidural cannulation such
as cutaneous or systemic infections, coagulopathies, or patient refusal (6,10).
Complications of EBP include backache, neck pain, leg pain, paresthesias, mild pyrexia,
bradycardia, pneumocephalus, intrathecal injection of blood, meningitis, arachnoiditis,
and the possibility that further epidural blockade quality may be affected (11).
FOLLOW-UP
• Routine spinal anesthesia or inadvertent puncture of the dura with an epidural needle:
Patients should be followed closely for potential PDPH development. Since the presentation
may be delayed, patients should be followed up at routine intervals following hospital
discharge and instructed to return to the ER if symptoms develop.
• EBP placement: Patients should be followed up at regular intervals to ensure that symptoms
have not returned and there have been no complications stemming from the EBP.
REFERENCES
1. Kuczkowski KM. The management of accidental dural puncture in pregnant women: What
does an obstetrician need to know? Arch Gynecol Obstet. 2007;275:125–131.
2. Kuczkowski KM. Post-dural puncture headache in the obstetric patient: An old problem.
New solutions. Minerva Anestesiol. 2004;70:823–830.
3. Hakim SM. Cosyntropin for prophylaxis against postdural puncture headache after
accidental dural puncture. Anesthesiology. 2010;113:413–420.
4. Al-metwalli RR. Epidural morphine injections for prevention of post dural puncture
headache. Anaesthesia. 2008;63:847–850.
5. Angle P, Tang SLT, Thompson D, et al. Obstetric and pediatric anesthesia expectant
management of postdural puncture headache increases hospital length of stay and
emergency room visits. Can J Anaesth. 2005;52:397–402.
6. Kuntz KM, Kokmen E, Stevens JC, et al. Post-lumbar puncture headaches: Experience in
501 consecutive procedures. Neurology. 1992;42:1884–1887.
7. Jeskins GD, Moore PAS, Cooper GM, et al. Long term morbidity following dural puncture
in an obstetric population. Int J Obstet Anesth. 2001;10:17–24.
8. Gaiser R. Postdural puncture headache. Curr Opin Anesthesiol. 2006;19:249–253.
9. Harrington BE. Postdural headache and the development of the epidural blood patch. Reg
Anesth Pain Med. 2004;29:136–163.
10. Williams EJ, Beaulieu P, Fawcett WJ, et al. Efficacy of epidural blood patch in the
obstetric population. Int J Obstet Anesth. 1999;8:105–109.
11. Scavone BM, Wong CA, Sullivan JT, et al. Efficacy of a prophylactic epidural blood patch
in preventing post dural puncture headache in parturients after inadvertent dural puncture.
12. Paech M. Unexpected postpartum seizures associated with post-dural puncture headache
treated with caffeine. Int J Obstet Anesth. 1996;5:43–46.
13. Thaw M, Paech MJ. Management of postdural puncture headache in the obstetric patient.
Curr Opin Anesthesiol. 2008;21:288–292.
14. Safa-Tisseront V, Thormann F, Malassine P. Effectiveness of epidural blood patch in the
management of post-dural puncture headache. Anesthesiology. 2001;95:334–339.
15. Bezov D, Lipton R, Ashina S. Post–dural puncture headache: Part I diagnosis,
epidemiology, etiology, and pathophysiology. Headache. 2010;50:1144–1152.
16. ezov D, Ashina S, Lipton R. Post–dural puncture headache: Part II–Prevention,
management, and Prognosis. Headache. 2010;50:1482–1498.
17. eeberger MD, Kaufmann M, Staender S, et al. Repeated dural punctures increase the
incidence of postdural puncture headache. Anesth Analg. 1996;82:302–305.
• Vaginal delivery
• Epidural
• Caudal epidural
• Epidural steroid injections
CODES
ICD9
349.0 Reaction to spinal or lumbar puncture
ICD10
G97.1 Other reaction to spinal and lumbar puncture
CLINICAL PEARLS
• Use smaller-sized and non-cutting needles for spinal and epidural procedures, when possible.
• Following inadvertent dural puncture with an epidural needle, consider maneuvers listed
above to help prevent PDPH development.
• After development of a PDPH, consider performing a therapeutic epidural blood patch if
symptoms are severe or persist, despite conservative therapeutic measures.
POSTOPERATIVE CHEST PAIN
Philip Levin, MD
BASICS
DESCRIPTION
• Postoperative chest pain can be caused/related to any part of the thorax, including the
heart, lungs, esophagus, muscle, bone, and skin. Despite the possibility for innocuous causes
(reflux), life-threatening causes (myocardial infarction [MI]) must be ruled out and, if
identified, treated quickly.
• It is a rare event that a patient complains of de novo anginal-type chest pain. Therefore, it is
important to review the patient’s history and assess risks to help distinguish and discern
chest pain due to cardiac origin.
EPIDEMIOLOGY
Prevalence
• Postoperative MI: 0–4%, depending on coronary artery disease (CAD) risk stratification.
• Those at-risk for, or have CAD: 3.9% (1) for a major perioperative cardiac event
Mortality
Patients that have an MI after noncardiac surgery have an in-hospital mortality rate of 10–
15%. They also have an increased risk that persists for at least a year compared to those who
did not have an MI.
• Acute MI, angina: CAD, anemia secondary to surgery, hypertension (HTN), preoperative use
of cocaine or other similar stimulants, recently placed coronary stents, high-risk surgery,
cerebrovascular disease, use of insulin therapy for diabetes, signs of heart failure on
preoperative examination, a preoperative serum creatinine >2 mg/dL, new long-standing
ST-T wave changes noted intraoperatively.
• Aortic dissection: s/p cardiac catheterization, aortic surgery.
• Pulmonary embolism (PE): Obesity, prolonged immobility, femur fracture, pregnancy,
cancer, history of prior PEs, family history of blood clots, arrhythmias, recently
discontinued anticoagulation or antiplatelet medications.
• Pneumothorax: Surgical injury to the chest or diaphragm, central line placement, brachial
plexus block, ventilator complication.
• Aspiration pneumonia: Poor motor control, extremes of age, emergency status, recent meal,
morbid obesity, events during intubation or extubation, delayed gastric emptying, decreased
gastric emptying, decreased lower esophageal sphincter tone.
• Gastroesophageal reflux disease (GERD): History of GERD, decreased lower esophageal
sphincter tone (e.g., pregnancy), certain medications (e.g., anticholinergics).
• Perforated viscus: Complicated abdominal or thoracic surgery.
• Costochondritis: Thoracic surgery, lateral position during surgery, repetitive minor trauma
to the chest wall during surgery.
• MI: Surgery with its associated trauma, pain, hypothermia, and anemia can induce an
inflammatory, hypercoagulable state that can lead to coronary plaque rupture and arterial
thrombosis. ST-segment elevated MI is associated with complete thrombotic occlusion of an
epicardial coronary artery. Severe imbalances in myocardial oxygen supply and demand can
also result in infarction.
• Angina: Chest pain results from an imbalance between myocardial oxygen supply and
demand that can result from increased levels of catecholamines and cortisol. It differs from
an MI in that the arteries are not completely blocked and there is little or no permanent
damage to the heart; however, it could be an indicator of impending MI.
• Aortic dissection: A tear in the intimal layer is followed by formation and spread of a
subintimal hematoma. This produces a false lumen, which can reduce blood flow to the
major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac
tamponade may result.
• PE: Occurs when a clot breaks loose and embolizes to block pulmonary blood vessels. Deep
vein thrombosis (DVTs) in the lower extremities are triggered by venostasis,
hypercoagulability, and vessel wall inflammation (increased in the perioperative period).
Patients who have undergone gynecologic surgery, or major trauma may have deep vein
thrombosis (DVTs) that move proximally to the popliteal vessels and from there embolize to
the lungs.
• Pneumothorax: Occurs with the entrance of air into the pleural cavity. A tension
pneumothorax (air enters, but cannot exit as a result of a “ball-valve" mechanism) results in
lung collapse, respiratory compromise, and mediastinal shifting.
• Perforated viscus: A hole or a tear in the wall of the gastrointestinal tract allows air to enter
the abdominal cavity, which irritates the diaphragm and can cause chest pain.
• Aspiration pneumonia: Occurs when material (food, foreign body) or fluid (gastric contents,
blood, or saliva) enters the lungs from the pharynx into the trachea. The consequences
depend on the type, amount, and pH of material aspirated. Acidic gastric contents cause
alveolar–capillary breakdown, resulting in interstitial edema, intraalveolar hemorrhage,
atelectasis, increased airway resistance, and commonly hypoxia.
• GERD: Occurs when gastric content refluxes into the esophagus, causing symptoms with or
without associated esophageal mucosal injury (i.e., esophagitis). Usually the result of lower
esophageal sphincter dysfunction.
• Esophageal spasm: Remains unknown; however, it is believed to relate to a loss of inhibitory
innervations in the body of the esophagus (2).
• Costochondritis: An inflammatory process of the costochondral or costosternal joints that
causes localized pain and tenderness.
• Cardiac events: Patients on beta-blockers or statins prior to surgery should receive their dose
in the perioperative period. Patients with recently placed bare metal stents should wait at
least 6 weeks and those with drug-eluting stents should wait at least 1 year before
discontinuing dual platelet therapy to decrease the risk of acute stent thrombosis. Treat
postoperative anemia, hypothermia, hypotension or HTN, and pain aggressively to decrease
myocardial oxygen demand/supply mismatch.
• PE: Early ambulation, mechanical and/or pharmacologic thromboprophylaxis have been
demonstrated to be effective.
• GERD: Administer acid reflux medication in the perioperative period.
• MI or angina: Variable and can include tachycardia or bradycardia, hypotension or HTN,
tachypnea, diaphoresis, and a fourth heart sound. Sign of CHF include S3 heart sound
(gallop), pulmonary rales, lower extremity edema, and elevated jugular venous pressure.
EKG changes: ST-segment elevation (≥2 mm in leads V1, V2 or V3 and ≥1 mm in the other
leads) or depression (≥1 mm) in at least 2 contiguous leads, or symmetric inversion of T
waves (≥1 mm) in at least 2 contiguous leads (3). New Q waves in two neighboring leads
may be seen.
• Aortic dissection: Hypertension (secondary to release of catecholamines), hypotension
(excessive vagal tone), cardiac tamponade, hypovolemia, syncope, altered mental status.
Dyspnea may be caused by CHF or tracheal/bronchial compression. Dysphagia form
esophageal compression. A new diastolic murmur and a decrease in oxygen saturation may
occur. A CT scan of the aortic vessels should be considered.
• PE: Unilateral leg swelling from DVT, hypoxemia (<95%), and pulse >94 bpm. Massive PE
causes hypotension due to acute cor pulmonale. Wheezing may be present. EKG changes:
Prominent S wave in lead I; Q wave and inverted T wave in lead III pattern due to right
ventricular strain. May also see peaked P waves in lead II, new right bundle branch block,
right axis deviation, or new onset atrial fibrillation. Decreased oxygen saturation. D-dimer is
a unique degradation product produced by plasmin-mediated proteolysis of cross-linked
fibrin; levels are increased in PEs (nonspecific). A high resolution CT angiograph is a
sensitive diagnostic tool; if it is not available, then a V/Q scan should be performed (less
sensitive and specific). A duplex ultrasound of a DVT can also aid with diagnosis.
• Pneumothorax: Decreased or absent breath sounds on the affected side with dyspnea,
decreased pulse oximetry. When large, hypotension can result.
• Aspiration pneumonia: Tachypnea, tachycardia; decreased breath sounds, rales, dullness to
percussion over the area of consolidation; and hypoxemia. Chest radiograph is usually
normal initially; a CT scan of the chest may yield results more quickly.
• Perforated viscus: Rebound abdominal tenderness and fever. Hypotension secondary to
significant blood loss or septic shock. An abdominal radiograph would show free air.
• Costochondritis: Pain on palpation of the affected costochondral joints.
• ECGs: Can be uninterpretable if the patient has known bundle branch block, chronic ST-
segment changes, or is pacer dependant.
• Blood troponin level: To identify infarction; a typical rise and gradual fall is a sign of cardiac
ischemia or PE.
• Transthoracic or esophageal echocardiogram (TTE or TEE): New wall motion abnormalities
on echocardiography are likely due to MI. New right ventricular dysfunction may also
suggest PE.
• Radionuclide scan: New fixed cardiac defects on radionuclide scan is likely due to
myocardial infarct.
• Chest x-ray: Can rule out pneumothorax, check for enlarged mediastinum (aortic dissection),
or infiltrate formation (aspiration pneumonia). For PE, the film may initially be normal;
occasionally there may be dilation of the pulmonary vessels proximal to an embolism along
with collapse of distal vessels. After 24–72 hours, the loss of pulmonary surfactant can cause
atelectasis and pulmonary infiltrates which may appear like pneumonia. Aspiration
pneumonia typically has a delayed presentation on radiography.
• Arterial blood gas: Hypoxia and possible respiratory acidosis in pneumonia, pneumothorax,
and PE.
• White blood cell count (WBC): Increased with bacterial infections associated with aspiration
pneumonia, as well as PE, and perforated viscus (if associated with sepsis). However, it can
also be elevated after trauma and major operations.
• Barium swallow: If a trial of proton pump inhibitors does not work and chest pain of an
esophageal origin is still suspected, then a barium swallow can be done to rule out diffuse
esophageal spasm or to detect hiatal hernias (associated with GERD).
• Esophagogastroduodenoscopy (EGD): Can be done to rule out esophagitis and peptic ulcer
disease. Esophageal manometry can be used to further detect diffuse esophageal spasm, and
monitor the lower esophageal sphincter (which can help detect GERD).
• Cardiac: Acute MI, angina, aortic dissection
• Pulmonary: Embolism, pneumothorax, aspiration pneumonia
• Gastrointestinal: Acid reflux, esophagitis, esophageal spasm, perforated viscus
• Musculocutaneous: Costochondritis
TREATMENT
• MI and hemodynamically stable: Consult a cardiologist and possibly an intensivist. Medical

management includes supplemental oxygen, morphine to adequately treat the patient’s pain
(decreases sympathetic stimulation and has preload-reducing properties), nitroglycerin
(decreases cardiac preload and causes coronary vasodilation), IV beta-blockers (decreases
myocardial O2 consumption; may not be appropriate in patients with decompensated CHF,
severe COPD, severe hypotension from shock), and aspirin 325 mg (decreases platelet
aggregation). IV unfractionated heparin may be given (to decrease thrombin formation) if
suspicion of plaque rupture is high and the bleeding risks are acceptable. The cardiologist
may also recommend starting an ACE inhibitor and a statin.
• MI and hemodynamically unstable: Consult a cardiologist; cardiac catheterization with
percutaneous coronary intervention may be necessary. Patients that have recently
discontinued antithrombotic medications for cardiac stent placement should be catheterized
immediately to rule out acute stent thrombosis.
• Aortic dissection: Consult a thoracic surgeon, keep the heart rate between 60 and 80 bpm
(beta-blockers), and systolic BP between 100 and 120. Treat pain adequately to maintain
pulse and BP within a target range. Urgent surgical intervention may be necessary
depending on the location and type of dissection.
• PE: Supplemental oxygen promotes pulmonary vascular dilation; vasoconstrictive agents and
IV fluids should be given to treat hypotension. Anticoagulation with heparin, either
unfractionated or low molecular weight, may be given to prevent clot progression;
thrombolytic therapy may be considered. Consultation with the surgeon and an intensivist
should be done prior to heparin and thrombolytic therapy since there is a great risk of
major bleeding in postoperative patients.
• Small pneumothorax: Typically resolves on its own without intervention. If large, a chest
tube should be placed to decompress the air around the lung and allow for re-expansion.
• Perforated viscus: Requires surgical intervention.
• Aspiration pneumonia: Suction upper airway for any gastric content, provide supplemental
oxygen, and consider intubation if signs of respiratory failure or poor oxygenation are
present. Consider a pulmonary/critical care consult on the basis of severity.
• GERD or esophagitis: Antacids, H2 blockers, or proton pump inhibitors.
• Costochondritis: Patient reassurance and adequate pain control.
REFERENCES
1. Devereaux PJ, Goldman DJ, et al. Perioperative cardiac events in patients undergoing
noncardiac surgery: A review of the magnitude of the problem, the pathophysiology of the
events and methods to estimate and communicate risk. CMAJ. 2005;173(6):627–634.
2. Krieger-Grubel C, Hiscock R, Nandurkar S, et al. Physiology of diffuse esophageal spasm
(DES)-when normal swallows are not normal. Neurogastroenterol Motil. 2010;22:1056–
e279.
3. Devereaux PJ, Goldman L, Yusuf S, et al. Surveillance and prevention of major
perioperative ischemic cardiac events in patients undergoing noncardiac surgery: A review.
CMAJ. 2005;173(7):779–788.
4. Priebe HJ. Myocardial infarction-aetiology and prevention. Br J Anaesth. 2005;95(1):3–19.
ADDITIONAL READING
• Adesanya AO, de Lemos JA, Grilich NB. Management of perioperative myocardial infarction
in noncardiac surgical patients. Chest. 2006;130:584–596.
• Pneumothorax
• Anemia
CODES
ICD9
• 338.18 Other acute postoperative pain
• 786.50 Chest pain, unspecified
ICD10
• G89.18 Other acute postprocedural pain
• R07.9 Chest pain, unspecified
CLINICAL PEARLS
• Postoperative chest pain can be caused by many different etiologies. It is critical to
immediately rule out and treat the life-threatening causes.
• Review the patient’s medical history and intraoperative record for clues on the cause of
postoperative chest pain. For example, does the patient have known CAD or GERD?
• Perform a physical examination and order diagnostic testing as indicated
• Implement treatment quickly and consult specialists as appropriate.
POSTOPERATIVE COGNITIVE DYSFUNCTION (POCD)
Richard M. Rivera, MD
BASICS
DESCRIPTION
• Postoperative cognitive dysfunction (POCD) describes a deterioration in cognition that can
be seen following surgery. It manifests as acute or persistent disturbances in the information
processing of the brain including:
– Executive function
– Language
– Attention
– Perception
– Verbal abilities
– Learning
– Memory
– Abstract thinking
– However, patients typically remain oriented
• The onset may begin within days of surgery and may last >1 year in 1% of elderly patients;
it is considered a reversible condition in the majority of elderly patients. In addition, POCD
differs from delirium, postoperative delirium (POD), and dementia.
– Delirium (DSMIV) is defined as a change in mental status characterized by a reduced
awareness of the environment and disturbance in attention; it may be accompanied by
hallucinations, disorientation, or temporary memory dysfunction. In addition, the patient
may express hypoactive, hyperactive, or mixed psychoactive behavior.
– POD describes delirium in the postoperative surgical patient. Patients are often lucid in
the recovery room, with onset developing between postoperative days 1–3.
– Dementia (DSMIV) is a progressive decline in cognition or behavior from a prior level of
functioning in one or more of the following: Memory, reasoning, language, visual
processes, executive functions, social-interpersonal behaviors, and personality. It is caused
by brain disease.
• At this time, POCD lacks a consensus definition and studies face several methodologic
limitations, despite the growing awareness within the field of anesthesiology and amongst
the public.
EPIDEMIOLOGY
Prevalence
• At 1 week postoperatively, POCD following:
– Cardiac surgery: 30–80%
– Major noncardiac surgery: 19–26%
– Minor surgery: 7%
• No difference seen with general versus regional anesthesia
Prevalence
Geriatric patients are more likely to have POCD at 1 week and 3 months postoperatively
compared to their younger cohorts
Morbidity
• Results in patients requiring longer hospital stays and greater assistance at home
• Increased likelihood of dropping out of the labor market.
Mortality
If present at the time of hospital discharge and persists at 3 months, there is an increased
mortality within 1 year after surgery.
• Increasing age
• Major surgery
• Stress response
• Hypotension
• Cerebral hypoxia
• Microemboli
• Cardiac surgery
• Anesthesia
• Genetics
• The definitive cause of POCD remains unknown.
– Age: Changes in the white and gray matter may decrease the “cognitive reserve.” This may
be somewhat offset by higher levels of education and physical activity.
– Stress response: Surgery results in the release of neuroendocrine hormones, cytokines, and
alterations in cortisol. Major procedures may have an increased stress response.
– Hypotension: Studies have shown that elderly, hypertensive patients with low
intraoperative mean arterial pressures have increased cognitive impairment at 1 day and 1
week postoperatively.
– Cerebral hypoxia: In cardiac surgery, a decrease in cerebral oxygen saturation has been
associated with an increased risk of POCD
– Microemboli, as measured by Doppler in orthopedic cases, may be a factor in the
development of POCD.
– Regional anesthesia does not reduce the risk of POCD as compared to general anesthesia.
However, a greater depth of anesthesia has been associated with a >1 year mortality in
elderly patients
– Genetically, the APO-E 4 allele is associated with Alzheimer’s disease and is present in a
subgroup of POCD patients
• Future research appears to be focused on:
– The mechanism by which age may play a role
– The effects of genetics on predisposition
– The relationship between POD and POCD
– Preoperative “mental exercise training” as well as postoperative interventions to decrease
the incidence and/or duration of POCD
• There are no specific, proven methods for prevention.
• Preoperative testing may be considered in patients at risk for POCD.
• Maintenance of systolic BP at >90 mm Hg, especially in hypertensive patients
• Maintain an adequate cerebral perfusion pressure, particularly in the beach-chair position or
cardiac surgical procedures
• Consider monitoring the depth of anesthesia with a BIS monitor to avoid excessive levels
• Reduce perioperative stress by placing continuous infusion neuraxial or regional blocks
preoperatively and maintaining them in the intraoperative and postoperative period.
• Anesthetic choice, regional versus general, does not appear to influence the incidence of
POCD
• At this time, there is no standard, consensus testing for POCD. Diagnosis is on the basis of
establishing a decrease between preoperative and postoperative cognitive functions.
• There are several tests available to aid in evaluating memory, sensorimotor speed, cognitive
flexibility, and aspects of motor performance:
– Mini mental status examination (MMSE): Frequently utilized and takes approximately 5–
10 minutes to administer
– Clock drawing test
– List learning test
– Paragraph or story learning test
• POD
• Dementia
• Acute alcohol withdrawal
• Residual anesthesia/analgesics
TREATMENT
There is no specific treatment of POCD at this time.
FOLLOW-UP
• If a patient is suspected of, or diagnosed with POCD, a discussion should be made with the
patient, family, and surgeon.
• Patients may require greater assistance after discharge and follow-up with a geriatrician or
neurologist should be considered and arranged, if appropriate.
REFERENCES
1. Silverstein H, et al. Central nervous system dysfunction after noncardiac surgery and
anesthesia in the elderly. Anesth. 2007;106(3):622–628.
2. Ramaiah R. Postoperative cognitive dysfunction in the elderly. Anesth Clin. 2009;27:485–
496.
3. Monk T, et al. Predictors of cognitive dysfunction after major noncardiac surgery. Anesth.
2008;108(1):18–30.
4. Monk TG, Price CC. Postoperative cognitive disorders. Curr Opin Crit Care.
2011;17(4):376–381.
5. Price CC, Garvan CW, Monk TG. Type and severity of cognitive decline in older adults after
noncardiac surgery. Anesthesiology. 2008;108(1):8–17.
6. ekker A, Lee C, de Santi S, et al. Does mild cognitive impairment increase the risk of
developing postoperative cognitive dysfunction? Am J Surg. 2010;199(6):782–788.
7. sai TL, Sands LP, Leung JM. An update on postoperative cognitive dysfunction. Adv Anesth.
2010;28(1):269–284.
ADDITIONAL READING
• Silbert B, Evered L, Scott DA. Cognitive dysfunction in the elderly: Is anesthesia implicated?
Best Pract Res Clin Anaesthesiol. 2011;25(3):379–393.
8. Bilotta F, Doronzio A, Stazi E, et al. Early postoperative cognitive dysfunction and
postoperative delirium after anaesthesia with various hypnotics: Study protocol for a
randomized controlled trial–the PINOCCHIO trial. Trials. 2011;6(12):170.
CODES
ICD9
293.9 Unspecified transient mental disorder in conditions classified elsewhere
ICD10
G97.82 Oth postproc complications and disorders of nervous sys
CLINICAL PEARLS
• When in the beach-chair position for neurosurgical procedures, the arterial line should be
placed and zeroed at the level of the auditory meatus
• Consider the use of preemptive analgesia with regional or neuraxial blocks to minimize the
surgical stress response.
• Consider BIS monitoring to titrate medication and volatile agent dosing.
POSTOPERATIVE DELIRIUM
Carlee Clark, MD
BASICS
DESCRIPTION
• The diagnostic and statistical manual (DSM) of Mental Disorders IV diagnosis of delirium is
a:
– Disturbance of consciousness with inattention accompanied by a change in cognition or
perceptual disturbance that develops over a short period of time (hours to days) and
fluctuates over time
• It exists on a continuum:
– Hyperactive: Abnormal psychomotor activity with picking or pulling at lines and
monitors, combative with staff and family, visual hallucinations, or increased state of
arousal and hypervigilance; more common during the night.
– Hypoactive: Uncomplaining, lying listless, and may even follow commands; most common
and most commonly undiagnosed.
– Hypoalert: May seem sedated or somnolent.
• Postoperative delirium has a temporal relationship with surgery and frequently occurs
between postoperative days 2 and 7 (1).
EPIDEMIOLOGY
Prevalence
– Hip fracture 4–53% (2)
– Postcardiac surgery 32–38.5% (3)
– Elderly patients 15–53% (4)
– General surgery 5–15% (5)
• Trauma and ICU patients 60–80% (6)
• Medical and surgical inpatients 15–60% (7)
Prevalence
Ranges from 5–50%
Morbidity
• Increased length of hospital and ICU stay
• Increased hospital cost
• Greater dependency of care on discharge
• Higher nursing home disposition rates
• Cognitive deterioration
Mortality
• Postoperative delirium patients have a 15–20% mortality rate (8)
• Elderly patients and ICU patients with delirium have an increased 6-month mortality (9,10).
• Patients with delirium have a 62% increase in 12-month mortality (11).
• Preoperative risk factors
– Critical illness
– Severity of illness
– Prior history of delirium
– History of alcohol abuse
– History of tobacco use
– Poor preoperative functional status
– Preoperative use of narcotic analgesics
– Preoperative depression and dementia
– History of Parkinson’s disease
• Intraoperative risk factors
– Vascular surgery
– Cardiac surgery
– Hip fracture
– Emergent surgery
– Greater intraoperative blood loss
• Postoperative risk factors
– Postoperative transfusions
– Postoperative hematocrit <30%
– Severe postoperative pain
– High doses of benzodiazepines
– Postoperative polypharmacy
– Electrolyte abnormalities
• The exact pathophysiology in the development and progression of delirium is unknown, but
it is associated with many different etiologies.
• Neurotransmitter imbalance: A relative deficiency of cholinergic transmission can result in
decreased central cholinergic and increased dopaminergic, GABA, and serotonergic
neurotransmission. The aging brain has a relative deficiency of acetylcholine, as do
dementia patients, resulting in greater susceptibility. Perioperatively:
– Medications: Steroids, anticholinergics, benzodiazepines, opioids, some anesthetics,
anticonvulsants, bromides, and antibiotics
– Metabolic and endocrine derangements: Electrolyte abnormalities, dehydration
– Withdrawal syndromes: Alcohol, benzodiazepines, or opioids
• Type of anesthesia: There is no difference in the incidence of delirium when comparing
patients having undergone MAC, general anesthesia, or a regional anesthetic (12,13).
• Systemic inflammation secondary to the surgical procedure: An inflammatory response to
surgical tissue injury can result in cytokine, TNK, histamine, and cortisol release, as well as
proliferation of macrophages. These inflammatory mediators may interfere with normal
metabolism and function, thereby, causing delirium (14–16).
• Anatomic defects: Anatomic changes in the brain seen on CT, MRI, and PET scanning have
implicated the prefrontal, non-dominant posterior parietal, basal ganglia, and temporal–
occipital cortex (17).
Identification of patients with preoperative risk factors and minimization of intraoperative
and postoperative risk factors. “Prophylactic” measures mimic therapeutic measures.
• Cardiac surgery delirium prediction score (18)
• General elective surgery delirium prediction score (19)
• Nonpharmacologic measures (see Treatment)
• Haloperidol prior to, and following, the surgical procedure; little data to support this
practice.
• Atypical antipsychotics; prophylactic efficacy is not supported by data
• Dexmedetomidine in ventilator-dependent patients may result in decreased delirium and
resolution of symptoms quicker than those sedated with benzodiazepines (20).
• Avoidance of benzodiazepines
• Avoidance of new polypharmacy
• Adequate pain control
• Delirium is a diagnosis based on clinical signs and symptoms defined in the DSM IV
– Rapid onset with a fluctuating course
– Disorganized thinking
– Alterations in level of consciousness with inattention
• It is a diagnosis of exclusion and organic causes need to be excluded:
– Thorough history and physical examination looking for risk factors or new pathology.
– Basic metabolic panel, CBC, arterial blood gas
– Pulse oximetry, temperature, telemetry, and BP monitoring
• Patients frequently have sleep disturbances
• Confusion assessment method for the ICU (CAM-ICU): Can be used in verbal and nonverbal
patients.
• Hypoxemia
• Hypercarbia
• CNS or systemic infection
• Cerebrovascular accident
• Hypoglycemia/hyperglycemia
• Urinary retention
• Alcohol or medication withdrawal
• Dementia
• Medication administration
TREATMENT
• Focus on improving patient cognition and decreasing adverse events such as aspiration,
prolonged immobilization, impaired cognition, or death.
• Non-pharmacologic interventions should be initiated first.
– Reorientation to person, place, and time is important. It is helpful to encourage the family
members to do the same.
– Improve sleep quantity and quality; sleep aids if necessary.
– Correct day/night cycle; lights on during the day and off at night.
– Stimulating activities multiple times a day; visiting with family, watching television,
puzzles
– Early mobilization, range of motion activities and physical therapy
– Replace glasses and hearing aids as soon as possible
– Remove unnecessary lines, particularly Foley catheters and central lines
– Avoid restraints if possible
– Nutrition and hydration
– Avoid urinary retention
– Patients may require sitters to prevent harm to themselves.
• Avoid medications that can worsen postoperative delirium such as benzodiazepines,
anticholinergics, steroids, and opioids.
• Optimize the postoperative pain regimen by using multimodal analgesia when possible to
decrease the amount of opioids required.
• Antipsychotics: IV haloperidol is the drug of choice for delirium treatment as recommended
by The American Psychiatric Association and the Society of Critical Care.
– Mechanism of action (MOA): Dopamine receptor antagonist resulting in decreased
dopamine neurotransmission.
– Dosing: Mild symptoms and for the elderly: 0.5–2 mg IV; moderate symptoms: 2.5–5 mg
IV; severe symptoms: 5–10 mg IV. Administer every 30 minutes until agitation has
resolved.
– Maintenance: Dosing should be scheduled every 4–6 hours with PRN dosing for acute
episodes. Maximum daily dosing is 20 mg.
– Side effects: Sedation, prolongation of QT on EKG, it is not FDA approved for this purpose
and carries a Black Box warning for arrhythmias (including Torsade de Pointes)
extrapyramidal signs, minimal anticholinergic effects.
– A baseline ECG should be available prior to initiation of therapy.
• Atypical antipsychotics should be considered when patients have a contraindication to
haloperidol.
– Quetiapine
MOA: Receptor antagonist at dopamine, serotonin, histamine and alpha 1 and 2
adrenergic receptors.
Dosing: 25 mg–100 mg PO BID. Maximum daily dose is 200–400 mg. Not appropriate for
acute agitation, as it is only available in oral form.
Side effects: Prolongation of QT on ECG, extrapyramidal signs, anticholinergic effects,
sedation
– Olanzapine
MOA: Receptor antagonist at dopamine, serotonin, and histamine receptors.
Dosing: 2.5–5 mg PO/IM/sublingual daily. Maximum daily dose is 20 mg. Can be given
IM for acute agitation.
Side effects: Prolongation of QT on ECG, extrapyramidal signs, anticholinergic effects,
sedation
– Dexmedetomidine
MOA: Alpha 2 adrenergic receptor agonist
Dosing: 0.2–1.0 mcg/kg/hr
Side effects: Bradycardia, hypotension
More data is needed before applying to nonventilated patients with delirium (20).
FOLLOW-UP
• Patients with delirium need to be continuously reassessed for clinical improvement or

deterioration. Transfer to an ICU is common.
• Pharmacologic agents can be stopped a few days after the cessation of delirium.
REFERENCES
1. arcantonio ER, Goldman L, Mangione CM. A rule for prediction of delirium after
noncardiac surgery. JAMA. 1994;27:134–139.
2. Bruce AJ, Ritchie CW, Blizard R, et al. The incidence of delirium associated with
orthopedic surgery: A meta-analytic review. Int Psychogeriatr. 2007;19(2):197–214.
3. ockalingam S, Parekh N, Bogoch I, et al. Delirium in the postoperative cardiac patient: A
review. J Cad Surg. 2005;20(6):560–567.
4. Demeure MJ, Fain MJ. The elderly surgical patient and postoperative delirium. J Am Coll
Surg. 2006;203:752–757.
5. Bekker AY, Weeks EJ. Cognitive function after anaesthesia in the elderly. Best Pract Res
Clin Anaesthesiol. 2003;17:259–272.
6. Ishaq L, McMillan M, Taylor S, et al. The impact of delirium on clinical outcomes in
mechanically ventilated surgical and trauma patients. Crit Care Med. 2009;37(6):1898–
1905.
7. Ely EW, Siegel MD, Inouye SK. Delirium in the intensive care unit: An underrecognized
syndrome of organ dysfunction. Semin Resp Crit Care Med. 2001;22:115–126.
8. Ansaloni L, Catena F, Chattat R, et al. Risk factors and incidence of postoperative delirium
in elderly patients after elective and emergency surgery. Br J Surg. 2010;97(2):273–280.
9. Fann JR.The epidemiology of delirium: A review of studies and methodological issues.
Semin Clin Neuropsychiatry. 2000;5:64–74.
10. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically
ventilated patients in the intensive care unit. JAMA. 2004;291:1753–1762.
11. Leslie D, Zhang Y, Holford T, et al. Premature death associated with delirium at 1-year
follow-up. Arch Int Med. 2005;165:1657–1662.
12. Papaioannou A, Fraidakis O, Michaloudis D, et al. The impact of the type of anaesthesia
on cognitive status and delirium during the first postoperative days in elderly patients.
Eur.J.Anaesthesiol. 2005;22:492–499.
13. Williams-Russo P, Sharrock NE, Mattis S, et al. Cognitive effects after epidural vs general
anesthesia in older adults: A randomized trial. JAMA. 1995;274:44–50.
14. Saper CB.Neurobiological basis of fever. Ann NY Acad Sci. 1998;856:90–94.
15. Bierhaus A, Humpert PM, Nawroth PP. NF-B as a molecular link betweenpsychosocial
stress and organ dysfunction. Pediatri Nephrol. 2004;19:1189–1191.
16. ichers MC, Maes M. The role of indoleamine 2,3-dioxygenase (IDO) in the
pathophysiology of interferon-α-induced depression. J Psychiatry Neurosci. 2004;29:11–
17.
17. Trzepacz P.Is there a final common neural pathway in delirium? Focus on acetylcholine
and dopamine. Sem ClinNeuropsychiatry.2000;5:132–148.
18. Rudolph JL, Jones RN, Levkoff S. Derivation and validation of a preoperative prediction
rule for delirium after cardiac surgery. Circulation. 2009;119:229–236.
19. arcantonio EJ, Goldman L, Mangione CM, et al. A clinical prediction rule for delirium
after elective noncardiac surgery. JAMA. 1994;271:134–139.
20. Riker RR, Shehabi Y, Bokesch PM, et al. Dexmedetomidine vs midazolam for sedation of
critically ill patients: A randomized trial. JAMA. 2009;301(5):489–499.
21. Jacobi J, et al.American Psychiatric Association and the Society of Critical Care practice
guidelines for delirium. Crit Care Med. 2002;30:119–141.
• www.ICUdelirium.org
CODES
ICD9
293.9 Unspecified transient mental disorder in conditions classified elsewhere
ICD10
G97.82 Oth postproc complications and disorders of nervous sys
CLINICAL PEARLS
• Postoperative delirium frequently occurs postoperative days 2–7
• Delirium has three subtypes: Hyperactive, hypoactive, and mixed. Hypoactive most
commonly goes undiagnosed because the patient is not disruptive.
• Delirium screening can aid with identifying patients at risk and minimizing perioperative
risk factors as well as implementing prophylactic measures. Nonpharmacologic therapy is
first-line for prevention and treatment of delirium.
• Haloperidol is the drug of choice for delirium treatment. The patient should have an ECG
before initiating haloperidol therapy secondary to the potential for QT prolongation.
POSTOPERATIVE HYPOXIA
Suzanne Strom, MD
BASICS
DESCRIPTION
Postoperative hypoxia is defined as an arterial oxygen tension (PaO2) <60 mm Hg, which
correlates with SpO2 <90%.
EPIDEMIOLOGY
Prevalence
• Postoperative respiratory problems are the most frequently occurring complication during
the recovery period.
• Up to 30% of postoperative patients have oxygen saturations (SpO2) <90% while breathing
room air.
• The major etiologies for postoperative hypoxia are airway obstruction and hypoventilation.
• Airway obstruction. Causes include:
– The tongue falling back against the posterior pharynx
– Laryngospasm
– Glottic edema
– Secretions
– Emesis or blood in the airway
– Hematoma in the neck from surgery; external pressure on the trachea
– Gauze packing left unintentionally in the mouth, airway, or esophagus. Can cause
immediate or delayed complete airway obstruction.
– Vocal cord paralysis
• Hypoventilation: Defined as a PaCO2 >45 mm Hg and is common following general
anesthesia. In most cases, the hypoventilation is mild and overlooked unless the PaCO2 is
>60 mm Hg or arterial blood pH is <7.25. Hypercarbia is a sympathetic stimulant that can
manifest as tachycardia, hypertension, and cardiac irritability. Decreased respiratory drive
can result from:
– Residual anesthetic agents and postoperative analgesics (most common)
– Residual neuromuscular blockade as a result of inadequate reversal, overdose,
hypothermia, pharmacologic interactions with antibiotics (clindamycin), renal or hepatic
dysfunction, or electrolyte disturbances.
– CNS lesion or ischemia
– Inadequate respirations can result from splinting with incisional pain, diaphragmatic
dysfunction, abdominal distention, or firm dressings.
• Decreased functional residual capacity (FRC) causes increased right-to-left intrapulmonary
shunting relative to closing capacity (common cause). Causes include:
– Atelectasis
– Parenchymal infiltrates (including those caused by aspiration)
– Large pneumothorax
– Pleural effusion
– Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS)
– Absorption atelectasis
– Bronchospasm
• Other causes that need to be ruled out when the above-mentioned do not appear to explain
hypoxia:
– Low cardiac output caused by myocardial infarction, congestive heart failure, shock,
arrhythmias, or cardiac tamponade.
– Increased O2 consumption from shivering
– Pulmonary embolism, especially if the patient complains of dyspnea
• Risk factors:
– Extremes of age
– Pregnancy
– Obesity
– Smokers
– Pre-existing cardiac or respiratory disease.
• Hypoxia results in inadequate oxygen supply for normal cellular metabolism and oxidative
phosphorylation. In low oxygen states, anaerobic metabolism proceeds to continue
manufacturing ATP; however, it is inefficient and produces lactic acid. Progressive lactic
acidosis impairs enzymatic function and concentration gradients.
• In the face of decreased oxygen delivery and increased myocardial oxygen demand,
ischemia and worsened acidosis can result. The final result of continued hypoxia is cell
death.
• Hypoxia is sensed in the carotid bodies (at the bifurcation of the common carotid arteries)
and the aortic bodies (surrounding the aortic arch). These peripheral sensors interact with
central respiratory centers via the glossopharyngeal nerves to produce reflexive increases in
alveolar ventilation. However, hypoxia receptor activity does not appreciably increase until
the PaO2 decreases <50 mm Hg, at which point the SpO2 is 80%.
• Signs: Hypoxia stimulates the sympathetic system and initially can cause tachycardia,
hypertension, and increased cardiac output. Late signs of hypoxia include myocardial
dysrhythmias, tachycardia, bradycardia, hypertension, hypotension, and cardiac arrest.
• Concomitant hypercarbia should also be considered, which can cause a respiratory acidosis
in addition to the metabolic (lactic) acidosis caused by hypoxia.
– Supplemental FiO2:
– Should be considered in all patients who have received deep sedation or general
anesthesia in the postoperative period; transient hypoxia can develop even in healthy
patients.
– Can be discontinued if room air SpO2 measurements are acceptable and the patient is
relatively alert and awake. An arterial blood gas can help guide decisions in challenging
cases.
– Longer periods of administration should be considered in patients at increased risk for
hypoxia (impaired baseline status, abdominal or thoracic procedures).
– When continued upon discharge from the recovery room, care should be taken in those
with COPD and a history of CO2 retention that are being transferred to a unit which does
not have constant pulse oximetry measurement.
• The head of the bed should be elevated at least 30° if the patient is responsive unless
contraindicated by the surgical procedure (e.g., recent femoral sheath access). Similarly,
coughing and deep breathing should be encouraged.
• Verify low SpO2 measurement.
– Ensure that the SpO2 rate correlates with the EKG tracing
– Verify accurate waveform
– Move pulse oximetry probe to different fingers, an earlobe, nostril or nasal ala
– Measure arterial blood gas to confirm; also aids with differentiating between absolute
shunt/large V/Q mismatching and low FiO2, hypoventilation, and smaller V/Q
mismatching.
• Correlation between PaO2 and SpO2 may be affected by hypothermia, poor circulation,
electrocautery, motion, ambient lighting, and methylene blue administration.
• Evaluate for
– Respiratory rate (opioid-induced hypoventilation presents with low respiratory rate and
large tidal volumes)
– Flow of air
– Respiratory pattern
– Labored breathing (accessory muscles)
– Chest wall movement
– Excessive somnolence
– Airway obstruction. In total obstruction, the chest wall descends as the abdomen rises
during each respiration instead of the abdomen and chest rising together. With partial
obstruction, usually presents as sonorous respirations.
• In an awake patient, assessment of neuromuscular blockade can be done by having the
patient sustain a head lift for 5 seconds or by a nerve stimulator in an unconscious patient.
• Portable chest x-ray should be obtained to ascertain atelectasis, infiltrates, or pneumothorax.
Evaluating alveolar to arterial (A–a) gradient may help determine the cause. The alveolar
oxygen equation is as follows:
• PAO2 = FiO2 (PB − PH2O) − (PaCO2/RQ)
– PAO2 = partial pressure of oxygen in the alveoli
– FiO2 = fraction of inspired oxygen
– Pb = barometric pressure (sea level = 760 mm Hg)
– PH2O = partial pressure of water vapor in the airway (47 mm Hg)
– PaCO2 = partial pressure of carbon dioxide in the blood
TREATMENT
• Increase the FiO2 while evaluating for reversible causes.

• Since airway obstruction is the most likely cause, start with arousal of the somnolent
patient, followed by chin lift, jaw thrust, oro- and nasopharyngeal airway insertion.
Elevation of the head of the bed can improve anatomic considerations.
• If laryngospasm is suspected, continuous positive pressure may be implemented to “break”
it. If unsuccessful, administer succinylcholine (20 mg/70 kg) with continuous positive
pressure ventilation.
• If respiratory depression is caused by opioids, consider reversal with naloxone titrated in
0.04 mg increments in adults. Watch for side effects such as pain, sympathetic stimulation,
and pulmonary edema.
• Treat residual neuromuscular paralysis with additional cholinesterase inhibitors if the
maximum dose has not been achieved. In the event that it has been attained, supportive
measures should be taken:
– Bag mask ventilation
– Invasive airway instrumentation (LMA or ETT) following induction
• Laryngeal mask airway (LMA) insertion or endotracheal intubation may be necessary to re-
establish ventilation if the patient is unconscious, hypercarbic, or acidotic. Repeated airway
instrumentation and intraoperative fluid administration can worsen the glottic view from
original laryngoscopy at the beginning of surgery; alternative techniques for securing the
airway should be available such as a bougie, cricothyrotomy, indirect video laryngoscopy,
or transtracheal jet ventilation.
• Glottic edema leading to stridor should be treated with IV dexamethasone 0.5 mg/kg up to
10 mg (slow onset) or aerosolized racemic epinephrine 0.5 mL of a 2.25% solution with 3
mL of normal saline (faster onset).
• If wound hematoma is suspected, immediately open the wound.
• Maintain adequate cardiac output and hemoglobin levels.
REFERENCES
1. Noble DW. Hypoxia following surgery – an unnecessary cause of morbidity and mortality?
Minerva Anestesiol. 2003;69(5):447–450.
2. Tyler IL, Tantisira B, Winter PM, et al. Continuous monitoring of arterial oxygen saturation
with pulse oximetry during transfer to the recovery room. Anesth Analg. 1985;64:1108–
1112.
3. Pedersen T, Moller AM, Hoyannisyan K. Pulse Oximetry for Perioperative monitoring.
Cochrane Database Syst Rev. 2009;(4):CD002013.
• Oxygen content
• Hypoxia intraoperative
• Laryngospasm
CODES
ICD9
• 799.02 Hypoxemia
• 997.01 Central nervous system complication
ICD10
• G97.82 Oth postproc complications and disorders of nervous sys
• R09.02 Hypoxemia
CLINICAL PEARLS
• Always assume that a low SpO2 is accurate until proven otherwise.
• Hypoxia should always be at the top of a differential diagnosis for abnormal cardiovascular
vital signs such as hypertension, tachycardia, and arrhythmia, as well as nausea and altered
mental status in a postoperative patient.
POSTOPERATIVE JAUNDICE
BASICS
DESCRIPTION
• Jaundice in the postoperative period may result from a combination of hypotension,
hypoxemia, pigment overload, or sepsis, with the clinical picture resembling hepatitis. It is:
– Usually evident within 2 weeks after surgery
– Can occur in up to 47% of patients with cirrhosis
– Unusual in patients without liver disease
• Abnormal liver chemistry tests (LCTs), on the other hand, can range from 25–75% in
patients without liver disease; mild elevations are thus considered typical.
• Postoperative LCT abnormalities and jaundice are usually categorized and worked-up in one
of the following 4 groups:
– Increased bilirubin production (pre-hepatic)
– Hepatocellular disease (intrahepatic)
– Cholestatic disorders (posthepatic)
– Pre-existing liver disease
EPIDEMIOLOGY
Prevalence
• Elective abdominal surgery: <1% (1)[A]
• Cardiac surgery: 26.5%
– Higher in mitral valve replacement (MVR) combined with coronary artery bypass graft
(CABG) than CABG alone and aortic valve replacement (AVR) plus CABG (2)[B]
– Heart transplantation: 57% (3)[B]
• Postoperative acute acalculous cholecystitis is more common in men than women,
represents 70% of all acute cholecystitis in children (1)[A].
Morbidity
A history of pre-operative cirrhosis is associated with a 30% complication rate with surgery,
the most common being pneumonia (4)[B]. Cirrhosis is a common cause of jaundice
Mortality
• Postoperative jaundice is associated with:
– A 5.5% mortality after CABG or MVR
– A 11.6% 30-day postoperative mortality in patients who have pre-operative cirrhosis
• Acalculous cholecystitis mortality can reach 70% (1,5)[A]
• Pre-existing liver disease: Viral hepatitis, cirrhosis, alcoholic hepatitis, mononucleosis, or
congenital disorders
• Major blood loss requiring blood transfusions
• Prolonged hypotension in surgery
• Medications: Erythromycin, chlorpromazine, halothane, enflurane, sulfonamides, penicillin,
phenytoin, methyldopa, acetaminophen, methyltestosterone, rifampin, isoniazid, and
nitrofurantoin
• Hemolytic blood diseases: Sickle cell, thalassemias, G6PD deficiency, autoimmune anemia
• Mechanical heart valves
• In cardiac surgery: Prolonged bypass, aortic cross clamping; intra-aortic balloon pump use;
pre-operative hepatic dysfunction due to heart failure; and type of surgery
• Total parenteral nutrition (TPN): Short-term use can cause fatty liver and cholestasis,
whereas long-term use can result in steatohepatitis, cholestasis, and acalculous cholecystitis
• Acalculous cholecystitis: Male; major surgery including cardiac and GI, trauma, burns, renal
failure; mechanical ventilation with positive end expiratory pressure (PEEP); TPN for at
least 3 months; and critically ill patients
• Heme is a prosthetic group with an iron atom in the center of a porphyrin group. It is most
commonly found in hemoglobin molecules within red blood cells.
– Normal breakdown of hemoglobin occurs in reticuloendothelial cells with unconjugated
(indirect) bilirubin byproduct.
– Unconjugated bilirubin is water insoluble, binds readily to albumin, and is conjugated
with glucuronic acid in the liver.
– Conjugated (direct) bilirubin is water soluble and excreted in bile and urine.
Normal lab values:
Total bilirubin: 0.2–1.9 mg/dL
Direct bilirubin: 0–0.3 mg/dL
Indirect bilirubin: 0.2–0.7 mg/dL
• Jaundice is the clinical manifestation of hyperbilirubinemia and describes a yellow
pigmentation of the skin, sclera, and mucus membranes.
• Pre-hepatic causes of postoperative jaundice result from increased red blood cell breakdown
and unconjugated bilirubin levels. This can overwhelm the liver’s capacity to conjugate
bilirubin. Perioperatively, this can result from:
– Hemolysis (the rupture and release of hemoglobin) can result from blood transfusions,
hemolytic diseases, mechanical heart valves, cardiac surgery.
– Hematoma resorption
• Intrahepatic causes of postoperative jaundice result in a reduced ability to conjugate
bilirubin. Perioperative causes include hepatocellular injury (ischemia, medications, viral)
or pre-existing liver disease.
– Ischemic injury may result from cardiogenic or noncardiogenic shock, hypoxemia, or
surgical injury (hepatic artery ligation, post-liver transplant)
– Medications, TPN, and volatile agents
– Viral infections can present after 3 weeks of surgery. In 2001, the Centers for Disease
Control and Prevention reported the risk of hepatitis C infection from a unit of transfused
blood in the US to be less than one per million transfused units.
– Pre-existing liver disease that was not recognized until after surgery is also possible. For
example, unrecognized cholestatic liver disease such as primary sclerosing cholangitis or
primary biliary cirrhosis. Gilbert’s syndrome, which is the most common inherited cause
of unconjugated hyperbilirubinemia, is another possibility.
• Posthepatic causes of postoperative jaundice result from an inability to excrete conjugated
bilirubin. Intrahepatic and extrahepatic causes can result in the obstruction of bile flow or
cholestasis.
– Intrahepatic cholestasis can be caused by benign postoperative cholestasis, acalculous
cholecystitis, sepsis, or medication induced.
– Extrahepatic cholestasis can be caused by choledocholithiasis, cholecystitis, acalculous
cholecystitis, upper abdominal surgery, postoperative pancreatitis, postoperative bile duct
injury, stricture or tumor, or unrecognized liver diseases like primary sclerotizing
cholangitis.
• Postoperative abnormal LCTs in normal individuals may be due to decreased hepatic blood
flow or the surgical procedure.
• Do not perform elective surgery in cirrhotic or acute viral hepatitis patients (5)[B].
• Avoid TPN or blood transfusions when possible.
• Avoid halothane.
• Avoid using same syringes or multidose vials on patients to prevent infectious disease spread
such as hepatitis.
• Avoid severe hypotension.
• Is based upon clinical and intraoperative history with laboratory results confirming the
diagnosis.
• Bilirubin overproduction (pre-hepatic) presents with elevated unconjugated bilirubin levels.
It may also result in:
– Elevated reticulocyte count
– Low haptoglobin
– Presence of schistocytes
– Elevated AST and LDH (alkaline phosphatase and ALT are not largely elevated) (5)[B]
• Decreased conjugation from hepatocellular injury presents with elevated unconjugated
bilirubin levels. It may also result in:
– Elevated aminotransferases (5–100 times normal)
– Elevated LDH
– Elevated alkaline phosphatase (2 times normal).
– Positive viral hepatitis A and B serologies, hepatitis C RNA by PCR; elevated ALT and AST
up to 10 times normal, LDH and alkaline phosphatase (small increases).
– Halothane hepatitis presents with fever, arthralgias, skin rash, eosinophilia, repeated
exposure to halothane
• Decreased bilirubin excretion presents with elevated conjugated bilirubin. It may also result
in:
– Elevated alkaline phosphatase (3 times normal)
– Acholic stools
– Pruritus
– Biliary strictures, bile leaks, retained common bile duct stones can present with epigastric
or right upper quadrant pain, fever, and jaundice
– Acalculous cholecystitis demonstrates increased gallbladder wall thickness on ultrasound
>4 mm, no response to cholecystokinin (CCK), intramural gas, and sloughed mucosal
membrane (1)[A].
Consider preeclampsia or acute fatty liver of pregnancy (AFLP) as possible diagnosis.
TREATMENT
• Defer all other elective procedures

• Discontinue medication if suspected to be drug-induced.
• In cholestasis, consider open or laparoscopic cholecystectomy or antibiotics, endoscopic or
radiologic interventions, or antibiotics. If seriously ill or unstable, percutaneous
cholecystostomy can be done (1)[A]. Consider Vitamin K when severe disease is causing
elevations in PT.
• In hepatic hypoperfusion, consider invasive BP monitoring with an arterial line to avoid
further hepatic hypoperfusion.
• In hypersensitivity-drug-related liver injury, consider corticosteroids.
• In fulminant hepatic failure, consider liver transplantation
• Elevated LCTs in otherwise normal patients may be observed without intervention.
However, if severe and getting worse, consider a hepatology consult
CLOSED CLAIMS DATA
• Halothane hepatitis: 38 claims
– Halothane plus patient with underlying condition: 2 claims
– Halothane plus a hepatotoxic chemo: 1 claim
– Of all 41 cases, 3 occurred after 1990, most recent was 1997
– 20 patients (49%) with halothane hepatitis died
• Infectious hepatitis: 2 claims
– Hepatitis B from reusing syringes for skin wheel
– Hepatitis C from reusing multidose vial (at least 41 patients in the claim)
REFERENCES
1. Molina EG, Reddy KR. Postoperative jaundice. Clin Liver Dis. 1999;3:477–488.
2. Mastoraki A, Karatzis E, Mastoraki S, et al. Postoperative jaundice after cardiac surgery.
Hepatobiliary Pancreat Dis Int. 2007;6:383–387.
3. Hsu RB, Lin FY, Chen RJ, et al. Incidence, risk factors, and prognosis of postoperative
hyperbilirubinemia after heart transplantation. Eur J Cardiothorac Surg. 2007;32:917–922.
4. Ziser A, Plevak DJ. Morbidity and mortality in cirrhotic patients undergoing anesthesia and
surgery. Anesthesiology. 1999;90:42–53.
5. Faust TW, Reddy KR. Postoperative jaundice. Clin Liver Dis. 2004;8:151–166.
ADDITIONAL READING
• Barash PG, Cullen BF, Stoelting RK. Clinicial Anesthesia, 5th ed. Chapter 39: Anesthesia and
the liver. New York, NY: Lippincott Williams and Wilkins, 2006.
• www.asaclosedclaims.org
• Cholecystectomy
CODES
ICD9
• 782.4 Jaundice, unspecified, not of newborn
• 997.49 Other digestive system complications
ICD10
• K91.89 Oth postprocedural complications and disorders of dgstv sys
• R17 Unspecified jaundice
CLINICAL PEARLS
• Perform a thorough history and physical examination with a focus on surgical causes,
intraoperative ischemic events, drugs, and pre-existing liver disease
• Consider ordering an ultrasound of the right upper quadrant to rule out acalculous
cholecystitis (high mortality).
• Avoid halothane when possible.
POSTOPERATIVE NAUSEA AND VOMITING (PONV)
BASICS
DESCRIPTION
• Postoperative nausea and vomiting (PONV) is still a leading adverse event and more
distressing for patients than postoperative pain
• PONV is multifactorial in its origin, as a consequence of emetogenic triggers (such as
inhaled anesthetics, opioids) to susceptible patients (women, history of motion sickness and
PONV, non-smokers, long surgery).
EPIDEMIOLOGY
Prevalence
Can reach up to 80%
Prevalence
Females are 3 times more likely, with up to 80%, to develop PONV
Morbidity
Vomiting can result in rare, but potentially severe issues such as retinal detachment, suture
dehiscence, wound bleeding, aspiration, subcutaneous emphysema, or esophageal rupture
Mortality
Not proven
• General anesthesia (GA) with volatile agents and opioids (most common) remain the most
relevant known causes.
• Risk factors and independent predictors:
– Women, until high age, independent of anesthesia technique (strongest predictor)
– Non-smoking (1.8 times more likely)
– History of PONV and/or motion-sickness
– Young age: Children >3 years, adolescents, young adults independent of gender
– Increased duration of anesthesia
– Postoperative opioid use
• Associated, evidence-based parameters:
– Weakly associated: Anxiety
– Unlikely associated: High FiO2, ginger
• NOT associated, evidence-based parameters (against individual impressions): Obesity,
facemask ventilation, use of nasogastric or orogastric tube, IV use of neostigmine, phase of
menstrual cycle, weather, and the phase of the moon.
• Regional anesthesia: Neuroaxial blockade and peripheral nerve blocks have more than a 4-
fold lower incidence of PONV. Risk factors and independent predictors include: Female
gender, history of motion sickness, preoperative tachycardia, preoperative IV opioids,
intrathecal procaine, use of phenylephrine or epinephrine, hypotension or high intrathecal
block above T4.
• Chemoreceptor trigger zone. Located in the area postrema at the bottom of the 4rd ventricle.
Receives afferent input from various peripheral and central emetogenic neurons in response
to toxic materials in the GI lumen, smell and sight, drugs (opioids), and toxins.
• Nucleus tractus solitarius receives input from vestibular and GI vagal afferents, as well as
the cortex, cerebellum, and vagal and glossopharyngeal nerves. The vestibular system is
stimulated by motion and possibly by anesthetics and opioids. The cortex is influenced by
emotions, pain, anticipation, and personality.
• Lateral reticular formation of the medulla oblongata coordinates vomiting in the medulla
and functions as the vomiting center.
• The reason that PONV is high in women and remains elevated until advancing age remains
unknown. It is obviously independent from the patient’s menstrual cycle.
• Nicotine stimulates indirect GABA-mediated cerebral dopamine release, and nicotine
withdrawal may lead to low postoperative cerebral dopamine levels, reducing activation of
dopaminergic circuits in the CRTZ.
• Children <3 years old do not suffer PONV; the risk becomes very high in adolescents and
young adulthood. In men, the incidence of PONV decreases with age. The reasons for this
effect remain speculative.
• Longer and more complex surgeries lead, accordingly, to more PONV, depending on the
administration of volatile anesthetics and intraoperative opioids. The type of surgery is not
an independent predictor for PONV; however, the underlying conditions are, such as
gender, length of surgery, volatile anesthetics, and intraoperative opioids. With maybe the
exception of strabismus surgery in children, there is only an assumed association between
different types of surgery and PONV.
• Opioids:
– Preoperative opioids: Few studies, irrelevant.
– Intraoperative opioids: Dose, and not type, of opioid is relevant for causing PONV.
– Postoperative opioids: Doubles the risk of PONV; dose, and not type, of opioids is relevant.
• Propofol possesses antiemetic properties, with a dose-dependent effect: Anesthetic doses are
most effective.
• Inhalational anesthetics strongly lead (dose-dependently) to PONV. There is no difference
between the volatile agents isoflurane, enflurane, sevoflurane and desflurane.
• Nitrous oxide weakly contributes to PONV and is additive to the effects of volatiles.
• Risk scores. The patient’s baseline risk is the main determinant of the effectiveness of
antiemetic interventions. A simplified risk score by Apfel, Koivuranta et al. identifies 4
predictors: Female gender, history of motion sickness and/or PONV, nonsmoking status, and
use of postoperative opioids. If 0, 1, 2, 3, or 4 of these risk factors are present, the
incidences of PONV over 24 hours in inpatients are 10%, 20%, 40%, 60%, and 80%.
– Prophylaxis in low risk patients (1 risk factor, risk score <10%): Prophylaxis is rarely
justified. The risks of treatment (sedation, headache, low BP, QT prolongations, Torsades
de pointes etc.) should be weighed against the patient’s preference and medical concerns
due to vomiting (e.g., a middle-aged male smoker having a microlaryngoscopy).
– Moderate risk patients (2–3 risk factors, risk score 20–40%): Consider 1 or 2 antiemetic
drugs or measures (e.g., total intravenous anesthesia [TIVA] with opioid and no other
antiemetic drugs, or 4 mg of dexamethasone and block to minimize opioid consumption).
An example is a middle-aged, non-smoking female with no other known risk factors
undergoing an appendectomy.
– High-risk patients (>3 risk factors, risk score >60%): Consider combination treatment
(e.g., regional anesthesia instead of GA, or TIVA with additional antiemetic). An example
is a young non-smoking female undergoing a craniectomy for the removal of a brain
tumor.
• Treatment guidelines suggest that outpatients should receive longer acting antiemetic
measures.
• Different mechanisms of antiemetic strategies have additive effects.
• Nausea: Feeling of urge to vomit with sickness of the stomach, which can be measured with
a VAS.
• Vomiting: Expelling stomach contents through the mouth and nose.
Differentiate between nausea and vomiting due to anesthesia and other causes related to
surgery or medical conditions; for instance, increased intracranial pressure, ileus, long fasting
period, pre-existing nausea and vomiting due to chemotherapy (CINV).
TREATMENT
• Although it is often self-limiting, PONV decreases patient satisfaction significantly

• D2 antagonists may be used prophylactically as well as acutely for PONV
– Metoclopramide (benzamide) 25–50 mg IV: Extrapyramidal side effects (dystonia,
akathisia, dysphoria, anxiety, restlessness) can occur in up to 0.8%.
– Droperidol (butyrophenone) 0.625–1.25 mg IV: Dose-dependent side effects include
sedation, extrapyramidal side effects. The FDA issued a Black Box Warning due to the
potential for lethal arrhythmias, including Torsades de pointes, under low dose
droperidol. Prior to administration, a 12-lead EKG should be performed and avoided in
females with a QTc >450 ms and in males with a QTc >440 ms. It should be noted that
other anesthetics generally have a more pronounced effect on QTc prolongation
– Haloperidol (butyrophenone) 1–2 mg IM: IV use is off-label in the US.
• Histamine (H1) antagonists can cause sedation, potentially leading to delayed awakening.
– Diphenhydramine 25 mg IV: Acts on H1 receptor antagonists in the nucleus tractus
solitarius, other vomiting centers, and the vestibular system. It also functions as a weak
anticholinergic.
– Cyclizine 50 mg IV, promethazine 25 mg IV: Are non-specific antihistamines and equally
potent anticholinergics; they are thus contraindicated in glaucoma and prostate
hypertrophy. Side effects include urinary retention, blurred vision, dry mouth, and very
rarely extrapyramidal side effects.
• Anticholinergics: Central, muscarinic receptor antagonist
– Atropine: Since it crosses the BBB, it has effects on PONV. However, it is less effective due
to its short half-life.
– Scopolamine TDS 1 mg/24 hr: Transdermal application as a patch effective up to 72
hours. Side effects include visual disturbances, dilated pupils, dry mouth, dizziness and
agitation, particularly if rubbing the patch and touching their eyes.
• Steroids: Dexamethasone 4–5 mg IV acts on the central inhibition of the nucleus tractus
solitarii, but not the area postrema. It is commonly administered after induction as it can
have severe and intense rectal burning and is slow in onset (commonly used
prophylactically)
• Serotonin (5-HT3) antagonists are the most popular class of prophylactic antiemetic drugs.
They appear to act on all levels of central structures involved in PONV. They are associated
with QTc prolongation and cardiac arrhythmias.
– Ondansetron 4 mg IV has a plasma half-life of 4 hours.
– Tropisetron 2 mg IV: QTc prolongation is observed only in high doses up to 80 mg IV.
– Dolasetron 12.5 mg IV is the minimum effective dose; 50 mg is the equipotent of
ondansetron. The plasma half-life is nearly twice as long as ondansetron.
– Granisetron 1 mg IV (lower doses of 0.1 mg have also been shown to be effective). Similar
plasma half-life to dolasetron.
• Neurokinin (NK1) antagonists act on vagal afferents in the GI tract and in the area postrema;
they are competitive inhibitors of substance P
– Aprepitant 40 mg PO is effective against vomiting, but not nausea
– Other NK antagonists in development: Casopitant and rolapitant; IV fosaprepitant is only
approved for CINV
• Miscellaneous drugs
– Mirtazapine 30 mg PO for premedication reduces PONV through reduction of anxiety
– Opioid antagonists have efficacy due to reduction of delay in gastric emptying. Naloxone
0.25 μg/kg/hr has been shown to be superior to placebo
• Alternative remedies and approaches:
– Ginger: Studies have not shown clear evidence for efficacy.
– Liberal crystalloid fluid supplementation: May be of benefit for late onset PONV,
potentially due to the lower need to drink early after surgery.
– P6-stimulation of “nei guan” point via acupressure, acupuncture, transcutaneous nerve
stimulation, laser stimulation, or acu-stimulation device: evidence for efficacy on PONV,
especially in high-risk patients
FOLLOW-UP
• Rescue treatment strategies need to be started early to improve outcomes (e.g., time to
discharge). Preferred pharmacologic rescue treatments include:
– Serotonin antagonists are the first choice, if not given in the OR before
– Dexamethasone
– Antidopaminergics
– Stimulation of P6 acupressure point
– Scopolamine TDS
– Non-opioid analgesics, such as NSAIDs
– It is more effective to choose an alternative acting antiemetic to the one previously given.
• Regional techniques such as peripheral nerve blocks or catheter techniques, to spare oral or
IV opioids for postoperative pain control.
CLOSED CLAIMS DATA
PONV is not mentioned in the 2011 Closed Claims’ Analysis
REFERENCES
1. Apfel CC, et al. A simplified risk score for predicting postoperative nausea and vomiting:
Conclusions from cross-validations between two centers. Anesthesiology. 1999;91(3):693–
700.
2. Carpenter RL, et al. Incidence and risk factors for side effects of spinal anesthesia.
Anesthesiology. 1992;76(6):906–916.
3. Eberhard LH, et al. The development and validation of a risk score to predict the
probability of postoperative vomiting in pediatric patients. Anesth Analg.
2004;99(60):1630–1637.
4. Fero KE, et al. Pharmacologic management of postoperative nausea and vomiting. Expert
Opin Pharmacother. 2011;12(15):2283–2296.
5. Pierre S, et al. A risk score-dependent antiemetic approach effectively reduces
postoperative nausea and vomiting – a continuous quality improvement initiative. Can J
Anaesth. 2004;51(4):320–325.
6. Apfel CC, et al. Transdermal scopolamine for the prevention of postoperative nausea and
vomiting: A systematic review and meta-analysis. Clin Ther. 2010;32(12):1987–2002.
7. Lee A, Fan LTY. Stimulation of the writs acupuncture point P6 for preventing postoperative
nausea and vomiting. Cochrane Database Syst Rev. 2009;15:CD003281.
• Wallenborn J, et al. The impact of isoflurane, desflurane, or sevoflurane on the frequency
and severity of postoperative nausea and vomiting after lumbar disc surgery. J Clin Anesth.
2007;19(3):180–185.
CODES
ICD9
• 787.01 Nausea with vomiting
• 997.49 Other digestive system complications
ICD10
• K91.89 Oth postprocedural complications and disorders of dgstv sys
• R11.2 Nausea with vomiting, unspecified
CLINICAL PEARLS
• An underappreciated risk factor for PONV is the length of surgery.
• The most effective antiemetic strategy would be to avoid emetogenic triggers, which are GA
with volatile agents and opioids, and perform opioid-free regional anesthesia instead.
• If a GA needs to be done in very susceptible patients, a TIVA with or without additional
antiemetic strategies is advisable.
• PONV properties of opioids seem to depend on the (equipotent) dose, not on type of opioid.
• The risk of PONV in local and regional anesthesia is not 0%; it is, however, at least 4 times
lower compared to general anesthesia.
• No available antiemetic strategy will completely eliminate PONV. In very high-risk patients,
multimodal therapy with independently acting measures and drugs should be chosen.
POSTOPERATIVE PULMONARY COMPLICATIONS (PPCS)
BASICS
DESCRIPTION
Postoperative pulmonary complications (PPCs) are as common as cardiac complications for
patients undergoing non-cardiothoracic surgery. Similarly, they contribute to morbidity,
mortality, and length of stay.
EPIDEMIOLOGY
Prevalence
5–10% of all surgical patients experience PPCs.
Morbidity
The most significant PPCs are: Atelectasis, pneumonia, respiratory failure, and exacerbation
of underlying chronic lung disease.
Mortality
Following abdominal aortic aneurysm (AAA) repair, patients who develop postoperative
respiratory failure (PPF) have an in-hospital mortality that reaches 40–42% (compared to 6%
for those without).
Patient-related risk factors
• Age: Appears to be an independent, significant risk factor. In a study of patients older than
80 years, the overall 30-day mortality rate was 6.2%. As age is obviously a nonmodifiable
risk factor, and the potential risk of complications does not invariably translate into
increased mortality, surgery should not be declined because of advanced age alone.
• Chronic obstructive pulmonary disease (COPD): The most common risk factor. Patients with
severe COPD (forced expiratory volume in 1 second [FEV1] <40% predicted) are 6 times
more likely to have a major postoperative complication. Despite the increased risk, a
prohibitive level of pulmonary function for an absolute contraindication is not apparent.
The benefits of surgery must be weighed against these complications. A careful preoperative
evaluation should include identification of high-risk patients and aggressive treatment.
Elective surgery should be deferred in symptomatic patients with poor exercise capacity or
having an acute exacerbation.
• Cigarette use: Patients who currently smoke have a 2-fold increased risk even in the absence
of COPD. The risk is highest in patients who smoked within the last 2 months. Patients who
quit smoking for more than 6 months have a risk similar to those who do not smoke. The
risk of postoperative pneumonia appears to remain elevated up to 1 year after smoking
cessation.
• ASA classification: The incidence of PPC increases with comorbidities. Class I: 1.2%; Class II:
5.4%; Class III: 11.4%; Class IV: 10.9%
• Obesity (BMI > 30): Causes a reduction in lung volume, V/Q mismatch, and relative
hypoxemia that are accentuated after surgery. In severe cases, pulmonary hypertension, cor
pulmonale, and hypercapnic respiratory failure (“pickwickian" syndrome) are seen.
• Asthma: Increases the risk of bronchospasm, hypoxemia, hypercapnia, inadequate cough,
atelectasis, and pulmonary infection following surgery. Inadequate preoperative control
may increase the risk.
• Obstructive sleep apnea (OSA): Patients are at increased risk of developing deterioration of
breathing, severe hypoxemia, and hypercapnia in the postoperative period. Obese patients
with sleep apnea may present difficulties with endotracheal intubation or early
postoperative upper airway obstruction, requiring reintubation or other therapies.
Procedure-related risk factors
• Surgical site: The incidence of PPC is inversely related to the distance of the surgical incision
from the diaphragm. The complication rates for thoracic surgery range from 19–59%, upper
abdominal surgery 17–76%, and lower abdominal surgery 0–5%. AAA repair is associated
with the highest risk.
• Duration of surgery: Patients undergoing procedures lasting longer than 3–4 hours have a
higher incidence rate (40%) compared to procedures less than 2 hours (8%).
• Anesthetic technique: General anesthesia (GA) appears to be associated with a higher risk of
clinically important complications compared with epidural or spinal anesthesia. The
associated mechanisms appear to be GA-associated respiratory changes, residual effects of
sedatives, narcotics and neuromuscular blockers. The duration of anesthesia also correlates
with PPC.
• Emergency surgery: The limited time available to implement protective strategies (e.g.,
intensive preoperative inspiratory muscle training) increases the incidence of PPC.
• Intraoperative changes: Many PPCs are related to the disruption of normal respiratory
muscle activity which begins at the time of induction and continues into the postoperative
period. The lack of coordinated activity decreases efficiency and impaired functional
residual capacity (FRC) causes atelectasis. Of note, chest wall distortion and atelectasis is
more pronounced with mechanical ventilation.
– Volatile and intravenous drugs affect the central regulation of breathing. The altered
neural drive to respiratory muscles results in respiratory depression.
– Airway instrumentation can result in reflex stimulation and the release of inflammatory
mediators with resultant bronchoconstriction. Increased airway resistance limits
expiratory gas flow, which can produce hyperinflation with risk of barotrauma and
abnormal gas exchange.
– Tracheal intubation and anesthetic vapors impair mucociliary transport.
– Prolonged anesthesia and surgery can impair the function of the inflammatory cells and
cause postoperative infections.
– Cardiopulmonary bypass can cause acute lung injury
– Surgical trauma and barotrauma can cause pneumothorax
– Laryngospasm can cause negative pressure pulmonary edema
– Aspiration of stomach contents can occur during induction and emergence, or
intraoperatively with supraglottic devices or deep sedation
• Postoperative changes: The role of surgical trauma is most pronounced after thoracic and
abdominal surgery. Causes include the functional disruption of respiratory muscles
(intercostals and abdominal muscles) by incisions; postoperative pain that limits voluntary
respiratory motion; and visceral stimulation that can decrease phrenic motor neuron output
and limit diaphragmatic descent. The persistent decrease in FRC and respiratory muscle
function lasts for several days after surgery. Prolonged atelectasis can result in pneumonia.
Even laparoscopic techniques can still stimulate abdominal viscera and affect pulmonary
mechanics.
• Preoperative risk assessment: A complete history and physical examination helps to identify
risk factors for PPC. Seek any history of smoking, exercise intolerance, unexplained
dyspnea, or cough. Note evidence of COPD, such as decreased breath sounds, wheezes,
crackles, or a prolonged expiratory phase. Consider further workup as needed.
– Pulmonary function tests (PFTs): Several retrospective studies of routine PFTs found only
a marginal benefit in predicting postoperative complications, other than in those
undergoing lung resection. Preoperative spirometry has not been shown to be predictive
of complications following abdominal surgery. Thus, testing should be restricted to those
patients with unexplained dyspnea or exercise tolerance, or undergoing resectional
surgery.
– Arterial blood gasses (ABGs): Measures of pH, PaO2, and PaCO2 may be utilized to
establish an objective baseline, or deviation from it.
– Chest radiography: Studies suggest that it adds little to the clinical evaluation in healthy
patients and routine preoperative evaluation is unnecessary.
– Polysomnographic sleep study: In patients with sleep apnea, the diagnosis should be
confirmed and the severity assessed with a sleep study. The severity is judged based on
the apnea–hypopnea index and the lowest oxygen saturation value during sleep.
• Multifactorial Risk Index for Predicting Postoperative Respiratory Failure: Developed and
validated respiratory failure risk index from 44 VA medical centers.
– Useful to evaluate the perioperative risk for developing PPF (defined as the inability to be
extubated 48 hours after surgery); considered the most serious of thePPCs.
– Operation-specific risk factors had the highest value, in particular, the type of surgery;
however, the ability to intervene and decrease these factors is minimal.
– Patient-related factors are amenable to treatment or optimization and play a role in
decreasing the PPF risk.
• Preoperative strategies to reduce PPC:
– Smoking cessation for 8 weeks
– Proper perioperative fluid management
– Correction of possible malnutrition
– Pulmonary rehabilitation
– Educate patients on lung expansion maneuvers and inspiratory muscle training
– Antibiotic therapy for acute bronchitis.
• Intraoperative strategies to reduce PPC:
– Intermediate and short-acting neuromuscular blocking agents
– Regional anesthesia when feasible
– In extremely high-risk patients, less invasive, shorter or modified procedures should be
considered.
– When possible, laparoscopic procedures should be substituted for open procedures.
– In patients with known or possible sleep apnea, the perioperative use of sedatives and
narcotics should be minimized.
• Postoperative strategies to reduce PPC:
– Lung expansion maneuvers (incentive spirometry, deep breathing exercises, intermittent
positive pressure breathing [IPPB], continuous positive airway pressure [CPAP]), postural
drainage, percussion and vibration, coughing, suctioning, and mobilization.
– Pain control: Adequate postoperative pain control helps minimize pulmonary
complications by facilitating earlier ambulation and lung expansion. In upper abdominal
procedures, epidural analgesia had lower rates of pulmonary complications and a shorter
hospital stay. Epidural narcotics provide a longer duration of action, a lack of excessive
sedation and respiratory depression, and a minimum or absence of sensory motor loss.
– Good glycemic control: Associated with a reduced duration of mechanical ventilation;
however, its specific impact on PPCs is unclear
– Nasogastric decompression: Selective use of nasogastric tubes in patients with
postoperative nausea and vomiting (PONV), inability to tolerate oral intake, or
symptomatic abdominal distention may be appropriate. However, the routine use
following abdominal surgery is associated with higher rates of pneumonia.
– Total parenteral nutrition: Although poor nutrition is a risk factor for PPC, the routine use
of total parenteral nutrition has no benefit over enteral nutrition or no hyperalimentation,
except in patients with severe malnutrition or prolonged inadequate enteral feeding.
– Prevention of venous thromboembolism (VTE): Surgery is a well-recognized risk factor for
the development of deep vein thrombosis and pulmonary embolism. The risk is influenced
by patient and procedure-related factors; appropriate thromboprophylaxis is essential in
high-risk patients.
See Table
REFERENCE
1. ong W, Weber E. Factors associated with postoperative pulmonary complications in
patients with severe COPD. Anaesth Analg. 1995;80:276–284.
2. Arouzullah A. Multifactorial risk index for predicting postoperative respiratory failure in
men after major noncardiac surgery. Ann Surg. 2006;232:242–253.
3. Lawrence V. Strategies to reduce postoperative pulmonary complications after
noncardiothoracic surgery: systematic review for the American College of Physicians. Ann
Int Med. 2006;144:596–608.
ADDITIONAL READING
• www.emedicine.medscape.com - perioperative pulmonary management
• Atelectasis
• Asthma
CODES
ICD9
• 518.0 Pulmonary collapse
• 997.32 Postprocedural aspiration pneumonia
• 997.39 Other respiratory complications
ICD10
• J95.2 Acute pulmonary insufficiency following nonthoracic surgery
• J95.821 Acute postprocedural respiratory failure
• J95.89 Oth postproc complications and disorders of resp sys, NEC
CLINICAL PEARLS
• PPCs contribute significantly to overall perioperative morbidity and mortality rates.
• The goal of perioperative pulmonary management is to identify patients at high risk for
significant postoperative pulmonary complications, so that appropriate interventions can be
implemented in order to minimize that risk.
POSTOPERATIVE RENAL DYSFUNCTION
Patrick Kim, MD
BASICS
DESCRIPTION
• Acute kidney injury (AKI) is a frequently encountered postoperative complication with
significant short-term and long-term consequences.
• The Acute Kidney Injury Network classifies AKI as:
– Stage 1: Increase in SrCr >0.3 mg/dL or 1.5–2-fold increase from baseline, or urine
output (UOP) <0.5 mL/kg/hr × 6 hours
– Stage 2: 2–3-fold increase in SrCr, or UOP <0.5 mL/kg/hr × 12 hours
– Stage 3: >3-fold increase in SrCr or an acute increase of >0.5 mg/dL in patients with a
baseline SrCr >4 mg/dL, or UOP <0.3 mL/kg/hr × 24 hours or anuria × 12 hours; or
patients requiring renal replacement therapy (RRT)
• Despite being the basis of the AKI definition, SrCr is not a very sensitive marker of the
condition:
– Changes in GFR are reflected by SrCr levels 2–3 days after an insult.
– Levels vary with the patient’s age, body habitus, and volume status.
• Newer biomarkers of AKI are being developed:
– Neutrophil gelatinase-associated lipocalin (NGAL). A protein is upregulated by tubular
endothelial cell after an ischemic injury. Urinary and plasma levels are being studied.
– KIM-1: Transmembrane protein that is highly expressed by de-differentiated tubular cells
following injury.
– Cystatin C: Produced by all nucleated cells. It is freely filtered and completely reabsorbed
and degraded by the tubules. Reflects glomerular filtration, not tubular injury. Value not
yet certain but could identify AKI before elevations of creatinine occur.
– IL-18: Tubular epithelial pro-inflammatory cytokine that gets activated in proximal
tubules following injury. May be a predictor of mortality in critically ill patients.
EPIDEMIOLOGY
Prevalence
• Difficult to ascertain due to the previously widely varying definitions of acute renal failure
in the literature.
• Varies widely depending on the surgery. Estimated at 1% in major non-cardiac surgery and
up to 25% in cardiovascular surgery patients
Prevalence
Varies according to patient population. Occurs in approximately 5–7% of hospitalized
patients and 30–35% of ICU patients.
Morbidity
Significant: Postoperative acute renal failure is associated with an increased risk of
perioperative infection, longer ICU and/or hospital stay, need for renal replacement therapy
(RRT), and acceleration of coronary vascular disease with increased long-term morbidity.
Mortality
Significant: Patients with an increase in serum creatinine by 2 mg/dL or who require
hemodialysis have an 8-fold increase in 30-day mortality. Even a modest increase in SrCr
>0.5 mg/dL in hospitalized patients is associated with a 6.5-fold increase in the odds of in-
hospital death.
• High risk surgical procedures include: Cardiac and vascular surgery, heart and liver
transplant, hepatobiliary surgery, and procedures utilizing radiocontrast
• High risk patients include:
– Renal insufficiency, both mild and moderate
– Ascites
– Active congestive heart failure
– Emergency surgery
– Age >56 years
– Hypertension
– Male sex
• Total renal blood flow (TRBF) is about 20% of the cardiac output with an oxygen delivery of
80 mL/min/100 g of tissue.
• The renal cortex receives most of the TRBF and has a low oxygen extraction ratio (∼20%).
• The renal medulla has a smaller blood flow and a high oxygen extraction ratio (∼80%),
consequent to the high metabolic demand of tubular reabsorptive function. Thus, the renal
medulla is susceptible to ischemic insults.
• In acute tubular necrosis (ATN), ischemia and/or direct toxicity result in apoptosis and
shedding of tubular cells as well as recruitment of vasoactive and inflammatory mediators
that worsen ischemic injury. Loss of tubular cells allows leakage of glomerular filtrate into
the interstitium which results in edema that may progress to chronic inflammation and
fibrosis, ultimately leading to chronic kidney disease.
• Perioperatively, a combination of factors contribute to renal dysfunction:
– Preoperatively: Hypovolemia due to preoperative fasting, bowel preparation
– Intraoperatively: Effect of anesthetics on hemodynamics and renal perfusion, effect of
surgical technique on renal blood flow (e.g., laparoscopic procedures), blood loss,
neuroendocrine response to anesthesia and surgery, excessive fluid resuscitation
– Use of nephrotoxins such as contrast media, antibiotics, NSAIDs, etc.
• The cornerstone of treatment is prevention.
• Pharmacologic interventions have been controversial, and as of yet, no pharmacologic
interventions have definitively been beneficial in the prevention of renal failure in the
perioperative period with the exception of mannitol administration prior to renal transplant
reperfusion.
• Maintain adequate blood pressure.
– Autoregulation maintains a constant renal blood flow between mean arterial pressures
(MAPs) of 80–160 mm Hg.
– Improved renal hemodynamics has been shown with MAPs around 75 mm Hg.
– The autoregulation curve may be shifted to the right in chronic hypertensives, so higher
pressures may be needed.
• Ensure euvolemia.
– Oxygen delivery to the kidneys may be reduced in hypovolemia, resulting in ischemic
ATN.
– Excessive fluid resuscitation may lead to abdominal compartment syndrome (intra-
abdominal hypertension [IAH]) and impaired renal perfusion.
– Normal saline given in volumes >30 mL/kg can cause a non-gap hyperchloremic
metabolic acidosis and hyperkalemia. Hyperchloremia may result in a decrease in renal
blood flow, glomerular filtration rate, and urine output.
– Albumin may not be more beneficial than crystalloids except in specific situations such as
in cirrhotic patients with spontaneous bacterial peritonitis.
– There is conflicting evidence on the renal safety of hydroxyethyl starch.
• Optimize the oxygen delivery to the kidneys by maintaining an adequate hemoglobin level
and cardiac output.
• Avoid nephrotoxins.
– Iodinated contrast agents are being used with increasing frequency and can cause contrast
induced-acute kidney injury (CI-AKI). In addition to being directly toxic to tubular cells,
they can cause renal vasoconstriction. Unfortunately at this time, no definitive technique
has been shown to consistently decrease or eliminate this risk. The following may be
considered: Adequate hydration to a goal of 100–150 mL/hr of UOP to potentially “wash
off” the agent and minimize contact time with tubular cells; antioxidants such as N-acetyl
cysteine, statins, and urine alkalinizers such as sodium bicarbonate may reduce free
radical-related tubular cell apoptosis; the use of low osmolar agents (approximately twice
the osmolarity of plasma) in normal patients and iso-osmolar agents in patients at risk of
CI-AKI; avoid concomitant use of other nephrotoxins as well as repeat exposure (within 72
hours) of receiving a contrast medium load.
– NSAIDs inhibit vasodilatory prostaglandins and can result in decreased glomerular
filtration pressure by vasoconstricting afferent arterioles. Consider avoiding in high-risk
patients. However, in one study, no long-term impairment in renal function was found
when given postoperatively to kidney donors.
– ACEI and ARBs: Decrease glomerular filtration pressure by vasodilating efferent arterioles.
Avoid in hypovolemia.
– Antibiotics such as aminoglycosides can cause ATN by accumulating in the proximal
tubules.
– Other nephrotoxins include antifibrinolytics such as aprotinin, immunosuppressants such
as cyclosporine and tacrolimus, and chemotherapeutic agents such as cisplatin.
• History and physical examination including medication review, perioperative exposure to
nephrotoxins, volume and hemodynamic assessment.
• On urinalysis, hyaline casts suggest prerenal azotemia, whereas pigmented casts are seen in
ATN.
• Concentration of urine solutes and avid sodium retention is seen in prerenal azotemia. This
will result in a specific gravity >1.015, osmolality >350 mOsm/kg, and urine sodium <20
mmol/L.
• Fractional excretion of sodium (FENa) is helpful in distinguishing between prerenal
azotemia and ATN. FENa levels <1% suggest prerenal azotemia and >3% suggest ATN;
however, patients with prerenal azotemia treated with diuretics may have high FENa.
• Fractional excretion of urea may be helpful in differentiating between prerenal azotemia and
ATN.
• Newer biomarkers such as NGAL and KIM-1 may play a role in distinguishing ATN from
other causes of AKI.
• Exclude urinary tract obstruction.
– Renal ultrasound
– High resolution CT scan of abdomen and pelvis
• Prerenal AKI results as a consequence of true hypovolemia or decreased effective circulating
blood volume (as in cirrhosis, CHF).
• Intrinsic AKI can be due to tubular, interstitial, or glomerular injury.
– ATN is the most common cause of intrinsic AKI. It occurs as a result of ischemia
(prolonged absolute or relative hypotension), exposure to nephrotoxins, and/or the
endotoxins and inflammatory mediators released in septic patients.
– Acute interstitial nephritis is infiltration of the interstitium by lymphocytes secondary to
the use of NSAIDs or antibiotics.
– Acute glomerulonephritis is characterized by rapid progression and may be seen in post-
streptococcal infection or in the setting of endocarditis.
• Postrenal AKI: Urinary tract obstruction can be seen perioperatively in pelvic surgery
following inadvertent injury to the bladder or ureter(s). Intraoperative identification may
include the use of intravenous methylene blue or indigo carmine.
TREATMENT
• Mainly supportive
• RRT may be initiated before the development of the classic indications of hyperkalemia,
metabolic acidosis, volume overload, and symptomatic uremia. Controversy still exists on
the best modality of RRT (continuous RRT or intermittent hemodialysis) and the dosing
(intensity of dialysis).
FOLLOW-UP
• Basic metabolic profile

• Free excretion of sodium, urea
• Urine specific gravity
• Postoperative urinary output
• 24-hour creatinine clearance
CLOSED CLAIMS DATA
Perioperative renal failure Closed Claims Data. There were 75 claims from 1978 to 2006:
• Male: 53%
• Age >53 years: 50%
• ASA 3–5: 45%
• Intraoperative oliguria or anuria: 31%
• Emergency surgery (ASA classification): 29%
• Vascular surgery: 16%
• Cardiac surgery: 3%
• Perioperative events leading to renal dysfunction/failure:
– Patient condition or surgical cause: 17%
– Wrong blood administered: 15%
– Electrolyte imbalance or inappropriate fluid therapy: 13%
– Medication error: 12%
– Excessive blood loss: 8%
• Outcome and liability:
– Mortality: 47%
– Substandard anesthesia care: 48%
– Payments/settlement to patient: 56%
– Median payment: $255,000 (range: $4,000–$3,625,000)
REFERENCES
1. agshaw SM, et al. Review article: Acute kidney injury in critical illness. Canadian J Anesth.
2010;57:985–998.
2. Kheterpal S, Tremper K, Heung M, et al. Development and validation of an acute kidney
injury risk index for patients undergoing general surgery. Anesthesiology. 2009;110:505–
515.
3. Crowley ST, Pexioto AJ. Acute kidney injury in the intensive care unit. Clin Chest Med.
2009;29–43.
4. Jones D, Lee H. Perioperative Renal Protection. Best Pract Res Clin Anesthesiol.
2008;22(1):193–208.
5. Khalil P, Murty P, Palevsky P. The patient with acute kidney injury. Prim Care Clin Office
Pract. 2008;35:239–264.
6. Posner KL. Personal communication. ASA Closed Claims Project N8954, March 1, 2011.
ADDITIONAL READING
• Chertow MG, Burdick E, Honour M, et al. Acute kidney injury, mortality, length of stay, and
costs in hospitalized patients. J Am Soc Nephrol. 2005;16:3365–3370.
• Friedwald VE, Goldfarb S, Laskey W, et al. The editor’s roundtable: contrast-induced
nephropathy. Am J Cardiol. 2007;100(3):544–51.
• Jarnberg P. Renal protection strategies in the perioperative period. Best Pract Res Clin
Anesthesiol. 2004;18(4):645–660.
• Sear JW. Kidney dysfunction in the postoperative period. Brit J Anesth. 2005;95(1):20–32.
• Tang I, Murray P. Prevention of perioperative acute renal failure: what works? Best Pract
Res Clin Anesthesiol. 2004;18(1):91–111.
CODES
ICD9
• 584.9 Acute kidney failure, unspecified
• 997.5 Urinary complications, not elsewhere classified
ICD10
• N17.8 Other acute kidney failure
• N99.89 Oth postprocedural complications and disorders of GU sys
CLINICAL PEARLS
• With the exception of maintaining adequate renal perfusion pressures and fluid hydration,
there are not many interventions that can actively prevent renal failure postoperatively.
• Low intraoperative urinary output is not always correlated with postoperative renal failure.
• Oliguria during laparoscopic procedures is due to compression of the kidneys and their
vessels by the pneumoperitoneum. It usually resolves after desufflation. Avoid insufflations
pressures >15 mm Hg.
POSTOPERATIVE SHIVERING
Jose M. Soliz, MD
BASICS
DESCRIPTION
Postoperative shivering is involuntary, oscillatory muscle activity that augments heat
production; it is common upon emergence from anesthesia.
EPIDEMIOLOGY
Prevalence
• Up to 40% of patients shiver during recovery after undergoing a general anesthetic (1)
• Up to 30% of patients shiver during epidural anesthesia
• The incidence of shivering is affected by the core body temperature:
– At 35.5°C, up to 50% of patients shiver.
– Between 34.5–35.4°C: Up to 90% of patients shiver.
Morbidity
• Increases O2 consumption by up to 300%; as a result, it may increase the incidence of
adverse myocardial events in high-risk patients.
• Increases CO2 production
• Increases plasma catecholamine levels
• Increases intraocular and intracranial pressures
• Increases postoperative pain and discomfort
• Hypothermia may exacerbate postoperative bleeding, prolong neuromuscular blockade,
delay emergence, delay wound healing, and increase the risk of surgical site infection (1).
Mortality
May indirectly increase due to adverse cardiovascular events and increased risk of infection.
Data is not currently available.
• Most commonly occurs as a complication of hypothermia (2)
• Normothermic shivering can also occur in:
– Younger patients
– Prolonged surgery
– Orthopedic surgery
• The preoptic region of the hypothalamus is the dominant autonomic thermoregulatory
center. When this region is cooled, shivering is believed to be mediated via recurrent
inhibition of a group of inhibitory neurons called Renshaw cells. Shivering thus serves as a
normal, physiologic, protective mechanism to create warmth by energy expenditure.
• Perioperative hypothermia
– During general peripheral vasodilation results in redistribution of heat from the core to
the periphery; this typically occurs over the first hour.
– Heat loss from the patient to the environment/surroundings occurs via radiation,
conduction, convection, and evaporation.
• Anesthetic agents and shivering. During surgery, anesthetic medications increase the
shivering threshold and protect against intraoperative shivering. However, as plasma
concentrations decrease in the postoperative period, shivering can occur (8).
• Neuraxial anesthesia and shivering. Spinal and epidural anesthetics produce sympathetic
blockade with resultant vasodilation and heat loss. The mechanism of postoperative
shivering is not fully understood.
– Shivering is a function of motor activity; thus dermatomes that have motor blockade will
not produce oscillatory muscle activity.
– Spinal blocks initially decrease core temperature faster than epidural anesthesia; thus, the
shivering threshold is achieved faster.
• Non-thermoregulatory shivering: Shivering is not isolated to hypothermic states; the
pathogenesis is not completely understood. Potential causes include:
– The release of pyrogenic mediators elicited by surgical tissue damage
– Anesthetic drugs
– Postoperative pain
– Decreased sympathetic activity
– Uninhibited spinal reflexes/loss of descending control
– Adrenal suppression
– Fever
– Respiratory alkalosis
• Neonates have an increased body surface area and are susceptible to hypothermia in the
perioperative period. In addition, neonates cannot respond to cold stress by shivering; these
mechanisms do not develop until the age of 6 months to 1 year. Measures to decrease heat
loss and generate heat include:
– Peripheral vasoconstriction via norepinephrine release: This can lead to pulmonary artery
constriction and right-to-left shunting (hypoxia, cyanosis), as well as decreased tissue
perfusion with subsequent tissue hypoxia and metabolic acidosis.
– Non-shivering thermogenesis (NST): Describes the metabolism of brown fat which
increases oxygen consumption and carbon dioxide production. The increased oxygen
requirements may lead to hypoxia and metabolic acidosis; the increased carbon dioxide
production may lead to tachypnea (if unable to adequately exhale the increased load, can
result in respiratory acidosis). Furthermore, inhalational anesthetics inhibit brown fat
metabolism, further increasing neonatal susceptibility to hypothermia in the operating
room.
Epidural meperidine, fentanyl, alfentanil, and morphine have been used to treat shivering in
the obstetric patient. Intravenous propofol has also been used to decrease cold responses.
Shivering can also occur in the laboring patient who did not receive neuraxial anesthesia,
which suggests a non-thermoregulatory mechanism for shivering during labor.
• Prevention of hypothermia is preferred to rewarming in the postoperative period (3). This
can be facilitated by:
– Intraoperative temperature monitoring: Core body temperature is measured in the distal
esophagus, nasopharynx, tympanic membrane, or pulmonary artery.
– Blankets and drapes to decrease radiation of heat into the cooler environment.
– Forced air warming decreases the radiation of heat into the cooler environment as well as
actively warms the patient. It is considered the most effective method.
– Increasing the ambient temperature of the surgical suite decreases the radiation of heat
into the environment
– Warm intravenous fluids and blood products
– Humidify anesthesia circuits
Visualized cutaneous muscle contractions
• Seizure
• Muscle spasms from hypocalcemia, hypokalemia
• Rigors in patients developing fever
• Extrapyramidal symptoms in patients with Parkinson’s disease or Parkinson-like syndrome.
TREATMENT
• Hypothermic shivering: Cutaneous warming with blankets or forced air in the recovery
room.
• Non-thermoregulatory (and hypothermic shivering, while simultaneously rewarming) can be
treated with pharmacologic agents:
– Meperidine 12.5 mg or 25 mg IV; via kappa receptor effects.
– Granisetron 40 mcg/kg IV (5); via 5-HT3 activity.
– Tramadol 0.1 mg/kg IV; via a modulatory effect on central monoaminergic pathways. It
has the benefit of decreased sedation compared to meperidine (6).
– Opioids (morphine, fentanyl); likely via analgesic effects.
– Physostigmine 0.04 mg/kg IV; crosses the blood–brain barrier and is a cholinesterase
inhibitor. Cholinergic stimulation of the hypothalamic–pituitary–adrenal axis and the
adrenal medulla enhance the secretion of arginine vasopressin, epinephrine, and
norepinephrine; these neurotransmitters are believed to be involved in body temperature
control. Physostigmine is associated with bradycardia and gastrointestinal upset.
– Ketamine 0.5 mg/kg IV prophylactically (7); mechanism via antagonism of the NMDA
receptor.
– Clonidine 75 mcg IV; a centrally acting alpha-2 receptor agonist. May decrease blood
pressure.
– Chlorpromazine 10–20 mg IV; exact mechanism to reduce shivering is unknown. It may
possibly occur via antidopaminergic or anticholinergic activity.
– Doxapram 100 mg IV (3); centrally acts to increase the shivering threshold, may also have
weak opioid receptor activity.
– Dexmedetomidine 1 mcg/kg; likely via reduced central adrenergic flow.
FOLLOW-UP
• If patients are hypovolemic, rewarming may cause vasodilatation leading to hypotension,
reflex tachycardia, and myocardial ischemia. Replacing intravascular volume while
rewarming may be necessary.
• Opioid-related side effects can occur when used for the treatment of shivering. Monitor for
respiratory depression, drowsiness, altered mental status, nausea, vomiting, and pruritus.
CLOSED CLAIMS DATA
Devices used to warm the patient’s skin resulted in 28 burns (N = 3000 total claims). 18 of
the 28 were from IV fluid bags or water bottles applied directly to the patient’s skin. 5 of the
28 burns resulted from circulating water mattresses (4).
REFERENCES
1. Bhattacharya PK, Bhattacharya L, Jain R, et al. Post anesthesia shivering (PAS): a review.
Indian J Anaesth. 2003;47(2): 88–93.
2. Leopold H, Eberhart J, Doderlein F, et al. Independent risk factors for postoperative
shivering. Anesth Analg. 2005;101:1849–1857.
3. Kranke P, Eberhart LH, Roewer N, et al. Pharmacological treatment of postoperative
shivering: a quantitative systematic review of randomized controlled trials. Anesth Analg.
2002;94:453–460.
4. Cheney FW, Posner KL, Caplan RA, et al. Burns from warming devices in anesthesia.
5. Sajedi P, Yaraghi A, Moseli HA. Efficacy of graniesetron in preventing postanesthetic
shivering. Acta Anaesthesiol Taiwan. 2008;46(4):166–170.
6. Tsai YC, Chu KS. A comparison of tramadol, amitryptyline, and meperidine for
postepidural anesthetic shivering in parturients. Anesth Analg. 2001;93(5):1288–1292.
7. Sagir O, Guthas N, Toprak H, et al. Control of shivering during regional anesthesia:
Prophylactic ketamine and granisetron. Acta Anaesthesiol Scand. 2007;51(1):44–49.
8. Horn EP. Postoperative shivering: Aetiology and treatment. Curr Opin Anaesthesiol.
1999;12(4):449–453.
ADDITIONAL READING
• Hypothermia
• Surgical site infection
• Chronic angina
CODES
ICD9
995.89 Other specified adverse effects, not elsewhere classified
ICD10
T88.51XA Hypothermia following anesthesia, initial encounter
CLINICAL PEARLS
• Prevention of hypothermia is key.
• Intraoperative forced air warming is the most effective method of preventing hypothermia.
• Various pharmacologic agents can be used as treatment. Meperidine (12.5 mg or 25 mg IV)
is the most consistently effective.
POSTRENAL ACUTE KIDNEY INJURY
Jonathan Anson, MD
BASICS
DESCRIPTION
• Acute kidney injury (AKI) is a sudden decrease in kidney function causing acid–base
imbalance along with fluid and electrolyte disturbances.
• AKI causes can be divided into:
– Prerenal
– Intrarenal
– Postrenal: Accounts for just 5–10% of all AKI, but is often easily reversible.
• In the perioperative period, patients may present:
– For temporary or definitive surgical treatment to relieve a pre-existing urinary obstruction
– For pre-emptive stent placement prior to abdominal or pelvic surgeries
– With anuria, oliguria, or signs and symptoms of AKI secondary to mechanical obstruction
• The reversible nature of postrenal disease makes a prompt diagnosis essential.
• Nephrons are the functional units of the kidney.
– Afferent arterioles form glomerular capillaries within the Bowman’s capsule (cup-like
structure). They exit via efferent arterioles after filtering into the nephron via hydrostatic
forces.
– Urine ultrafiltrate passes from the proximal convoluted tubule to the loop of Henle to the
distal convoluted tubule and finally to the collecting ducts.
• Glomerular filtration rate (GFR) is the plasma volume filtered by the kidneys per unit of
time and is used to assess the kidney function. GFR can be estimated by calculating a
patient’s creatinine clearance. Additionally, trends in creatinine clearance can be used to
predict perioperative outcomes.
ANATOMY
• Gross anatomy of the kidney:
– Consists of an outer cortical layer and inner medulla.
– Renal artery, renal vein, and ureter enter/exit the kidney at the hilus on the midportion of
the concave side.
– At the hilus, the ureter dilates into the renal pelvis. The renal pelvis further divides into
many tube-like calyces that combine to form the renal parenchyma.
– Sympathetic innervation is via the T8-L1 preganglionic fibers.
– Parasympathetic input is from the vagus nerve.
• Gross anatomy of the ureter:
– Muscular tubes propel urine from the renal pelvis to the bladder.
– The lumen is lined with transitional epithelium.
– Descends anterior to the psoas muscle and crosses the pelvic brim at the bifurcation of the
iliac arteries.
– Ureters enter the bladder at the vesicoureteric junction.
– Ureterovesical valves prevent backflow of urine.
• Gross anatomy of the bladder:
– Hollow, muscular, elastic organ that collects urine excreted by the kidney.
– The bladder wall is composed of a smooth muscle called detrusor.
– Internal surface consists of the transitional epithelium, cuboidal cells that can expand and
contract to support volume fluctuations.
– Sympathetic innervation is via T11-L2
– Parasympathetic innervation is from S2–S4. Bladder stretching induces the
parasympathetic nervous system to contract the detrusor muscle and expel urine to the
urethra
• Postrenal failure occurs when urine flow from both kidneys is obstructed. This can result
from obstruction of a single kidney in the presence of a diseased contralateral kidney or
partial or complete obstruction of the bladder or urethra. Specific instances where this can
occur are:
– Urethral obstruction bilaterally, such as stones or strictures
– Bladder obstruction
– Neurogenic bladder
– Prostatic hypertrophy
– Obstruction of the renal pelvis
– Blood clots
– Cancer of the bladder, prostate, or cervix
– Mechanical obstruction of a Foley catheter
• Urinary obstruction increases renal intraluminal pressure with resultant:
– Decreased renal blood flow
– Decreased glomerular filtration rate
– Decreased tubular function; distal tubule injury impairs sodium reabsorption with
accompanying hyperkalemic renal tubular acidosis
– Systemic hypertension via an unknown mechanism, but possibly involving renin–
angiotensin activation and volume overload
– Pain from distension of the renal capsule, collecting system, or bladder. More common
with acute complete obstruction such as ureteral calculus; slow-developing obstructions
such as tumors tend to cause less pain
– Prolonged obstruction leads to tubular atrophy and irreversible injury
Anatomic abnormalities are the most common cause of urinary obstruction in children. They
include urethral strictures and stenosis of the ureteropelvic or ureterovesical junctions.
The incidence of benign prostate hypertrophy (BPH) increases with age. Eighty percent of
men over the age of 80 years have BPH and therefore are at a higher risk for urinary
obstruction and postrenal failure
• Hydronephrosis and hydroureter without evidence of obstruction is a normal finding present
in 80% of pregnancies
• More likely to occur on the right side
• A dilated collecting system is a risk factor for pyelonephritis
• Patients at increased risk for postrenal dysfunction:
– Anticholinergic drugs (acute or chronic): Decreased detrusor contractility places patients
at increased risk postoperatively.
– Narcotics: Decreased detrusor contractility and ureteral colic.
– Benign prostatic hypertrophy: Risk is increased with intraoperative narcotics and missed
doses of chronic alpha blockade.
– Neuraxial blocks: Blocking the S2–S4 nerve roots can lead to decreased bladder
contractility. Advanced age, history of BPH, and neuraxial narcotics can further increase
this risk. A urinary catheter should always be used intra-operatively with a neuraxial
block.
– Preoperative renal impairment: The stress response to surgery can induce a decrease in
RBF and GFR, ultimately leading to ischemic damage. This can exacerbate a co-existing
postrenal disorder.
• Postrenal AKI in the intraoperative period: Usually noticed as a decrease or cessation of
urinary output in patients with a bladder catheter. Kinks, clots, or other reversible
obstructions should be ruled out prior to presumptively assuming that there is a prerenal or
intrarenal cause. It may also present as hypertension or hypervolemia.
• Postrenal AKI in the Post Anesthesia Care Unit (PACU) typically presents as an inability to
void. Tachycardia, hypertension, and abdominal pain are also common. Bladder ultrasound
scan may be considered and can avoid the placement of a catheter. A catheter should be
placed if there is evidence of bladder distension on ultrasound. Ability to void is not a
criterion for discharge at all institutions (some may use it for urologic or laparoscopic
procedures or if neuraxial anesthesia is used).
• Postrenal AKI on the floor or ICU: Presents with signs of fluid overload (tachycardia,
hypertension, or pulmonary edema in severe cases) as well as decreased or absent urine
output. Electrolyte disturbances such as hyperkalemia and metabolic acidosis can be present
as well.
• Diagnosis
– A serum BUN:Cr >15 can result from increased tubular pressure causing BUN
reabsorption. However, this is not a marker of acute change. Trends can be monitored to
track progression of renal impairment over time.
– Fractional excretion of sodium (FENa) may initially be <1% before tubular function is
compromised
– Renal ultrasound is the test of choice to diagnose urinary tract obstruction. It can assess
for hydronephrosis or hydroureter without the risk of radiocontrast. It has a 25% false
positive rate. False negatives may initially occur due to the low compliance of the
collecting system (negative for dilation) or in the setting of retroperitoneal fibrosis or
tumor surrounding the collecting system (prevents dilation).
– CT scans should be considered as a follow up to a positive ultrasound
– Intravenous pyelogram (IVP) should be considered if there is a high suspicion for calculi.
It has a low false positive rate, can identify the exact level of obstruction, and requires
contrast agent. Contrast agents should be used with caution as they can be highly
allergenic and may worsen kidney injury. Bicarbonate infusions are often co-administered
to reduce the risk of kidney injury.
• Management of postrenal AKI: The primary goal of treatment is to re-establish urine output,
especially if there is complete obstruction. Definitive treatment is a secondary goal.
– Obtain early urologic consult
– Insert a urinary catheter if one is not already in place
– Temporary treatments are typically reserved for complete obstruction, infection, AKI,
transplanted kidney, or pregnancy and are meant to quickly relieve obstruction and
prevent deterioration. They include a cystoscopy with retrograde stent placement or
percutaneous nephrostomy tubes. Both have a high success and low complication rate.
– A meta-analysis that compared retrograde stents to percutaneous nephrostomy tubes did
not show one to be superior to the other at relieving obstruction and resolving sepsis (2)
[B].
– Antibiotic therapy may be started if the urine is cloudy after the obstruction is relieved.
Typically, either a fluoroquinolone or ampicillin/gentamicin is started empirically and
titrated to culture results.
– Diuresis after the obstruction is relieved can result in a UOP as high as 500–1,000 mL/hr
(secondary to overaggressive IV fluid administration causing volume expansion and
continued high urine output). Hypovolemia and hypotension may result, requiring fluid
administration and monitoring, as appropriate.
– Definitive treatment is usually delayed for 2–3 weeks until the acute infection is treated.
– Renal recovery after correction of the obstruction is dependent on the severity and
duration of obstruction.
EQUATIONS
• Fractional excretion of sodium (FENa) = (Urine sodium / Plasma sodium) / (Urine
creatinine / Plasma creatinine)
• The RIFLE criteria provide a uniform definition for AKI created by the Acute Dialysis
Quality Initiative. It is based on the elevation of SCr and change in urine output and consists
of 3 graded levels of injury and 2 outcome measures.
– Risk = 1.5 × increase SCr, GFR decrease 25%, Uo <0.5 mL/kg for 6 hours
– Injury = 2 × increase SCr, GFR decrease 50%, Uo <0.5 mL/kg for 12 hours
– Failure = 3 × increase SCr, GFR decrease 75%, Uo <0.5 mL/kg for 24 hours or anuria for
12 hours
– Loss = complete loss kidney function requiring dialysis for >4 weeks
– ESRD = complete loss of kidney function requiring dialysis for more than 3 months
• As the RIFLE stage increases, mortality increases (3)[A].
REFERENCES
1. Licurse A. Renal Ultrasonography in the evaluation of acute kidney injury. Arch Intern
med. 2010;170(21):1900–1907.
2. Ramsey S. Evidence-based drainage of infected hydronephrosis secondary to ureteric
calculi. J Endourol. 2010;24(2):185–189.
3. Uchino S. An assessment of the RIFLE criteria for acute renal failure in hospitalized
patients. Crit Care Med. 2006;34:1913–1917.
ADDITIONAL READING
• http://www.asn-online.org/publications/ (American Society of Nephrology)
• Cystoscopy
• Postrenal acute kidney injury
• Ureteral reimplantation
• Glomerular filtration rate
CODES
ICD9
• 584.9 Acute kidney failure, unspecified
• 599.60 Urinary obstruction, unspecified
ICD10
• N13.8 Other obstructive and reflux uropathy
• N17.9 Acute kidney failure, unspecified
CLINICAL PEARLS
• Mechanical obstruction of the urinary catheter is a common cause of anuria in the PACU.
Early recognition of a kinked catheter can prevent an expensive workup and harm to the
patient.
• Renal ultrasound is a non-invasive test to evaluate for hydronephrosis. It avoids the use of
potentially nephrotoxic contrast in patients who already have AKI.
• Careful attention must be paid to a patient’s volume status after reversal of urinary
obstruction and subsequent post-obstructive diuresis.
• Dosing of renal metabolized or eliminated drugs may have to be adjusted.
• Electrolyte disturbances may be present.
– Hyponatremia: If due to water excess, UNa >20 mmol/L; if due to excessive sodium
retention, UNa <20 mmol/L.
– Hyperkalemia: May see peaked T-waves, arrhythmias. Chronic hyperkalemia is better
tolerated than acute.
POTASSIUM
Suzanne Strom, MD
BASICS
DESCRIPTION
• Potassium is necessary for the maintenance of the cellular membrane potential, intracellular
osmotic pressure, and transmission of action potentials.
• Normal plasma [K+] is 3.5–5 mEq/L; normal intracellular [K+] is 140 mEq/L. A
redistribution or shifting of K+ between the ECF and ICF compartments can result in
marked changes in their concentration without a change in total body potassium content
• Hypokalemia is defined as a plasma [K+] <3.5 mEq/L and can result in arrhythmias,
decreased cardiac contractility, myalgias, and respiratory depression.
• Hyperkalemia is defined as a plasma [K+] >5.5 mEq/L and can result in weakness and
arrhythmias that can progress to cardiac arrest.
• Intracellular K+ comprises 98% of total body stores; whereas intravascular and extracellular
compartments comprise 2%. This discrepancy is the result of maintaining the cell
membrane’s resting potential.
• The membrane resting potential is an electrochemical gradient that plays a role in transport,
signal transduction, myocardial pacemakers and contractility, and cell volume homeostasis.
– The Na+–K+ ATPase enzyme pump (embedded in the cell membrane) exchanges 3 Na+
ions extracellularly for 2 K+ ions intracellularly while consuming one ATP molecule. In
doing so, it maintains the electrochemical gradient with an intracellular [K+] of 150
mEq/L, compared to an intravascular concentration of approximately 3.5–5 mEq/L.
• Additional mechanisms: K+ concentrations between the two compartments are also affected
by pH, insulin, and catecholamines or sympathomimetics with beta-adrenergic receptor
activity.
– pH: The Na+–H+ ion exchanger allows for the cells to function as a buffer against
alkalemia or acidemia. In alkalemia, H+ ions move extracellularly to offset the
disturbance; Na+ moves intracellularly. This increase in intracellular Na+ stimulates the
Na+–K+ ATPase; thus the buffering effect results in a secondary intracellular shifting of
K+. Conversely, in acidemia, H+ ions move intracellularly in exchange for extracellular
Na+ movement; this process reduces intracellular shifting of K+ via the Na+–K+ ATPase.
– Insulin: Activates the Na+–K+ ATPase in cells.
– Beta-adrenergics: Activates adenylyl cyclase and increases cAMP levels, which, in turn,
activates protein kinase A. This results in the activation of calcium-gated K+ channels as
well as Na+–K+ ATPase with resultant intracellular shifting of potassium.
• K+ excretion: In addition to intracellular shifting, K+ levels are also regulated by the
kidneys (90%), the gastrointestinal tract, and sweat. Aldosterone, a mineralocorticoid,
lowers the plasma K+ concentration at several levels in the renal tubule.
ANATOMY
Depolarizing cells (with potassium repolarization)
• Pacemaker cells spontaneously depolarize (sodium enters the cell and makes the resting
potential positive). Depolarization serves as an electrical signal that passes to adjacent
conduction and myocardial cells in a domino-like fashion. Repolarization of pacemaker cells
is primarily via potassium efflux (Phase 3).
• Myocardial cell depolarization is coupled to mechanical contraction and blood being
“pumped.” Repolarization is mediated via potassium efflux; however, it is divided into an
early (phase 1) and late (phase 3) phase by an extended plateau.
• Nerve cells communicate and transmit their signal via electrical signaling that involves
changes in resting membrane potential. Repolarization occurs via potassium efflux.
• Acute [K+] changes are less well-tolerated than chronic changes.
• Hypokalemia is the result of either reduced total body stores, or redistribution into the
intracellular space.
– Reduced total body K+ stores may result from reduced intake or increased excretion
(renal or extra-renal).
Reduced intake: The minimum daily requirement is 40–50 mEq/day
Increased renal excretion: Type I and II renal tubular acidosis, diabetic ketoacidosis,
diuretic therapy, carbonic anhydrase inhibitors, ureterosigmoidostomy, post-
hypercapnia, increased mineralocorticoid activity (aldosterone), and hemodialysis.
Increased extra-renal excretion: Diarrhea, vomiting and nasogastric suction, increased
sweat loss, and laxative abuse.
– Intracellular shifting can occur perioperatively via alkalemia, exogenous insulin
administration, and beta-adrenergics.
Alkalemia can be metabolic and result from excessive bicarbonate administration or
hyperventilation (mechanical ventilation, pain, stimulation).
Exogenous insulin may be administered for glucose control. Hyperalimentation may
increase endogenous insulin release.
Beta-adrenergic excess may be exogenous (administration of epinephrine, dobutamine,
isoproteronol, ephedrine; nebulizer/inhaler) or endogenous (thyrotoxicosis).
• Clinical manifestations of hypokalemia result from hyperpolarization of the cell membrane.
In cardiac pacemaker cells, it also increases the duration of repolarization.
– Cardiac: Dysrhythmias (premature atrial contractions, premature ventricular contractions,
AV block, ventricular tachycardia, ventricular fibrillation), conduction defects (increased
PR and QT intervals, reduced T wave amplitude, T wave inversion or U waves, and ST
segment depression), and potentiation of digitalis toxicity.
– Skeletal muscle: Weakness, paralysis, rhabdomyolysis, fasciculations and tetany (typically
do not manifest until the serum [K+] <3 mEq/L).
– Gastrointestinal: Ileus, constipation.
– Renal: Nephrogenic diabetes insipidus, impaired urinary concentrating abilities, increased
NH3 production, and hypokalemic nephropathy.
• Hyperkalemia is the result of either increased total body stores or redistribution out of the
intracellular compartment into the serum.
– Increased total body K+ stores may result from increased intake or decreased excretion
(renal or extra-renal).
Increased intake: Transfusions, intake of sodium substitutes, potassium penicillin, or
increased absorption from a ureterojejunostomy.
Decreased renal excretion: Marked reductions in glomerular filtration, decreased
mineralocorticoid (aldosterone) activity, or a defect in potassium secretion in the distal
nephron (distal RTA).
– Extracellular shifting can occur perioperatively with succinylcholine administration,
acidemia, hemolysis, rhabdomyolysis, massive tissue trauma, hyperosmolality, digitalis
overdoses, and beta-adrenergic blockade. It can also occur with cell lysis following
chemotherapy, administration of arginine hydrochloride, and during episodes of
hyperkalemic periodic paralysis.
Succinylcholine: Plasma [K+] can increase 0.5–1 mEq/L with administration of an
intubation dose.
Acidemia: Hypoventilation results in hypercarbia and can be caused perioperatively by
respiratory depression from inhalational anesthetics, benzodiazepines, and opioids.
Cell destruction: K+ release may occur with trauma, burns, rhabdomyolysis, hemolysis,
tumor lysis, or reperfusion of an ischemic limb or organ.
Beta-adrenergic blockade: Increased potassium may be seen in patients receiving beta-
adrenergic blockade
Insulin deficiency
• Clinical manifestations of hyperkalemia result from hypopolarization of the cell membrane.
In cardiac pacemaker cells, it also decreases the duration or repolarization.
– Cardiac: Dysrhythmias leading to CV collapse. Peaked T waves (6–7 mEq/L), ST
depression, prolonged P–R interval and widened QRS (10–12 mEq/L), ventricular
fibrillation or asystole.
– Skeletal muscle: Weakness, paralysis.
– Gastrointestinal: Ileus, constipation.
– Renal: Metabolic acidosis by interfering with renal ammonium (NH4+) excretion.
• Potassium artifact might be seen with hemolysis of blood sample from venipuncture.
• Hypokalemia: [K+] values of 2.0–2.5 mEq/L are likely to cause arrhythmias and muscular
weakness; furthermore, it can potentiate the effects of neuromuscular blocking agents and
can delay recovery.
– Potassium replacement: Oral and intravenous preparations are available. Perioperative
correction often involves intravenous KCl preparations. The maximum recommended rate
of infusion via a peripheral IV is 10 mEq/hr and via a central line is 20 mEq/hr. Higher
rates of administration carry the risk of hyperkalemia or arrhythmias.
– Urgent or emergent surgery may be performed with careful EKG monitoring and
avoidance of hyperventilation, alkalosis, and beta-adrenergics. Potassium and magnesium
replacement should be concurrently performed.
• Hyperkalemia
– Urgent or emergent surgery may be performed with careful EKG monitoring and
avoidance of hypoventilation or acidosis.
– Treatment involves:
Membrane stabilization. Calcium gluconate 10% (70 kg patient): 10–30 mL IV over 10–
20 minutes.
Intracellular shift (for a 70 kg patient): Glucose 25–50 g IV (avoid hypoglycemia) with
regular insulin 10–20 units IV. Sodium bicarbonate: 50–100 mEq IV. Hyperventilation:
With each pH change of 0.1, there is an inverse change in [K+] of 0.5 mEq/L (goal:
PaCO2 = 25–30 mm Hg).
Removal: Diuretics, exchange resins (Kayexalate), dialysis.
REFERENCES
1. Katerinis I, Fumeaux Z. Hypokalemia: Diagnosis and treatment. Rev Med Suisse.
2007;3(101):579–582.
2. Parham Q, Mehdirad A, Biermann K, et al. Hyperkalemia revisited. Tex Heart Inst J.
2006;33(1):40–47.
ADDITIONAL READING
• Lin SH, Halperin ML. Hypokalemia: A practical approach to diagnosis and its genetic basis.
Curr Med Chem. 2007;14(14):1551–1565.
• QT prolongation
• Hyperkalemia
• Hypokalemia
CLINICAL PEARLS
• Disturbances with either total body or plasma K+ concentrations can cause weakness and
possibly lethal arrhythmias. Careful preoperative and intraoperative monitoring of both K+
levels and factors that affect intracellular shifting is crucial.
• Anaesthetists must determine whether to delay surgery in order to optimize plasma
potassium levels or proceed.
PREECLAMPSIA
Henry Ra, MD
BASICS
DESCRIPTION
• Preeclampsia is a pregnancy-specific, multi-organ system disease characterized by
hypertension and proteinuria beginning after 20 weeks gestation and resolving by 6–12
weeks postpartum.
• May be mild, severe, or part of a larger spectrum of diseases, including pregnancy-induced
hypertension, eclampsia, and hemolysis, elevated liver enzymes, and low platelet count
(HELLP) syndrome.
EPIDEMIOLOGY
Prevalence
5–8% of all pregnancies; rising incidence in the US.
Morbidity
• Maternal morbidity: Seizures (eclampsia), HELLP syndrome, renal disease, pulmonary
edema, hemorrhage, disseminated intravascular coagulation (DIC), cerebrovascular
accident.
• Fetal morbidity: Placental abruption, fetal growth restriction, preterm delivery.
• Increased incidence of Cesarean section in severe cases.
• Early onset preeclampsia (before 34 weeks gestation) associated with increased risk for
future cardiovascular disease.
Mortality
• Comprises ∼10–15% of maternal death worldwide.
• Third leading cause of maternal mortality in the US (behind pulmonary embolus and
hemorrhage).
• Late onset preeclampsia (after 34 weeks gestation) has lower maternal and fetal morbidity
and mortality compared to early disease.
• Maternal factors:
– Nulliparity
– Preeclampsia in previous pregnancy
– Family history of preeclampsia
– Pre-gestational diagnosis of chronic hypertension, diabetes, vascular, or renal disease
– Obesity (BMI >35)
– Presence of antiphospholipid antibodies
– African American or Filipino race
– Age >40 years
• Paternal factors: Male who previously fathered a preeclamptic pregnancy; male born from a
preeclamptic pregnancy.
Two proposed hypotheses:
• An atypical maternal immune response to embryonic trophoblasts results in impaired
invasion of trophoblastic cells into the uterine wall. This leads to maladaptation of
myometrial spiral arteries with reduced, high-resistance, utero-placental flow. The irregular
placental perfusion can cause placental hypoxia and the release of inflammatory cytokines
into the maternal circulation with consequent endothelial dysfunction.
• An imbalance of placental production of prostacyclin and thromboxane can result in
systemic vasoconstriction and placental ischemia.
• Assess the severity of disease and end-organ damage.
• Avoid hemodynamic extremes, especially when general anesthesia is attempted (intubation
and extubation).
• Gentle fluid resuscitation with caution of excess fluid administration.
• Delivery of fetus/placenta is the only cure.
SYMPTOMS
• Seizures, visual disturbances, headaches
• Pulmonary and peripheral edema
• Abdominal pain
• Nausea/vomiting
• Vaginal bleeding
• Decreased urine output
History
• Prenatal history and care, including pre-gestational diagnoses of hypertension and renal
disease.
• Fetal anomalies/intrauterine growth restriction (IUGR).
• Family history
• History of preeclampsia with previous pregnancy
• Reduced fetal movement
Signs/Physical Exam
• Hypertension
• Proteinuria
• Hypovolemia
– ∼10% fluid deficit in mild preeclampsia
– ∼35% fluid deficit in severe preeclampsia
• Pharyngolaryngeal edema
• Tachypnea, crackles at lung bases
• Right upper quadrant pain
• IUGR
MEDICATIONS
• Prevention: Aspirin may be prescribed for high-risk patients (abnormal uterine artery
Doppler at 16 weeks gestation). It is not recommended for prophylactic use in low-risk
patients.
– Hydralazine (first line): 5–10 mg IV q15 minutes
– Labetalol (first line): 20 mg IV q10 minutes up to a maximum dose of 300 mg.
– Nifedipine (second line): 10 mg PO TID titrated to effect for maximum dose of 120 mg
daily. Should be avoided in women with CAD, DM >15 years, or >45 years old.
– Continuous epidural infusion can block sympathetic nerve fibers and may assist with BP
control.
• Magnesium sulfate (first line): 4–6 g IV bolus over 15 minutes, followed by 1–2 g/hr for
seizure, prophylaxis. Therapeutic level ∼6–8 mEq/mL
• Ergot alkaloids (e.g., Methergine) should be avoided as it may cause a hypertensive crisis.
Labs/Studies
• 24-hour urine protein
• Urine protein: urine creatinine ratio
• Hgb/Hct/platelet count
• Liver enzymes to assess for HELLP syndrome
• Blood type and screen or cross-matching, as appropriate
• Fetal ultrasound
• Echocardiogram if suspicion for cardiomyopathy
• CNS: Visual disturbance, headache, eclamptic seizures, or cortical blindness may be due to
cerebral edema.
• CV: Vasoconstriction due to endothelial dysfunction and consequent hypertension.
• Respiratory: Increased risk of pulmonary edema due to lower colloid oncotic pressures and
increased capillary permeability
• Renal: Proteinuria due to increased permeability of albumin and other plasma proteins.
• Hematologic: Microconsumption coagulopathy, and/or thrombocytopenia.
• GI: Hepatic edema causing RUQ pain; rupture of Glisson’s capsule in severe disease may
lead to hepatic hemorrhage; elevated liver enzymes in HELLP syndrome.
• Appropriate BP control is necessary before induction of general anesthesia, even in emergent
cases.
• Coagulopathy may preclude the use of neuraxial anesthesia.
CLASSIFICATIONS
• Mild preeclampsia: Systolic >140 mm Hg or diastolic >90 mm Hg with proteinuria (>300
mg/24 hrs)
• Severe preeclampsia: Systolic >160 mm Hg or diastolic >110 mm Hg and/or end-organ
damage.
– Renal involvement defined as proteinuria >3 g/24 hrs, 3+ on urine dipstick, or sudden
oliguria
– CNS involvement
– Pulmonary edema
– Liver dysfunction
– RUQ/epigastric pain
– Thrombocytopenia
– HELLP syndrome
– Evidence of fetal compromise
• Eclampsia: New onset of grand mal seizures occurring during or after pregnancy that do not
have another identifiable cause.
TREATMENT
Premedications
• Avoid benzodiazepines and limit narcotics.
• Nonparticulate antacid (i.e., bicitrate)
• MgSO4 infusion for seizure prophylaxis

• Regional anesthesia and coagulopathy
• Possible need for blood transfusion
• Possible need for invasive monitoring
INTRAOPERATIVE CARE
• ACOG and ASA recommend regional anesthesia in patients without evidence of
coagulopathy.
• Early placement of epidural should be considered to avoid general anesthesia.
• Spinal anesthesia is a suitable alternative to epidural for Cesarean section even in severe
preeclampsia.
Monitors
• Consider arterial line for better hemodynamic monitoring.
• CVP and PAP monitoring is rarely necessary.
• Neuraxial techniques: Consider supplemental O2 via facemask or nasal canula for patients
with neuraxial anesthesia/analgesia.
• General endotracheal anesthesia (GETA)
– Rapid sequence induction, along with aspiration precautions.
– Difficult airway: There is an increased risk of failed intubation due to pharyngolaryngeal
edema. Be prepared for a difficult airway, including having a supraglottic device
available.
– Careful attention to BP management with induction and intubation; intracranial
hemorrhage, secondary to severe hypertension, is the leading cause of morbidity and
mortality in preeclamptic women. Consider having esmolol and nitroglycerin available.
– Hypotension with induction may lead to fetal compromise/distress.
Maintenance
• Neuraxial. In the OR, intermittent boluses with high concentration local anesthetics
(possibly without epinephrine) for surgical anesthesia/analgesia.
• GETA. Less than 0.5 MAC of volatile anesthetic supplemented by nitrous oxide after delivery
of the fetus. All inhalational agents cause uterine relaxation and can contribute to
postpartum hemorrhage.
– MgSO4 causes prolonged duration of non-depolarizing neuromuscular blockade.
• Gentle fluid resuscitation with caution to avoid fluid overload
• The patient is considered to have a full stomach.
• Avoid severe hypertension.
FOLLOW-UP
BED ACUITY
• ICU admission may be indicated if there is evidence of severe end-organ damage, including
renal failure, cerebral hemorrhage, hepatic rupture, and/or pulmonary edema.
• Routine postpartum ward may be appropriate in a patients without pulmonary edema or
hemodynamic derangements.
• Preeclampsia and all of its associated complications may present de novo after delivery.
• IV MgSO4 should continue for 24 hours postpartum.
COMPLICATIONS
• HELLP, DIC, eclampsia, pulmonary edema, cerebral hemorrhage, placental abruption.
• MgSO4
– Toxicity: Decreased deep tendon reflexes, EKG changes, respiratory depression (10–15
mEq/L), cardiac arrest (25 mEq/L)
– Fetal depression
REFERENCES
1. Turner JA. Diagnosis and management of pre-eclampsia: An update. Int J Womens Health.
2010;2:327–337.
2. Steegers EA, von Dadelszen P, Duvekot JJ, et al. Lancet. 2010;376(9741):631–644.
3. Gogarten W. Preeclampsia and anaesthesia. Curr Opin Anaesthesiol. 2009;22:347–351.
4. American Society of Anesthesiologists Task Force on Obstetric Anesthesia. Practice
Guidelines for Obstetric Anesthesia. Anesthesiology. 2007;106:843–863.
5. Visalyaputra S, Rodanant O, Somboonviboonvv W, et al. Spinal versus epidural anesthesia
for cesarean delivery in severe preeclampsia: A prospective randomized, multicenter study.
Anesth Analg. 2005;101:862–868.
ADDITIONAL READING
• American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin: Diagnosis
and management of preeclampsia and eclampsia. Obstet Gynecol. 2002;99 (1):159–167.
• Lewis G , ed. 2007. The confidential enquiry into maternal and child health (CEMACH).
Saving mothers’ lives: Reviewing maternal deaths to make motherhood safer-2003–2005.
6. The Seventh Report on Confidential Enquiries into Maternal Deaths in the United Kingdom.
London: CEMACH.
• www.preeclampsia.org
• HELLP syndrome
• Eclampsia
CODES
ICD9
• 642.40 Mild or unspecified pre-eclampsia, unspecified as to episode of care or not applicable
• 642.50 Severe pre-eclampsia, unspecified as to episode of care or not applicable
ICD10
• O14.00 Mild to moderate pre-eclampsia, unspecified trimester
• O14.10 Severe pre-eclampsia, unspecified trimester
• O14.90 Unspecified pre-eclampsia, unspecified trimester
CLINICAL PEARLS
• Preeclampsia is a relatively common, transient multi-organ system disease diagnosed after
20 weeks gestation.
• Early placement of a epidural should be considered to assist with BP control and as a
preferred alternative to general anesthesia. Rule out coagulopathy and thrombocytopenia
before neuraxial anesthesia is attempted.
• When a GETA is indicated, be prepared for a difficult tracheal intubation and have back-up
airway equipment, including supraglottic devices, if available.
PREGNANCY INDUCED HYPERTENSION
Richard C. Jensen, MD
BASICS
DESCRIPTION
• Pregnancy-induced hypertension (PIH) is a spectrum of hypertensive disorders of pregnancy
including gestational hypertension (GH), chronic hypertension, preeclampsia, and
eclampsia.
• GH is defined as systolic blood pressure (SBP) >140 mm Hg or diastolic blood pressure
(DBP) >90 mm Hg in a woman without preexisting hypertension or signs of preeclampsia.
It manifests after 20 weeks gestation and resolves by 12 weeks postpartum.
• Chronic hypertension involves either pre-pregnancy hypertension (SBP >140 mm Hg or
DBP >90 mm Hg) or failure of hypertension to resolve within 12 weeks postpartum.
• Preeclampsia is the onset of hypertension and proteinuria after 20 weeks gestation with
remission by 6–12 weeks postpartum. Eclampsia is new onset of seizures or unexplained
coma in a woman with signs and symptoms of preeclampsia.
EPIDEMIOLOGY
Prevalence
• Hypertension complicates ∼20% of pregnancies
• GH is encountered in ∼5% of pregnancies.
• Chronic hypertension is present in 1–2% of pregnancies.
• Preeclampsia–eclampsia develops in ∼5% of pregnancies in the US; nearly 20% of women
with chronic hypertension develop preeclampsia.
Morbidity
• Sustained hypertension can result in end-organ damage such as renal failure, left ventricular
hypertrophy, and/or cerebrovascular accident.
• Maternal morbidity associated with preeclampsia–eclampsia includes pulmonary edema,
disseminated intravascular coagulation, hepatic rupture, HELLP syndrome (hemolysis,
elevated liver enzymes, low platelets), and seizures.
• Fetal morbidity is due to increased incidence of placental abruption, intrauterine growth
restriction, and preterm delivery.
Mortality
• PIH is the third leading cause of maternal mortality in the US behind pulmonary embolus
and hemorrhage. It accounts for ∼10% of all deaths, with intracranial hemorrhage as the
primary cause.
• Approximately 10% of neonatal deaths occur in the presence of PIH.
• GH risk factors: History of GH in a previous pregnancy.
• Chronic hypertension risk factors
– Essential chronic hypertension: Obesity, African American ethnicity, increased salt intake,
hyperlipidemia, family history
– Secondary chronic hypertension: Oral contraceptive use, renal disease, aortic coarctation,
endocrine disorders
• Preeclampsia-eclampsia risk factors
– Maternal: Age >40 years, African American ethnicity, obesity, hypertension, diabetes,
thrombotic vascular disease (interestingly, smoking decreases the risk)
– Pregnancy-associated: Nulliparity, multiple gestations, molar pregnancy
– Fetal: Gestational age <28 weeks
– Paternal: History of fathering a preeclamptic pregnancy with another woman
• Chronic hypertension: Adrenergic hyperactivity and altered calcium homeostasis leading to
decreased peripheral vascular resistance and cardiac stimulation; increased vasoreactivity
leading to elevated systemic vascular resistance; increased renal reabsorption of salt and
water leading to increased circulating blood volume.
• The cause of preeclampsia remains unclear.
• Control hypertension (target SBP <140 mm Hg; DBP <90 mm Hg).
• Assess the severity of disease and end-organ damage.
• Evaluate for preeclampsia and implement seizure prophylaxis if severe.
• Accelerate fetal lung maturity for gestational age <36 weeks with betamethasone if preterm
delivery is anticipated.
• Regional anesthesia is preferred in the absence of coagulopathy and/or thrombocytopenia.
Neuraxial analgesia may facilitate management of hypertension and avoidance of general
endotracheal anesthesia for an emergent procedure.
• Prepare for urgent delivery if indicated. Indications for emergent delivery include non-
reassuring fetal heart tones lasting >10 minutes, placental abruption, end-organ damage,
and/or seizure.
SYMPTOMS
• Decreased fetal movement
• Preeclampsia: Shortness of breath, abdominal pain, seizures, visual disturbances, headaches
History
• Prenatal history: Nulliparity, multiple gestations, molar pregnancy
• PIH risk factors
• Fetal anomalies/intrauterine growth restriction
• Fasting status if urgent/emergent Cesarean delivery becomes necessary.
Signs/Physical Exam
• Airway: Pharyngolaryngeal edema
• Pulmonary: Pulmonary edema, hypoxemia.
• Cardiovascular: Hypertension, LV hypertrophy, and/or decreased CVP.
• Hematologic: Anemia, thrombocytopenia, and/or disseminated intravascular coagulation
(DIC).
• Renal: Decreased GFR, increased proteinuria, increased uric acid, increased urine
protein:creatinine ratio, and/or oliguria.
• Hepatic: Increased serum transaminases, hepatic edema, hepatic hematoma, periportal
hepatic necrosis, rupture of Glisson’s capsule with hepatic hemorrhage
• Neurologic: Cerebral edema, cerebral hemorrhage.
• Placental: Intrauterine growth restriction, non-reassuring fetal heart tracing, and/or
placental abruption.
MEDICATIONS
• GH or chronic hypertension: Methyldopa 250 mg PO BID, maximum dose 3g/day; Labetalol
100 mg PO BID or TID, maximum dose 1,200 mg/day; Nifedipine 30–90 mg PO/day,
maximum dose 120 mg/day.
• Preeclampsia–eclampsia. antihypertensives: Hydralazine 5–10 mg IV q15 minutes; Labetalol
20 mg IV every 10 minutes, maximum dose of 300 mg. Seizure prophylaxis: Magnesium
sulfate 4–6 g IV bolus over 15 minutes, followed by 1–2 g/hr.
• Ergot alkaloids (e.g., Methergine) should be avoided due to risk of causing hypertensive
crisis.
• Betamethasone to stimulate fetal lung maturity in the setting of preterm delivery.
Labs/Studies
• Labs: Urinalysis for proteinuria, CBC (especially platelets and Hct), CMP (magnesium),
coagulation studies, type and cross.
• Imaging studies (if indicated): Chest x-ray (pulmonary edema), head CT (useful in
identifying cerebral edema, loss of cortical sulci, and/or cerebral hemorrhage), abdominal
ultrasound, CT, or MRI (if hepatic infarction, hematoma or rupture suspected),
echocardiogram (if cardiac dysfunction is suspected).
• In cases of severe PIH prior to fetal lung maturity (24–34 weeks gestational age), consider
delaying delivery for 48 hours after the administration of systemic steroids.
• BP control is necessary prior to induction of general anesthesia, even in emergent deliveries.
CLASSIFICATIONS
• GH: Elevated BPs after 20 weeks gestation that resolves by 12 weeks postpartum.
• Chronic hypertension: Pregnancy hypertension or hypertension in pregnancy that fails to
resolve following delivery.
• Preeclampsia–eclampsia: The new onset of hypertension and proteinuria after 20 weeks
gestation.
• Chronic hypertension with superimposed preeclampsia: The development of preeclampsia in
a parturient with chronic hypertension.
TREATMENT
Premedications
• Aspiration prophylaxis in the setting of GETA (nonparticulate antacids, metoclopramide, H2
blockers)
• BP control
• Seizure prophylaxis for preeclampsia–eclampsia.
• Regional anesthesia and coagulopathy.
• Blood products in the setting of thrombocytopenia, coagulopathy, and/or hemorrhage.
• Possible need for invasive monitoring if severe, refractory hypertension and/or evidence of
end-organ damage.
INTRAOPERATIVE CARE
• Neuraxial anesthesia (spinal or epidural) preferred. Contraindications for neuraxial
anesthesia include patient refusal, elevated intracranial pressure (ICP), inability to
cooperate, evidence of coagulopathy, signs of local infection.
• General anesthesia may be necessary in emergent deliveries (fetal distress, placental
abruption, hepatic rupture, severe pulmonary edema, seizure, and/or end-organ
dysfunction).
– Associated with increased risk of aspiration, transient neonatal depression, severe
hypertension, and cerebral hemorrhage.
– Maternal mortality is 7-fold greater with GETA compared with neuraxial anesthesia.
Failed intubations are 10 times more likely in obstetric patients compared with general
population.
Monitors
• Pulse oximetry: Decrease in SpO2 in the setting of pulmonary edema, respiratory depression,
and/or pulmonary aspiration.
• BP monitoring: Consider invasive BP monitoring in the setting of refractory hypertension
(BP >180/120) or for frequent blood sampling.
• Central venous pressure: May be useful in determining volume status and for infusion of
vasodilators.
• Pulmonary arterial catheter rarely indicated but may be useful in the setting of severe
cardiac disease and/or pulmonary hypertension.
• Urinary output: Useful in evaluation of volume resuscitation and renal function.
• Fetal heart tracing
• Limit use of benzodiazepines and opioids prior to delivery; use is associated with neonatal
depression.
• General anesthesia for emergent deliveries.
– Rapid sequence intubation with cricoid pressure to minimized risk of aspiration.
– Avoid hypertensive response to laryngoscopy with deepening of anesthetic, remifentanil,
and/or esmolol.
Maintenance
General anesthesia may be maintained with a combination of volatile anesthetic and nitrous
oxide. Volatile anesthetic at <0.5 MAC minimizes a decrease in the uterine tone. IV opioids
and benzodiazepines can be given following clamping of the cord. Magnesium sulfate
prolongs duration of non-depolarizing neuromuscular blockade.
• Airway edema may necessitate reintubation.
• Severe hypertension and cerebral hemorrhage may accompany emergence and extubation.
FOLLOW-UP
BED ACUITY
• Hemodynamically stable patients may be monitored on regular postpartum wards.
• Magnesium sulfate should be continued for 24 hours postpartum in patients with
preeclampsia/eclampsia. Preeclampsia and its associated complications may present de novo
after delivery.
• ICU admission may be indicated if there is evidence of severe end-organ damage including
renal failure, cerebral hemorrhage, hepatic rupture, and/or pulmonary edema.
• Continue antihypertensive therapy until the BP normalizes.
• Follow platelets, INR/PT, hepatic enzymes, BUN/Cr until values normalize.
• In the setting of eclampsia, continue seizure prophylaxis for 24 hours following last seizure.
COMPLICATIONS
• GH and chronic hypertension: Development of preeclampsia–eclampsia, hemorrhagic stroke,
placental abruption
• Complications associated with magnesium sulfate for seizure prophylaxis: Maternal toxicity,
uterine atony, postpartum hemorrhage, fetal depression
REFERENCES
1. urner JA.Diagnosis and management of preeclampsia, an update. Int J Womens Health.
2010;2:327–337.
2. American College of Obstetricians and Gynecologists (ACOG) Practice bulletin. Diagnosis
and management of preeclampsia and eclampsia. Obstet Gynecol. 2002;99(1):159–167.
3. Practice guidelines for obstetric anesthesia: An updated report by the American Society of
Anesthesiologists Task Force on Obstetric Anesthesia. Available at:
http://www.asahq.org/publicationsAndServices/OBguide.pdf. Accessed on Jan 08, 2011.
ADDITIONAL READING
• www.preeclampsia.org
• HELLP Syndrome
• Preeclampsia
• Eclampsia
• Hypertension
CODES
ICD9
642.90 Unspecified hypertension complicating pregnancy, childbirth, or the puerperium,
unspecified as to episode of care or not applicable
ICD10
• O13.1 Gestational htn w/o significant proteinuria, first trimester
• O13.2 Gestatnl htn w/o significant proteinuria, second trimester
• O13.9 Gestational htn w/o significant proteinuria, unsp trimester
CLINICAL PEARLS
• PIH describes a spectrum of diseases: Gestational hypertension, preeclampsia, and chronic
hypertension (with or without superimposed preeclampsia).
• Preeclampsia is characterized as hypertension and proteinuria diagnosed after 20 weeks
gestation. Management involves aggressive BP control, seizure prophylaxis, and monitoring
for end-organ damage. Delivery of the fetus and placenta is the only definitive treatment
• Regional anesthesia is preferred over general anesthesia for Cesarean delivery. When GETA
is necessary, anticipate and treat BP lability and be prepared for a difficult airway.
PRELOAD
Larry C. Field, MD
Daniel M. Rusu, MD
BASICS
DESCRIPTION
• Unless otherwise specified, preload describes the volume of blood distending the left
ventricle at the end of diastole (i.e., end of the ventricular filling phase), also known as left
ventricular end-diastolic volume (LVEDV). The concept of preload can also be applied to
any chamber of the heart
• Direct assessment of cardiac preload requires measurement of the blood volume within the
reference chamber. This is generally done via echocardiography which can be performed
intraoperatively but is also possible by MRI, CT, radionuclide angiography, and cardiac
catheterization. In the perioperative period, preload is often assessed indirectly via
interpretation of static cardiac filling pressures and/or the dynamic relationship of filling
pressures on cardiac output.
• Static measures of preload: Cardiac preload is a major determinant of cardiac performance
via the Frank–Starling mechanism. The curvilinear Frank–Starling curve demonstrates the
effect of preload versus contractility (as measured by stroke volume). Until the chamber is
grossly overdistended, increasing preload [end-diastolic volume (EDV)] will increase the
intrinsic strength of the systolic contraction and increase the stroke volume.
FIGURE 1. Frank—Starling curve: http://www.ncbi.nlm.nih.gov/books/NBK2220/

FIGURE 2. Stroke volume preload dependence
• Ventricular preload (filling volume) is increased by: Increased filling pressure (increased
total blood volume, decreased venous compliance, or gravity/Trendelenburg position) or
increased myocardial compliance. Chamber compliance determines how much the EDV
increases relative to the increased pressure.
• Ventricular preload is decreased by: Hypovolemia (dehydration, hemorrhage), impaired
atrial contraction (loss of ‘atrial kick’), increased heart rate (decreased filling time),
decreased afterload (smaller residual end-systolic volume), and diastolic heart failure
(impaired relaxation/compliance).
• Although pressure measurements are commonly used as surrogate measures of preload
(EDV), it is important to note that the pressure–volume relationship is not linear and is
often dynamic.
– In the absence of significant lung disease or mitral valve disease, pulmonary artery
occlusion pressure (PAOP) approximates LVEDP; LVEDP is assumed LVEDV
– In the absence of tricuspid valve pathology, central venous pressure (CVP) or right atrial
pressure (RAP) approximates right ventricular end-diastolic pressure (RVEDP); RVEDP is
assumed RVEDV
– In the absence of significant right heart pathology, pulmonary disease, or mitral valve
disease, adequate RVEDV (as suggested by its CVP surrogate) is also assumed to translate
into adequate LVEDV (preload for the systemic circulation).
– Surrogate pressure measurements may not begin to increase from near zero (slope of
pressure–volume relationship is near zero) until ventricular volumes are above 40–50 mL.
A curvilinear increase in filling pressure per unit preload volume is then seen until
ventricular volumes near their end-diastolic capacity, where the pressure–volume slope
increases (this slope assumes a more linear relationship if the pericardium is removed).
FIGURE 3. Pressure-volume relationship of the left ventricle. http://www.cvphysiology.com
• Dynamic measures of preload: Trends indicating the change in stroke volume or blood
pressure over different preload conditions are more useful indicators of ongoing volume
responsiveness than static pressure surrogates.
– When total blood volume is low compared to vascular capacitance (relative hypovolemia
with low preload), an adequate fluid challenge (>10 mL/kg of crystalloid given in <30
min) may provide only a transient increase in blood pressure and little (<3 cm H2O)
sustained increase in CVP/PAOP
– When total blood volume is approaching vascular capacity and cardiac preload is still low,
an adequate fluid challenge should provide a sustained blood pressure increase and a
sustained (>3 cm H2O) increase in CVP/PAOP.
– When total blood volume is in excess and cardiac preload reserve has been exhausted,
ongoing fluid challenges will not further increase blood pressure/cardiac output, but
significant sustained CVP/POAP increases will still be seen.
– Passive leg raises or Trendelenburg positioning may provide the patient with a significant
enough “volume challenge” to determine volume responsiveness.
• Under the conditions of regular controlled positive pressure ventilation (>8 mL/kg tidal
volumes) and regular sinus heart rhythm, heart–lung interactions will cause cardiac preload
conditions to change throughout the respiratory cycle.
– Increased systolic pressure, pulse pressure, and stroke volume variations indicate
increased cardiac preload dependence and can predict ongoing fluid responsiveness.
Depending on the non-invasive cardiac output measuring device and variable selected, a
variation of >11–13% of stroke volume often predicts volume responsiveness (1)[A].
Respiratory variation of the pulse oximetry plethysmograph of >14% may also suggest
volume responsiveness (2)[B].
Aortic blood flow velocity variation >12% (measured by echocardiography or
esophageal Doppler) is similarly highly predictive of volume responsiveness (3)[B].
– Looking at the venous system via bedside ultrasound, an inferior vena cava (IVC)
distensibility index >12% predicts volume responsiveness (4)[B]. IVC engorgement
occurs as positive pressure ventilation inhibits blood return to the right heart.
• In spontaneously ventilating patients, IVC collapse of >50% suggests a CVP <10 and
predicts volume responsiveness.
ANATOMY
• Microscopically, preload describes the sarcomere length related to myocyte stretching.
• Macroscopically, preload is the three-dimensional volume of blood within the chamber that
is responsible for the one-dimensional sarcomere length of the stretched myocytes.
• To avoid IVC compression by the uterus, left uterine displacement (rotation of hips/torso
towards left side) is suggested when a parturient (of >24 weeks gestation) would otherwise
be positioned supine.
• Uterine compression of the IVC may impair venous return and decrease preload, resulting in
up to a 30% reduction of cardiac output.
• Volume overload. Upon gross overdistention of the chamber, microscopic myofibrils
(myosin and actin) are stretched beyond their ability to optimally overlap, decreasing their
strength/contractility and heart failure ensues (Figure 1).
• Diastolic dysfunction results in increased filling pressures as a compensatory mechanism to
maintain adequate/minimal EDV. Such compensated patients often appear more sensitive to
filling pressure/volume decreases and are relatively “preload dependent.”
• Myocardial ischemia. Filling of a cardiac chamber during diastole involves both the active
(early) relaxation by the myocytes and the passive compliance of chamber’s wall. Active
relaxation of a cardiac chamber is decreased during myocardial ischemia. Relaxation
(diastolic) abnormalities occur in the ischemic tissue before contraction (systolic)
dysfunction is seen. Impaired active relaxation (during ischemia) will result in reduced
ventricular filling during diastole, contributing to the appearance of decreased compliance
(decreased ventricular volume for same filling pressure).
• Left ventricular hypertrophy (LVH). As the ventricular wall thickens, it becomes less
compliant. LVH can develop with:
– Increased afterload: Hypertension, morbid obesity, and aortic stenosis that result in a
chronic increase in work.
– Reduced compliance: Infiltrative diseases such as amyloidosis or cardiac tumors where
there is an increase in myocardial stiffness.
• Rhythm disturbances (tachycardia, heart block, atrial fibrillation, or atrial flutter) may
impair filling by decreasing coordinated active relaxation or by simply decreasing the total
filling time.
• Tricuspid stenosis and mitral stenosis result in increased measured CVP and PAOP,
respectively, while RVEDP and LVEDP may remain normal (valvular stenosis creates a
pressure gradient and violates the assumptions required for CVP and PAOP approximate
RVEDP and LVEDP, respectively).
• External compression from pericardial effusion, positive end-expiratory pressure (PEEP),
tension pneumothorax, pleural effusions, or greatly increased abdominal pressures may
reduce passive ventricular compliance.
• Intraventricular filling defects (tumors and clots) and septal shifts causing ventricular
interdependence (severe pulmonary hypertension, high levels of PEEP, and RV infarction)
may restrict diastolic filling of cardiac chambers.
• Surrogate filling pressures (CVP and PAOP) cannot reliably discern diastolic dysfunction
from systolic dysfunction. In several studies in critically ill patients, volume assessment via
transesophageal echocardiography disagreed with static pulmonary artery catheter pressure
assessments in up to 55% of patients and significantly altered medical management in 32–
44% of those patients (5)[B].
• Volume responsiveness refers to the ability of an increase in preload (volume challenge) to
produce a clinically significant increase in stroke volume (resulting in increased blood
pressure and cardiac output).
– Ongoing volume responsiveness suggests that the LV is still on the upslope of the Frank–
Starling curve (increased LVEDP generates the expected increased ventricular
contractility).
– Lack of volume responsiveness suggests that the LV has “fallen off” the Frank–Starling
curve (meaning increased LVEDP no longer generates increased contractility).
• Many pathophysiologic processes disrupt the normal relationship between measured filling
pressures and actual preload volumes, making appropriate interpretation of filling pressures
difficult.
EQUATIONS
• SV = EDV – ESV; where SV is stroke volume, EDV is end diastolic volume, and ESV is end
systolic volume
• Ejection fraction = [(EDV – ESV)/EDV]
• Stroke volume variation (SVV) = [(SVmax − SVmin)/SVmean] where SV is proportional to the
area under the pulse contour curve
REFERENCES
1. Hofer CK, Senn A, Weibel L, et al. Assessment of stroke volume variation for prediction of
fluid responsiveness using the modified FloTrac and PiCCOplus system. Critical Care.
2008;12:R82.
2. Cannesson M, Desebbe O, Rosamel P, et al. Pleth variability index to monitor the
respiratory variations in the pulse oximeter plethysmographic waveform amplitude and
predict fluid responsiveness in the operating theatre. Br J Anaesth. 2008;101:200–206.
3. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial
pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am
J Respir Crit Care Med. 2000;162:134–138.
4. Feissel M, Michard F, Faller JP, et al. The respiratory variation in inferior vena cava
diameter as a guide to fluid therapy. Intensive Care Med. 2004;30:1834–1837.
5. Beaulieu Y. Bedside echocardiography in the assessment of the critically ill. Crit Care Med.
2007;35:S235–S249.
ADDITIONAL READING
• Bar-Yosef S, Schroeder RA, Mark JB. Hemodynamic Monitoring. In: Longnecker et al., eds.
Longnecker DE, Brown DL, Newman MF, et al. Anesthesiology. New York, NY: McGraw-Hill
Medical; 2008:519–551.
• Chappell D, Jacob M, Hofman-Keifer K, et al. A rational approach to perioperative fluid
• Left ventricular end diastolic pressure
CLINICAL PEARLS
• Echocardiographic assessment of EDV is the gold standard for preload determination. When
echocardiography is performed to optimize preload, the filling pressures required to achieve
that desired preload should be noted and maintained (although compliance may still change
over time).
• Dynamic pressure changes (both arterial and venous) in response to fluid challenges are
better guides to ongoing fluid resuscitation than static preload pressure surrogates
(CVP/PAOP).
• During positive pressure mechanical ventilation, the SVV induced by the heart–lung
interaction is a more reliable assessment of volume responsiveness than static filling
pressure.
– CVP/PAOP should always be measured during the passive exhalation phase of the
respiratory cycle to avoid artifactual changes due to active inspiratory forces (PEEP
transmitted during this exhalation will still elevate the measured filling pressures).
– Due to higher intrathoracic pressures, positive pressure ventilation (especially with higher
PEEP) impedes diastolic ventricular filling, so higher filling pressures (CVP/PAOP) are
then required to maintain the normal preload.
• Measures of preload or volume responsiveness do not necessarily indicate volume need. If a
patient is normotensive with presumed normal cardiac output as measured by the end organ
function (e.g., urine output), conservative fluid management is likely appropriate regardless
of SVV or CVP.
• Expect the need for higher filling pressures to maintain normal/adequate EDV in patients
suspected of LVH. In the absence of echocardiography, LVH may be clinically suspected in
hearts that have been working against high afterload over many years (e.g., chronic poorly
treated hypertension or morbid obesity) or when high voltage changes are seen on the
electrocardiogram.
• While low filling pressures (CVP/PAOP) are generally associated with suboptimal filling
volumes (i.e., additional volume responsiveness), high filling pressures often correlate
poorly with filling volumes (due to coexisting pathophysiology or measurement difficulties).
Confidence in the presumed pressure–volume relationships should decrease as measured
filling pressures increase (echocardiography or dynamic preload measures should be
considered for confirmation of preload status when deciding to restrict further fluids due to
high CVP/PAOP measurements).
PREMATURE ATRIAL CONTRACTIONS
Dwayne E. McClerklin, MD
BASICS
DESCRIPTION
• Premature atrial contractions (PACs) describe the initiation of a discordant atrial contraction
by an ectopic atrial pacemaker focus.
• In the perioperative period, PACs are seen
– In patients with a chronic, baseline occurrence (most common)
– In response to hypoxia, hypercarbia, or metabolic derangements (e.g., hypokalemia,
hypomagnesemia).
EPIDEMIOLOGY
Prevalence
Information not available
Prevalence
Very common and often asymptomatic; therefore, difficult to quantify with any accuracy.
Morbidity
• In isolation, PACs usually do not indicate heart disease.
• Under certain circumstances, premature atrial depolarizations may trigger re-entrant
tachycardias or atrial fibrillation. Atrial fibrillation is the most common secondary
dysrhythmia associated with premature atrial depolarizations.
Mortality
Not fatal intrinsically; however, death can occur from the secondary arrhythmia.
• Extremes of age
• Excessive caffeine consumption
• Hyperthyroidism
• Alcohol abuse
• Tobacco abuse
• Chronic lung disease
• Ischemic heart disease
• Digitalis toxicity
• Anxiety
• Pregnancy
• Perioperative causes
– Hypoxia
– Hypercarbia
– Sympathetic stimulation
– Metabolic abnormalities
Hypokalemia
Hypomagnesemia
Hypercalcemia
• Following cardioversion
• Pacemaker cells: Spontaneous (phase 4) diastolic depolarization conveys the property of
automaticity (pacemaking) that is characteristic of cells in the following:
– Sinoatrial (SA) node: Action potentials are characterized by a membrane potential of –40–
60 mV (vs. –85 mV in the ventricular myocyte), slow and spontaneous phase 4 upstroke,
and rapid phase 0 depolarization after the threshold potential is reached.
– Atrioventricular (AV) nodes
– His–Purkinje system
– Cells surrounding the coronary sinus
– Cells surrounding the pulmonary veins
• Hierarchy: The intrinsic rates of depolarization in cardiac pacemakers are greatest in atrial
pacemakers, followed by AV junctional pacemakers, followed by ventricular pacemakers.
– The sinoatrial node (SA), located at the junction of the right atrium and superior vena
cava, functions as the primary pacemaker of the heart. It displays the highest intrinsic rate
of action potential discharge at 80–100 bpm.
– Packemaker cells in the AV node may initiate an action potential if the SA node is not
functioning properly. Consequently, pacemaker cells in the ventricle may initiate an
action potential in the event that the SA and the AV node do not fire.
• P wave: The action potential generated by the SA node is transmitted rapidly through the
atria, to the AV node, and is the source of the P wave seen on the ECG.
• Autonomic nervous system: Dynamically regulates the rate of phase 4 depolarization and,
therefore, the firing rate of pacemaker cells.
• Premature atrial depolarization and contraction: A known or unknown eliciting factor
results in an ectopic atrial depolarization that occurs prior to SA node depolarization; it fires
early and out of turn, subverting the hierarchy. The premature depolarization can then, in a
domino-like fashion, depolarize adjacent cells in the atrium, travel to the AV node, and
produce a normal ventricular depolarization. Consequently, a premature mechanical
contraction will result.
• Premature atrial depolarization and abnormal accessory tracts: A circus rhythm may result
in patients with abnormal pathways that connect the atria and ventricles (normally, the AV
node is the only connection between the atria and ventricles).
– If the accessory pathway is still refractory when the premature atrial depolarization
encounters it, then the impulse will conduct normally through the AV node.
– However, if the premature atrial depolarization impulse encounters the accessory pathway
when it is out of its refractory period, it can result in a self-sustaining “circus rhythm.”
Antidromic tachycardia: When the accessory tract is excited in the atria, conduction to
the ventricles is via the accessory node. Subsequent atrial depolarization occurs from
retrograde transmission (ventricles to the atria) via the AV node. A widened QRS
complex is seen on the EKG.
Orthodromic tachycardia (more common): When the accessory tract is excited in the
ventricles, retrograde transmission (ventricles to the atria) is via the accessory tract and
subsequent atrial depolarization occurs through the AV node. A normal width QRS is
seen on the EKG.
• Maintenance of physiologic acid-base status as well as avoidance of hypoxia, hypercarbia,
electrolyte derangements, and sympathetic stimulation.
• Anxiolysis
• Treatment of underlying chronic condition
• Avoidance of alcohol use, tobacco use, and caffeine consumption.
• Intraoperatively:
– Early P wave of different sizes, shapes, or axes than the patient’s sinus P wave complex.
However, if the ectopic focus occurs near the atrial pacemaker, the P wave may appear
identical to the patient’s normal sinus P wave.
– The P–R interval varies.
Premature atrial depolarizations that originate near the AV node may feature a shortened
PR interval due to the proximity of the ectopic focus to the AV node.
A longer P–R interval may be seen if the premature atrial depolarization reaches the AV
node during the relative refractory period.
If the premature atrial depolarization reaches the AV node during the absolute refractory
period, it is not conducted. It appears as an isolated P wave.
– QRS complexes are normal and narrow; they are conducted normally via the AV node and
through the right and left bundle branches.
– Aberrant, wide QRS complexes may be seen when the premature atrial depolarization is
conducted to ventricular tissue before complete repolarization has occurred.
– Compared to premature ventricular depolarizations, premature atrial depolarizations are
not associated with a full compensatory pause.
• Awake or outpatient setting.
– Symptoms: Often asymptomatic; patients who are symptomatic endorse a “wavering”
heartbeat or a “skipped” beat.
– Holter monitoring is the most sensitive method of diagnosing PACs.
• Premature ventricular depolarizations: Lack an associated P wave complex and feature a full
compensatory pause prior to initiation of the successive depolarization.
• Sinus arrhythmia: Features normal sinus P waves and P–R intervals and 1:1 AV conduction.
Sinus arrhythmia may be associated with inspiration and expiration.
• Digitalis effect: The ECG demonstrates ST segment sloping and a regular rhythm.
TREATMENT
• Rule out hypoxia, hypercarbia, myocardial ischemia, sympathetic stimulation (pain,

awareness), and metabolic abnormalities. If present or suspected, therapy should be aimed
at the underlying cause.
• Determine hemodynamic stability.
– Stable: No treatment is required.
– Unstable: Beta-blockade and calcium channel blockers may be necessary.
• Chronic therapy: Ranolazine is a novel antianginal agent that alters the trans-cellular Na+
current and has been shown to be effective in terminating premature atrial depolarizations.
FOLLOW-UP
• For intraoperative PACs, inform the patient’s family if the PACs were associated with
hemodynamic instability or anesthetic cause.
• Hemodynamic causes: If from hypoxia, hypercarbia, hypotension, hypertension, or ischemia,
ensure that the underlying cause has been treated and resolved.
• If the intraoperative PACs were secondary to an anesthetic cause, careful examination of the
intraoperative anesthetic record may provide information regarding the potential triggering
agents or conditions. Documentation of the findings is warranted to prevent recurrence or
replication of the onset of PACs.
• Consider a telemetry bed, particularly if associated with hemodynamic instability.
REFERENCES
1. Perez MV, Dewey FE, et al. Electrocardiographic predictors of atrial fibrillation. Am Heart
J. 2009;158:622–628.
2. Sosalla S, Wagner S, et al. Altered Na+ currents in atrial fibrillation: Effects of ranolazine
on arrhythmias and contractility in human atrial myocardium. J Am Coll Cardiol.
2010;55:2330–2342.
3. Narayan SM, Kazi D, et al. Repolarization and activation restitution near human pulmonary
veins and atrial fibrillation initiation: Mechanisms separating persistent from paroxysmal
atrial fibrillation. J Am Coll Cardiol. 2008;52: 1222–1230.
4. Stein PK, Barzilay JI, et al. Heart rate variability and its changes over 5 years in older
adults. Age Ageing. 2009;38:212–218.
5. Folkeringa RJ, Hartgers J, et al. Atrial extrasystoles after exercise predict atrial fibrillation
in patients with left ventricular hypertrophy. Heart. 2006;92:545–546.
• Premature ventricular contractions
• Pacemaker cells of the heart
CODES
ICD9
427.61 Supraventricular premature beats
ICD10
I49.1 Atrial premature depolarization
CLINICAL PEARLS
• Premature atrial depolarizations are commonly benign dysrhythmias. They can, however,
trigger a circus rhythm via an accessory tract or atrial fibrillation (rare).
• Intervention is warranted only if there is an associated compromise in hemodynamic
stability.
• Beta blockers and calcium channel blockers are the most commonly used agents to
terminate PACs in the event of hemodynamic compromise.
PREMATURE VENTRICULAR CONTRACTIONS
J. Aaron Williams, MD
BASICS
DESCRIPTION
• Premature ventricular contractions (PVCs) describe a discordant ventricular contraction that
is caused by an ectopic ventricular pacemaker focus. PVCs are also referred to as ventricular
premature beats (VPBs) and ventricular extrasystoles.
• Although PVCs can be a common, non-pathologic occurrence, the new onset or an increased
frequency in the perioperative period should alert the anaesthetist to the possibility of
ominous underlying pathology:
– Hypoxia
– Hypercarbia
– Acidosis
– Myocardial ischemia
EPIDEMIOLOGY
Prevalence
• True incidence is hard to ascertain secondary to most being asymptomatic at onset and over
time.
• Increases primarily with age.
• Predilection toward males, and African Americans (vs. Caucasians).
Prevalence
• Numbers vary greatly with the length of the monitoring period; longer periods result in a
much higher detection rate (e.g., single EKG versus 2 minute EKG versus 24-hour Holter
monitoring).
• PVCs are detected in at least 50% of young men and women (on 24-hour Holter monitoring)
(1,2).
• Elderly patients in one study had a nearly 30% incidence of >30 PVCs/hr (Lown
classification 2) (3).
Morbidity
• Palpitations causing distress, or uncommonly, pre-syncopal or syncopal episodes.
• Related to underlying condition.
• Bigeminy, over time, can lead to cardiomyopathy irrespective of other disease processes (4).
Mortality
• Related to the underlying condition or progression to more malignant arrhythmias.
• Increased mortality has been associated with:
– Increased frequency/number
– Multiform waves
– Runs of PVCs (couplets, NSVT)
– Complex arrhythmias during exercise, and particularly after exercise (5).
• Perioperative
– Normal variant
– Hypoxemia
– Hypercarbia/acidosis
– Myocardial ischemia/infarction
– Pulmonary embolism
– Electrolyte imbalance: Hypokalemia, hypomagnesemia, and hypercalcemia (can result
from intraoperative furosemide, mannitol, and IV contrast dye)
– Any high-catecholamine state
– Medications: Epinephrine, norepinephrine, dopamine, digoxin, tricyclic antidepressants,
aminophylline, other anti-arrhythmic agents (flecainide, etc.)
– Bradycardia
– Anxiety
– Localized irritation/mechanical factors: Central venous line introducer wire or catheter,
pulmonary artery catheter, surgical tools or hands in the operative field (particularly in
open heart surgery as well as in thoracic surgery, Nuss procedures, etc.)
• Chronic conditions: Hypertension, left ventricular hypertrophy, prior myocardial infarction,
cardiomyopathy, and valvular heart disease
• Provocative events: Exercise, smoking/nicotine exposure, caffeine and chocolate ingestion
• Three mechanisms in general:
– Enhanced automaticity: Electrolyte disturbances and elevated-catecholamine states can
affect the membrane resting potential/automaticity of ventricular pacemakers
– Triggered activation: Ischemia, digoxin
– Re-entrant phenomenon: Ischemic pathways or old infarcts can delay normal impulse
conduction and cause delayed firing that is “off-cycle” or “out-of-sync.”
• May originate from one focus or multiple foci within one or both ventricles (i.e., outside the
SA–AV-nodal or His–Purkinje systems)
• Hemodynamic concerns:
– Can cause hemodynamic instability; the lack of an atrial kick during ventricular diastole
can decrease the stroke volume and cardiac output (particularly with bigeminy or
frequent PVCs).
– Although commonly benign in nature, may signify a more sinister underlying disorder.
– May progress to malignant dysrhythmias in certain conditions (6).
• In the operating room, avoid hypoxemia, hypercarbia/acidosis, hypotension or tachycardia
(myocardial ischemia), and other above-mentioned causes.
– Chronic beta-blocker therapy may be appropriate in certain settings (i.e., symptomatic,
post-MI arrhythmias, etc.) (7).
• Outpatient setting: Avoid caffeine, nicotine, alcohol, and chocolate, as well as herbals and
diet pills containing stimulants (pseudoephedrine, etc.).
Intraoperatively
• Primarily an EKG diagnosis: Level 1A (7)
– Premature ventricular depolarization
– No P wave (as seen with a premature atrial depolarization/contraction)
– Irregular, wide-complex QRS
– Compensatory pause takes place prior to the next normal beat.
– R–R interval of surrounding beats is usually constant
– If multifocal, it will show various QRS morphologies.
• Pulse oximeter or arterial line waveform can be observed to rule out electrical artifact,
patient movement, or movement around the patient. If it is “real” one would see an
irregularly placed pulsation/beat with a smaller waveform (amplitude).
• Initial diagnostic tests
– 12-lead EKG would be helpful if new-onset ischemia is suspected
– Arterial blood gas to check for acidosis, hypoxia, hypercarbia
– Electrolyte studies
– Initial cardiac enzymes if ischemia is suspected
• Other diagnostic tests:
– CXR if a central venous line or retained wire is suspected
– Digoxin level (if applicable)
– Urine drug screen
– Echocardiogram
Awake or outpatient setting:
• History
– Many are asymptomatic
– Can be associated with palpitations (from the augmented beat after the PVC) or a “pause”
in the heartbeat from non-sustained ventricular tachycardia (NSVT) or ventricular
tachycardia (VT)
– Previous presyncopal or syncopal episodes from bigeminy or progression to NSVT/VT
– Presence on the preoperative EKG; however, it is more likely to be detected on
intraoperative EKG (longer duration of monitoring than preoperative 10-second EKG)
• Diagnostic tests
– 24-hour Holter monitoring: Level 1A (7)
– Cardiac stress testing
– Coronary angiography
– Electrophysiologic testing
• Lown classification system: (8)
– 0 = No PVCs
– I = <30 PVCs/hr
– II = ≥30 PVCs/hr
– III = Multiform PVCs
– IVa = Couplets (normal beat followed by two PVCs sequentially)
– IVb = Ventricular tachycardia (≥3 PVCs sequentially)
• EKG artifact from motion (patient or other people touching the patient)
• EKG artifact from electrocautery or ESWL
• Premature atrial contractions
• Sinus pauses
• Second-degree type I or II heart block
• Third-degree heart block
TREATMENT
• Management involves concurrent correction or treatment of the underlying cause as well as

ensuring hemodynamic stability.
– Stable: If new-onset, investigate for ominous causes. If absent, remain vigilant to possibly
detect any secondary causes.
– Unstable: Consider stopping the surgical interventions (pneumoperitoneum, pericardial
manipulation, etc.), and/or finishing/canceling the case. Consider implementing the
BLS/ACLS algorithms (i.e., defibrillation for pulseless VT, etc.).
• Treat secondary causes as appropriate:
– Electrolyte replacement
– Ventilator changes for respiratory acidosis
– Central venous line manipulation if it is in too deep.
– Optimizing myocardial oxygen supply and demand if acute coronary syndrome or
ischemia may be present.
• Symptomatic treatment: Suppression of PVCs in the perioperative period with lidocaine or
metoprolol may aid with hemodynamic stability. However, there are no studies on this
particular scenario and, thus, it should not delay the above-mentioned therapies.
FOLLOW-UP
• If a history of pre-syncope or syncope is uncovered preoperatively, one may consider

cardiology evaluation prior to elective procedures.
• If new onset occurs intraoperatively, a cardiology consult, telemetry monitoring, and/or
further diagnostic tests may be warranted depending on the history and situation.
• Patients with malignant arrhythmias or frequent PVCs may benefit from ablation therapy
(7).
REFERENCES
1. Brodsky M, Wu D, Denes P, et al. Arrhythmias documented by 24-hour continuous
electrocardiographic monitoring in 50 male medical students without apparent heart
disease. Am J Cardiol. 1977;39:390–395.
2. Sobotka PA, Mayer JH, Bauernfeind RA, et al. Arrhythmias documented by 24-hour
continuous ambulatory electrocardiographic monitoring in young women without apparent
heart disease. Am Heart J. 1981;101:753–759.
3. Glaser SP, Clark PJ, Appelbaum HJ. Occurrence of frequent complex arrhythmias detected
by ambulatory monitoring. Chest. 1979;75:565–568.
4. Chugh SS, Shen WK, Luria DM, et al. First evidence of premature ventricular complex-
induced cardiomyopathy: A potentially reversible cause of heart failure. J Cardiovasc
Electrophysiol. 2000;11(3):328–329.
5. Dewey FE, Kapoor JR, Williams RS, et al. Ventricular arrhythmias during clinical testing
and prognosis. Arch Intern Med. 2008;168:225–234.
6. Dalal D, Nasir K, Bomma C, et al. Arrhythmogenic right ventricular dysplasia: A United
States experience. Circulation. 2005;112:3823–3832.
7. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of
patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report
of the American College of Cardiology/American Heart Association Task Force and the
European Society of Cardiology Committee for Practice Guidelines. Circulation.
2006;114:e385–e484.
8. Lown B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation.
1971;44:130–142.
• Intraoperative hypoxia
CODES
ICD9
427.69 Other premature beats
ICD10
I49.3 Ventricular premature depolarization
CLINICAL PEARLS
• PVCs can represent a varied clinical picture from benign to suggestive of severe pathology.
• Uncommonly, they may progress to more malignant arrhythmias.
• Treatment revolves around identifying and treating the underlying disease process.
• Uncommonly, direct treatment of PVCs is indicated (beta-blockers, ablation).
PRERENAL ACUTE KIDNEY INJURY
BASICS
DESCRIPTION
• Acute renal failure (ARF), also known as acute kidney injury (AKI), is characterized by a
rapid decline in the glomerular filtration rate (GFR), accompanied by azotemia with, or
without, oliguria.
• Prerenal AKI describes the loss of kidney function secondary to the flow of blood before it
reaches the kidneys; it is also termed prerenal azotemia. This differs from renal AKI that
affects the kidney itself and postrenal AKI where the movement of urine out of the kidneys
is impaired. Prerenal AKI is the most common cause of ARF and can result from:
– Decreased blood volume
– Low blood flow states
– Interrupted blood flow to the kidneys
• Early recognition and treatment of underlying causes is critical, as prerenal AKI is usually
reversible
EPIDEMIOLOGY
Prevalence
• Varies widely across studies and patient population.
• All cause AKI may be seen in ∼5–8% of hospitalized patients and ∼50% of ICU patients.
• Prerenal causes are estimated to comprise ∼75% of AKI cases.
Morbidity
AKI (all cause) can result in:
• Fluid overload
• Electrolyte imbalance
• pH abnormalities
• Impaired metabolism/clearance of drugs
• Impaired excretion of waste products (uremia)
Mortality
Although most patients who develop prerenal AKI have complete recovery of their kidney
function, they have a greater than two-fold increase in in-hospital mortality.
• Causes of prerenal AKI can be classified as:
– Low volume states: Hypovolemia (burns, edema, diarrhea, vomiting, hemorrhage,
dehydration)
– Low perfusion states: Hypotension, shock (cardiac, septic, anaphylactic), cirrhosis, drugs
(ACE inhibitors, NSAIDs) that decrease glomerular capillary perfusion
– Interrupted blood flow to the kidneys: Renal artery stenosis or embolus, trauma to the
kidney, aortic cross clamping
• There is an increased risk for prerenal AKI in:
– Critically ill patients
– Patients who are exposed to nephrotoxic agents (intravenous contrast, aminoglycosides,
NSAIDs, etc.)
– Patients with pre-existing renal disease
• Determinants of renal blood flow (RBF):
– Cardiac output: The kidney receives ∼20% of the cardiac output; this is equivalent to 1
L/min in a 70 kg adult. The kidneys not only have a high metabolic requirement, but they
also function as a filtering and homeostatic organ.
– Renal perfusion pressure is dependent on the mean arterial pressure (MAP) in the renal
artery and vascular resistance of the renal arterioles, primarily the afferent and efferent
arterioles.
– Autoregulation (intrinsic mechanism) of the RBF and GFR blunt the otherwise deleterious
effects of variable blood pressure; it does not entirely negate the changes. Within MAPs of
80–180 mm Hg, RBF and GFR are relatively constant. Autoregulation occurs via two
mechanisms: A myogenic response of vascular smooth muscle (fast response to stretch)
and tubuloglomerular feedback (vasoconstrictive transmitters released by salt-sensing cells
within the macula densa).
– Extrinsic factors (humoral and nervous system): Bidirectional regulatory influences occur
between the vasoconstrictor and vasodilatory hormonal systems.
Renin–angiotensin–aldosterone feedback mechanism
Antidiuretic hormone (ADH)
Sympathetic system/adrenergic activity
It appears that adrenergic activity and angiotensin II are the dominant influences that
independently and synergistically impact the determinants of glomerular filtration.
Interactions between the two are complex and significant.
• Reduced renal perfusion stimulates intrinsic and extrinsic regulatory mechanisms in an
attempt to compensate and maintain the GFR.
• Early stages:
– Renal parenchyma usually remains intact and functional
– Lab tests demonstrate sodium reabsorption and urine concentration; FENa <1%
• Sustained decreases in blood flow:
– The time to, and level of, decrease varies widely amongst patients
– Typically, a complete lack of blood flow for 30–60 minutes can result in permanent,
irreversible cell damage; results in a secondary intrarenal AKI (acute tubular necrosis)
• Severe hypoperfusion results in selective vasoconstriction of the renal and splanchnic beds
in order to preserve perfusion to the brain and heart.
• The cornerstone of treatment is prevention, prevention, and prevention. Goal-directed
therapy that optimizes preload, afterload, and contractility with fluids,
vasopressors/inotropes, and blood transfusions may decrease the development of AKI.
• Low blood volume requires volume resuscitation.
– Carefully monitor insensible and blood losses, as well as urine output in the perioperative
period so that interventions can be made early and preemptively.
– Volume status assessment is a clinical judgment that is based upon vital signs (heart rate,
blood pressure), monitors (urine output, arterial line variation, central venous pressures,
pulmonary artery catheter measurements, echocardiogram), and physical examination
(mucus membranes, capillary refill).
– Replacement may be with isotonic crystalloid or colloid solutions and possibly blood.
Controversy surrounds the best modality and outcome studies.
– Excessive fluid resuscitation may lead to abdominal compartment syndrome and impaired
renal perfusion.
– Normal saline given in volumes greater than 30 mL/kg can cause a non-gap
hyperchloremic metabolic acidosis and hyperkalemia. Hyperchloremia may decrease RBF,
GFR, and urine output.
• Low blood flow states require interventions to restore renal perfusion.
– Treatment or optimization of the underlying etiology is key.
– Autoregulation maintains a constant RBF between MAPs of 80–160 mm Hg; however, this
curve may be shifted to the right in chronic hypertensives and thus require higher
pressures.
– Consider the use of inotropic medications and vasoconstrictors, as appropriate, to facilitate
forward flow and perfusion.
• Renal protection: The use of pharmacologic agents such as dopamine, fenoldopam, statins,
and bicarbonate are aimed at decreasing potential intraoperative pathology. However, these
agents have not consistently been shown to prevent or decrease AKI.
• Avoid potential renal insults: Nephrotoxic agents such as iodinated contrast agents, NSAIDS,
ACE inhibitors, and aminoglycoside antibiotics.
• The RIFLE/AKIN classification has standardized the definition of renal failure.
• Prerenal disease is distinguished by:
– Urinalysis that is usually normal; positive ketones may be present
– BUN/Cr ratio of >20:1; the decrease in flow to the kidneys results in more time for BUN
to be reabsorbed.
– Urine sodium <20 mEq/L
– FENa <1%
– Urine osmolality > 500 mOsm/kg
• Note that the laboratory values in isolated prerenal AKI reflect “normal” renal function that
attempts to conserve sodium and concentrate urine
Although causes of AKI are differentiated into prerenal, intrarenal, and postrenal, AKI with
resultant acute tubular necrosis is commonly the consequence of multiple insults.
TREATMENT
• Based upon treating the underlying cause.

• Consider invasive monitoring with arterial line and central venous pressure or pulmonary
artery catheter in order to provide goal-directed therapy.
– Volume repletion with crystalloid, colloid, or blood. Caution should be exercised to avoid
over-hydration with resultant tissue edema.
– Improve cardiac function/output
– Support renal perfusion pressure
• In patients that develop intrarenal failure
– Renal replacement therapy (RRT)
– Dopamine and loop diuretics have not been shown to improve recovery, decrease the need
for RRT, or improve survival.
FOLLOW-UP
• Kidney function should return to normal within 24–72 hours
REFERENCES
1. houdhury D.Acute kidney injury: Current perspective. Postgrad Med. 2010;122:29–40.
2. Bagshaw SM, Bellomo R. Acute kidney injury in critical illness. Can J Anesth.
2010;57:985–998.
3. Liano F, Pascual J. Epidemiology of acute renal failure: A prospective, multicenter,
community-based study. Kidney Int. 1996;50: 811–818.
4. Blantz RC, Singh P. Analysis of the prerenal contributions to acute kidney injury. Contrib
Nephrol. 2011;174:4–11.
5. Kramer HJ, Horacek V, Backer A, et al. Relative roles of nitric oxide, prostanoids and
angiotensin II in the regulation of canine glomerular hemodynamics. A micropuncture
study. Kidney Blood Press Res. 2004;27(1):10–7.
• Intrarenal disease
• Postrenal disease
• Renal blood flow
CODES
ICD9
584.9 Acute kidney failure, unspecified
ICD10
N17.8 Other acute kidney failure
CLINICAL PEARLS
• Prerenal azotemia (and postrenal AKI) “spare” damage to the kidney tissue compared to
intrarenal causes. Laboratory values of prerenal disease, thus, reflect the kidney’s
(maintained) ability to conserve sodium and concentrate urine.
• Severe azotemia can lead to decreased protein binding and increased effect for some
anesthetic agents.
PRESSURE–VOLUME LOOPS
Emily K.B. Gordon, MD
BASICS
DESCRIPTION
• Ventricular pressure–volume loops depict the relationship between pressure and volume in
the left ventricle (LV). They aid with assessment of preload, contractility, and afterload as
well as other physiologic parameters.
• Commonly used techniques to acquire this data include left heart catheterization (direct
measurements) and pulmonary artery catheters (extrapolation).
• The pressure–volume relationship delineates a single cardiac cycle. This is comprised of four
basic phases:
– Phase a (Points 4–1): Ventricular filling: Begins with the mitral valve open and blood from
the left atrium passively enters the ventricle. This is followed by the atrial kick and ends
with mitral valve closure.
– Phase b (Points 1–2): Isovolumetric contraction: Begins with the mitral and aortic valve
closed and contraction without ejection of blood. It ends with aortic valve opening.
– Phase c (Points 2–3): Ejection: Begins with the aortic valve open and blood being
propelled into the systemic circulation. It ends with aortic valve closure. Note that
electromechanical diastole begins during ejection of blood from the aorta; the ventricle
begins to relax and the aortic valve does not close until the LV pressure drops below aortic
pressure.
– Phase d (Points 3–4): Isovolumetric relaxation: Begins with the mitral and aortic valve
closed and relaxation of the ventricle without a change in volume. It ends with mitral
valve opening.
• Preload is depicted by the end diastolic volume (EDV; Point 1).
• Afterload is represented by the pressure at the end of isovolumetric contraction (Point 2).
• Inotropy can be assessed by the end-systolic pressure–volume relationship (ESPVR). The
ESPVR curve becomes steeper and shifts to the left as inotropy (contractility) increases.
• Stroke volume is represented by the difference between the EDV and end-systolic volume
(ESV).
• Left ventricular compliance is depicted by the reciprocal of the slope seen at end-diastole
(Point 1); this is called the end-diastolic pressure–volume relationship (EDPVR).
• Stroke work (SW) describes the work performed by the ventricle to eject the stroke volume
into the aorta. It can be assessed by the area within the pressure–volume loop or pressure–
volume area (PVA) (Points 1–4). This combines the external stroke work (SW) with the
potential energy (PE) remaining at the end of systole. Myocardial oxygen consumption can
be estimated by the PVA (recall that the primary determinants of VO2 are preload,
afterload, and contractility).
ANATOMY
• The ventricle is best described as an ellipsoid shape and its volume is best described by the
geometric formula V = 4/3πr3, where r is the radius.
• Systolic dysfunction signifies a loss of inotropy.
– End-diastolic volume (preload): Increase
– ESV: Increase
– Stroke volume: Decrease
– Inotropy: Decrease; ESPVR slope decreases and shifts rightwards
– Compliance: A dilated ventricle will exhibit an increase; EDPVR slope will decrease and
shift rightward
– Afterload: For any given afterload, there is a decreased velocity of fiber shortening
– Stroke work: Decreased
– Tension: Increase
• Diastolic dysfunction signifies a decrease in ventricular filling secondary to hypertrophy or
impaired relaxation (decreased lusitropy).
– End-diastolic volume (preload): Decrease
– ESV: Decrease or no change
– Inotropy: No change or increases
– Compliance: Decrease; EDPVR slope will increase
– Afterload: Increases when secondary to hypertrophy
– Stroke work: Decreased secondary to a decrease in stroke volume
– Tension: Decrease
• Aortic stenosis (AS): The narrowing of the LVOT requires the LV to generate a much higher
pressure in order to create an adequate stroke volume per each ventricular contraction. The
amount of pressure that the LV must generate to create an adequate stroke volume is
dependent on the degree of stenosis and the flow rate across the valve. Chronically, the total
coronary flow increases in proportion to the increased LV wall stress and mass, but
eventually, adequate subendocardial flow becomes difficult to attain leading to ischemia.
– End-diastolic volume (preload): Increases acutely
– ESV: Increase (to a greater extent than EDV)
– Inotropy: Increases; slope of ESPVR increases and shifts leftward
– Compliance: Decreases; slope of EDPVR increases secondary to the left ventricular

hypertrophy that is typically associated with AS
– Afterload: Increase
– Stroke work: Decrease
– Tension: Increase
• Mitral stenosis (MS) is marked by the pathologic obstruction of flow from the left atrium to
the LV. This obstruction results in elevated LA pressure and pulmonary pressures. There is a
decrease in stroke volume secondary to a decrease in end-diastolic volume (preload). This
decrease in preload leads to a decrease in cardiac output (CO) and aortic pressure,
particularly aortic diastolic pressure.
– End-diastolic volume (preload): Decrease
– ESV: Decrease or no change
– Inotropy: No change
– Compliance: No change
– Afterload: No change
– Stroke work: Decrease
• Aortic regurgitation (AR), also known as aortic insufficiency (AI), is caused by the aortic
valve not closing at the end of systolic ejection which allows blood to flow back from the
aorta to the LV during the diastolic relaxation. As a result, there is no true LV isovolumic
relaxation because blood is flowing back into the LV before the mitral valve even opens.
– End-diastolic volume (preload): Increase
– ESV: Initially, mild increase or no change; with failure, significant increase
– Stroke volume: Initially, increase in stroke volume; if the ventricle goes into systolic
failure, there is a decrease
– Inotropy: Mild decrease or no change; does not change significantly in the chronic state
– Compliance: Increase; slope of EDPVR decreases and shifts rightward
• Mitral regurgitation (MR) results in blood from the LV entering the left atrium during
ventricular systole. This results in an increase in the LA’s volume and pressure during
ventricular systole. There is no true isovolumetric contraction phase because as soon as the
LV pressure exceeds LA pressure, blood flows backwards across the mitral valve and into the
atrium. Additionally, there is no true isovolumetric relaxation because as the aortic valve
closes and the ventricle relaxes, the MV remains open and blood flows back into the LA.
This leads to an even smaller ventricular volume.
– End-diastolic (preload): Increase
– ESV: Small decrease or no change
– Stroke volume: “Increase;” this is because the loop accounts for both the blood ejected
forward into the aorta as well as the blood ejected back into the left atrium
– Inotropy: No change or mild decrease
– Compliance: Increases; the slope of EDPVR decreases and shifts rightward
– Afterload: Decrease
– Stroke work: Increase
– Tension: Decrease
• Aortic stenosis
– Prevent hypotension
– Prevent events that decrease CO
– Maintain normal sinus rhythm
– Avoid tachycardia and bradycardia
• Mitral stenosis
– Maintain heart rate slightly lower to allow sufficient time in diastole and flow across the
MV
– Avoid atrial fibrillation in order to maintain the atrial kick
– Carefully titrate fluid administration in order to avoid volume overload
• Aortic regurgitation
– Maintain HR >80 beats/min to avoid increased diastolic time and therefore LV overload
– Avoid an increase in systemic vascular resistance (SVR)
– Treat acute overload with vasodilators
– Prevent events that would decrease CO
– Maintain normal to fast heart rate
– Afterload reduction
– Maintain adequate preload
EQUATIONS
• T = (ΔP × R)/2 h; where T is tension, ΔP is change in pressure, R is radius, and h is wall
thickness.
• EF = [EDV − ESV]/EDV = SV/EDV
• Cardiac work = (stroke work) × (heart rate)
REFERENCES
1. Fonseca J, Andrade A, Nicolosi DE, et al. Cardiovascular simulator improvement: Pressure
versus volume loop assessment. Artif Organs. 2011;35(5):454–458.
2. Andrews DT, Royse AG, Royse CF. Functional comparison of anaesthetic agents during
myocardial ischaemia-reperfusion using pressure–volume loops. Br J Anaesth.
2009;103(5):654–664.
3. Sasayama S, Nonogi H, Sakurai T, et al. Assessment of cardiac function by left heart
catheterization: An analysis of left ventricular pressure–volume (length) loops. J Cardiogr
Suppl. 1984;(1):25–34.
4. Katz AM. Influence of altered inotropy and lusitropy on ventricular pressure–volume loops.
J Am Coll Cardiol. 1988;11(2):438–445.
5. eremias A, Brown DL. Cardiac Intensive Care, 2nd edition. Philadelphia, PA: Elsevier; 2010
• Contractility
• Preload
• Afterload
• Ejection fraction
• Lusitropy
CLINICAL PEARLS
• Preload can be increased by giving intravenous fluids.
• Stroke volume can be increased by instituting inotropic therapy and optimizing preload and
afterload.
• Afterload can be reduced with the use of vasodilators (i.e., calcium channel blockers,
nitroglycerin, etc.).
PRETERM INFANT
John T. Chalabi, MD
Samuel H. Wald, MD
BASICS
DESCRIPTION
The premature infant is defined as being born before 37 weeks of gestation.
EPIDEMIOLOGY
Prevalence
• Comprises 12.3% of all births in the US annually (1)
• The highest rates are seen in non-Hispanic Americans and African Americans; and the lowest
are seen in Asians or Pacific Islanders.
Prevalence
Greater than 500,000 births
Morbidity
• CNS: Intraventricular hemorrhage (IVH), retinopathy of prematurity (ROP)
• Cardiac: Patent ductus arteriosus (PDA)
• Pulmonary: Respiratory distress syndrome (RDS), meconium aspiration syndrome,
bronchopulmonary dysplasia (BPD), apnea of prematurity (AOP), persistent pulmonary
hypertension
• GI: Necrotizing enterocolitis (NEC), gastroesophageal reflux disease (GERD),
jaundice/hyperbilirubinemia
• Infectious: Bacterial sepsis
• Metabolic: Hypoglycemia, hypocalcemia
Mortality
Although two-thirds of infant deaths in the US occur among infants born prematurely, only
17% of infant deaths are classified as being attributable to premature birth.
• Birth defects
• Maternal risk factors
– History of premature birth
– Twins, triplets, or other multiple pregnancy
– Uterine or cervical abnormalities
– Poor prenatal care
– Smoking
– Alcohol consumption
– Substance abuse
– Select medication exposure
– Physical, sexual, or emotional abuse
– Infection
– Hypertension and preeclampsia
– Diabetes
– Obesity or malnutrition
– Short time period between pregnancies
– In vitro fertilization
– Vaginal bleeding
– Non-Hispanic, African-American race
– Extremes of maternal age (<17, >35)
– Low socioeconomic status
• Nervous system
– IVH has a 20–30% incidence in infants born <31 weeks and weighing <1,500 g at birth.
– ROP has a higher incidence in lower post-conceptual age infants. Hyperoxia causes
abnormal neovascularization. However, because normal photoreceptor development
requires high levels of oxygen, the underdeveloped retinal vasculature cannot meet the
oxygen demands and hypoxia-inducible factor and vascular endothelial growth factor are
consequently released. These factors result in “neovascularization" with abnormal
proliferation from the retina to the vitreous. Neovascularization can cause fluid leak,
hemorrhage, and retinal scar formation with traction of the retina. In severe case it can
cause retinal detachment.
– Cognitive impairment is more likely.
• Cardiovascular
– A less compliant ventricle is more dependent on heart rate for cardiac output.
– Decreased sensitivity to catecholamines.
– Small absolute blood volume.
– Underdeveloped baroreflex.
– Higher incidence of PDA.
• Respiratory
– Low levels of surfactant cause RDS, ventilation/perfusion mismatch, and hypoxia.
– Small airways are prone to obstruction (subglottic stenosis, laryngotracheomalacia).
– There is an increased susceptibility to oxygen toxicity and barotrauma resulting in BPD
from prolonged intubation.
– Apnea of prematurity (AOP) reflects immaturity of the respiratory control system that
manifests as an unstable respiratory rhythm. The neonatal neurotransmission pathway is
underdeveloped and both central and peripheral chemoreceptors are impaired. The
preterm neonate displays a reduced ventilatory response to hypercapnia; a biphasic
response to hypoxia (initial increase in ventilation for 1 minute, followed by a phase of
decreased ventilation; severely preterm infants typically do not display a period of
hyperventilation); and an enhanced inhibitory response by upper and lower airway
afferent innervation secondary to stimulation (i.e. negative pressure and positive airflow).
– Persistent pulmonary hypertension from persistent right-to-left shunt through a foramen
ovale, PDA, or both.
• Immune system: Increased susceptibility to infection is related to the immaturity of both
cellular and hormonal aspects.
• Renal function is dependent upon the post-conceptual age: A 28–30 week post-conceptual
age infant has a GFR that is almost half that of a term infant. The initial creatinine value
reflects the maternal creatinine and should decrease within 3–4 weeks.
• Gastrointestinal: Preterm infants frequently have an immature gag reflex and are unable to
coordinate sucking, swallowing, and breathing until 34–36 weeks post-conceptual age; this
makes feeding difficult.
• Metabolic
– Temperature dysregulation can result from a lack of brown fat, high body surface area to
body mass ratio, lack of adequate insulation, and high evaporation rate.
– There is an increased risk of developing hypoglycemia due to immature hepatic
glycogenolysis and adipose tissue lipolysis, hormonal dysregulation, and deficient hepatic
gluconeogenesis and ketogenesis.
– Anemia due to repeated phlebotomy, shortened RBC survival, rapid growth, and transition
from fetal to neonatal life.
Anesthetic goals should be centered around maintaining baseline ventilatory and circulatory
status while providing an adequate level of analgesia, amnesia, and immobility.
SYMPTOMS
• Body hair (lanugo)
• Abnormal breathing patterns (shallow, irregular pauses in breathing)
• Enlarged clitoris (female infant)
• Small scrotum, smooth without ridges, and undescended testicles (male infant)
• Low muscle tone
• Feeding problems
• Soft, flexible ear cartilage
• Thin, smooth, shiny skin
History
• Vital signs
• Current weight and birth weight
• Gestational and post-conceptual age
• Type of delivery
• Lung disease
• Cardiovascular history (structural anomaly, history of apnea and/or bradycardia)
• Presence of genetic abnormalities or other syndromes
• Infections
Signs/Physical Exam
• The Ballard Score is a set of procedures developed by Dr. Jeanne L Ballard, MD to determine
the gestational age through neuromuscular and physical assessment of a newborn fetus. It
consists of multiple charts and diagrams with neonates in different postures; the combined
score determines the gestational age.
• Attention should also be given to the following: Hypotonia, respiratory distress, failure to
thrive, temperature dysregulation, small for gestational age, jaundice, and anemia
TREATMENT HISTORY
History of treatment for specific conditions should be clarified and investigated, noting if the
condition was treated completely, or if there are any residual effects, and if there are any
physiologic changes from the disease. For instance:
• Prolonged intubation
• Cardiac failure/arrest, cardiac surgeries
• Apnea
• Seizures
• IVH
MEDICATIONS
The prescribed medications can alert the anaesthetist to a number of preexisting conditions:
• Prostaglandin: PDA, pulmonary hypertension
• Caffeine: Apnea
• Vasopressors: Heart failure, septicemia
• ACE inhibitors: Hypertension, heart failure
• Digoxin: Right heart failure, hypertrophic obstructive cardiomegaly
• Diuretics: Heart failure, acute renal failure, hypervolemia
• Beta-blocker: Hypertrophic obstructive cardiomegaly
Labs/Studies
• Chemistry
• Bilirubin level
• Arterial or venous blood gas
• Chest radiograph
• Echocardiogram
See Pathophysiology
• Emergency cases should be done as the stability of the patient allows.
• Elective cases should be postponed until apnea, the major risk of anesthesia, is reduced; this
can last for up to 60 weeks post-conceptual age.
CLASSIFICATIONS
• Low birth weight infants: 1,500–2,500 g
• Very low birth weight infants: 1,000–1,500 g
• Extremely low birth weight infants: <1,000 g
TREATMENT
Premedications
Vagolytics may be used to reduce salivation and increase the heart rate (atropine,
scopolamine, glycopyrrolate)
The consent should detail the risks of anesthesia in the perioperative period and the
possibility of post-operative ventilation, the post-anesthesia recovery plan, and any special
concerns about the disease.
INTRAOPERATIVE CARE
• General anesthesia is commonly used.
• Regional techniques (caudal blocks, spinal anesthesia) as a sole technique may be used for
lower abdominal and lower extremity procedures, particularly in infants that have
developed BPD or are at increased risk of apnea.
Monitors
• ASA standard monitors.
• Depending on the surgical procedure and comorbidities, an arterial line or central venous
line may be needed.
• Neuromonitoring: The train of four may not be reliable.
• Induction consists of appropriate preoxygenation, the possible administration of vagolytics,
and the use of propofol, barbiturates, opioids, ketamine, benzodiazepines, and/or
dexmedetomidine
• Increased total body water increases the volume of distribution for muscle relaxants
compared to older children and adults.
• Airway considerations: In general, pediatric patients have a relatively small oropharyngeal
space, higher larynx at the C3 level, anterior position of glottic opening, large head and
tongue, and floppy epiglottis
• Airway equipment
– Oral airway size 000, 00, 0, 40 mm
– Endotracheal tube (ETT) sizes 2.0–3.5
– Pediatric laryngoscope handle with Miller blade 00 or 0
– ETT usually secured at 6–9 cm at the gum
Maintenance
• Preterm infants have lower minimum alveolar concentration requirements compared to term
infants.
• Oxygen concentration should be kept as low as possible to reduce the possibility of ROP.
• Active warming should be implemented during surgery with the knowledge that the preterm
infant’s skin is more fragile and susceptible to burns.
• The patient should be fully awake and have full return of the neuromuscular function
• Good respiratory effort
• Stable hemodynamics
• Acceptable body temperature
• Equipment available for re-intubation
FOLLOW-UP
BED ACUITY
Almost all preterm infants should be admitted to the neonatal intensive care unit, pediatric
intensive care unit, or monitored bed for continuation of care, recovery, and detection of
apnea up to 60 weeks post-conceptual age.
Labs should be ordered with consideration that blood draws in excess may cause anemia and
prolong recovery.
REFERENCES
1. Martin JA, Osterman MJK, Sutton PD. Are preterm births on the decline in the United
States? Recent data from the National Vital Statistics System. NCHS Data Brief. 2010;39:1–
8.
2. Goldenberg RL, Culhane JF, Iams JD, et al. Epidemiology and causes of preterm birth.
Lancet. 2008;371:75–84.
3. Mathew OP. Apnea of prematurity: pathogenesis and management strategies. Journal of
Perinatology. 2010;1–9.
ADDITIONAL READING
• www.ballardscore.com
• Apnea of prematurity
• Anemia of prematurity
CODES
ICD9
765.10 Other preterm infants, unspecified [weight]
ICD10
P07.30 Preterm newborn, unspecified weeks of gestation
CLINICAL PEARLS
• Immaturity of the organ systems is the main concern for the anesthetic care of premature
infants.
• The increased risk of apnea in the perioperative period should be a consideration.
• Prematurity affects both the pharmacokinetics and pharmacodynamics of the commonly
used anesthetic agents.
PRETERM LABOR
Shetal H. Patel, MD
Mark Zakowski, MD
BASICS
DESCRIPTION
Preterm labor describes the onset of uterine contractions of sufficient strength and frequency
to result in progressive cervical dilatation and effacement between 20 and 37 weeks of
gestation.
EPIDEMIOLOGY
Prevalence
• Premature births have increased by 40% in the last 2 decades.
• The highest rates of preterm births are in Africa (12%) and North America (11%), and the
lowest rate is in Europe (∼6%).
• In the US, 3.5% of births occur at <34 weeks of gestation
• 30% of preterm labor resolves spontaneously.
• 50% of women with preterm labor will deliver at term.
Morbidity
• Neonatal:
– Long-term consequences: Mental retardation, developmental delay, cerebral palsy, seizure
disorders, blindness, deafness, hyaline membrane disease, chronic pulmonary disease, and
retinopathy of prematurity.
– Infants delivered at <32 weeks gestation (∼2% of all births) account for the greatest
amount of health care dollars spent on the neonate
• Maternal morbidity is often associated with tocolytic therapy:
– Magnesium sulfate: Respiratory arrest, cardiac arrest
– Beta-agonists: Hypokalemia, hyperglycemia, cardiac arrhythmias, hypotension, pulmonary
edema
– Calcium channel blockers: Hypotension, headache, nausea
Mortality
Preterm birth is the second leading cause of perinatal mortality after fetal anomalies.
• Greater than 50% of preterm births occur in women who have no apparent risk factors.
• A previous history of preterm labor is the most predictive risk factor.
– 14% incidence in a subsequent pregnancy after one previous preterm delivery
– 28% incidence in a subsequent pregnancy after two previous preterm deliveries
• Maternal characteristics (1):
– African-American > Caucasian women
– <18 years old or >35 years old
– Lower socioeconomic status
– History of tobacco use
– History of cocaine or amphetamine use
• Maternal anatomic features:
– Uterine overdistention: Multiple gestations, polyhydramnios, macrosomia, and/or fibroids
– Cervical dilatation >2 cm at 32 weeks
– Short cervix
– Bleeding after 12 weeks gestation
• Surgical risk factors:
– Abdominal surgery after the 1st trimester
– History of surgery on the cervix
– History of first or second trimester abortion
• Infectious exposure:
– Bacterial vaginosis
– Pyelonephritis
– Severe periodontal disease
• Inflammatory insults such as infections, ischemia, trauma, or allergic reactions incite the
production of cytokines and prostaglandins. These inflammatory intermediates initiate
uterine contractions and the release of proteases which damage the fetal membranes and
decidua.
• These events can result in cervical ripening, dilation, and possible rupture of membranes.
Tocolytics are used to prolong gestation and enable fetal growth and development, as well as
enable corticosteroids to exert a beneficial effect on fetal lung maturation. They are not
recommended after 34 weeks gestation.
• Calcium channel blockers (e.g., nifedipine)
– Decreases the concentration of free calcium within the myometrium by blocking voltage-
dependent calcium channels in the cell membrane
– Dose: Loading dose of 10 mg PO every 20 minutes until contractions stop to a maximum
of 30 mg; then 10 mg PO every 6 hours
– Maternal side effects: Vasodilation, headache, nausea
– Fetal side effects: No direct effects
• Prostaglandin synthetase inhibitors (indomethacin)
– Inhibit production of prostaglandins F2α and E2α, which are potent stimulators of uterine
activity
– Dose: Loading dose of 50 mg PO then 25 mg PO every 6 hours for 48 hours
– Maternal side effects: Gastric irritation, coagulation abnormalities (rare)
– Fetal side effects:
Premature closure of fetal ductus arteriosus; less likely if indomethacin given prior to 32
weeks gestation
Decreased fetal urine excretion leading to oligohydramnios and, rarely neonatal renal
failure
Increased incidence of necrotizing enterocolitis, intracranial hemorrhage, and
bronchopulmonary dysplasia
• Magnesium sulfate
– Decreases uterine activity by decreasing intracellular calcium concentrations as well as
competitively binding to calcium receptors.
– Dose: Loading dose of 4 g IV over 30 minutes; then infusion of 2 g/hr (with normal renal
function) to achieve a serum concentration of 5–8 mg/dL (4–7 mEq/L)
– Maternal side effects depend on serum magnesium concentration
Loss of deep tendon reflexes: 10–12 mg/dL (>7 mEq/L)
Respiratory paralysis: 12–18 mg/dL (>10 mEq/L)
Cardiac arrest: >25–30 mg/dL (>25 mEq/L)
– Fetal side effects: Decreased fetal heart rate variability, hyporeflexia, decreased tone,
respiratory depression
• Beta-2-adrenergic agonists (terbutaline and ritodrine)
– Binding to beta-2-adrenergic receptors within the myometrium activates adenyl cyclase
and increases cyclic-AMP. Increased cyclic-AMP decreases intracellular calcium and
contractile activity.
– Ritodrine dose: Initial dose of 0.05–0.1 mg/minute IV and increased at 15 minute intervals
to 0.35 mg/minute
– Terbutaline dose: 0.25 mg SQ every 1–6 hours
– Maternal side effects: Hypokalemia, hyperglycemia, chest pain, shortness of breath,
cardiac arrhythmias, hypotension, pulmonary edema
– Fetal side effects: No direct effects
• Oxytocin antagonist (atosiban): Currently only available in Europe
• Screening for bacterial vaginosis (BV)
– BV can increase the risk of preterm birth by two-fold.
– Anaerobic organisms replace normal lactobacilli
– BV present in up to 25% of pregnant women
• Symptoms:
– Pelvic pressure
– Abdominal cramping
– Increase in vaginal discharge
– Backache
– Painless in up to 50% of instances
• Signs/physical examination:
– Uterine contractions lasting >30 seconds and occurring at least every 10 minutes
– Cervical dilation ≥2 cm
– Cervical effacement ≥80%
• Fetal fibronectin (FFN)
– A basement membrane protein produced by the fetal membranes and functions as an
“adhesion binder”
– Appearance of FFN in cervical secretions after 22 weeks may indicate disruption of the
normal adhesion between chorioamnion and the underlying decidua
– Most useful test when cervical length 16–30 mm
– The negative predictive value for preterm delivery (within 7 days of test) is up to 99.5%
and 99.2% (within 14 days)
• Cervical ultrasonography
– Cervical shortening is one of the earliest indicators of cervical incompetency or the onset
of labor
– Cervical length <25 mm between 16–24 weeks may increase the risk of preterm delivery.
TREATMENT
• Increase fetal lung maturity with corticosteroids (betamethasone) (1)

– Can decrease the risk of cerebral palsy by up to 45%
– Recommended to be administered between 24 and 34 weeks of gestation
– Dose: 12 mg IM, repeat in 12–24 hours
– The optimum treatment to delivery interval is after 48 hours and within 7 days of steroid
use
– Contraindications: Chorioamnionitis with sepsis, uncontrolled diabetes mellitus
• Fetal neuroprotection with magnesium sulfate (2)
– Decreases risk of cerebral palsy up to 45%
– Dose: Loading dose of 6 grams IV over 30 minutes, followed by an infusion of 2
grams/hour for a minimum of 12 hours prior to delivery.
– Recommended for neonates <32 weeks gestational age
• Management of delivery
– Cesarean delivery is indicated for breech presentation and low gestational weight
(relative). There is some concern that a vaginal delivery may lead to head trauma and
subsequent intracranial hemorrhage in neonates with an estimated gestation weight
<1,500 grams. A classical or T-incision may be indicated if <32 weeks gestation.
Regional anesthesia is preferred over general anesthesia.
– Vaginal delivery: The goal is to avoid precipitous delivery that may increase stress on the
fetal head. Neuraxial analgesia provides the benefit of a well-relaxed perineum for a
controlled delivery. Take into account possible interactions with tocolytic therapy,
especially when beta-adrenergic agonists and calcium-channel blockers/antagonists are
utilized.
• Uterotonic agents following delivery:
– At <28 weeks gestation, the uterus may not respond to oxytocin due to insufficient
quantity and responsiveness of oxytocin receptors within the myometrium.
– Direct-acting uterotonic agents, including methylergonovine and carboprost, may be more
effective in achieving adequate uterine tone.
REFERENCES
1. COG Practice bulletin No. 80: Premature rupture of membranes. Obstet Gynecol.
2007;109(4):1007–1019.
2. ACOG Committee opinion no. 455: Magnesium sulfate before anticipated preterm birth for
neuroprotection. Obstet Gynecol. 2010;115(3):669–671.
ADDITIONAL READING
• Beck S, Wojdyla D, Say L, et al. The worldwide incidence of preterm birth: A systematic
review of maternal mortality and morbidity. Bull World Health Organ. 2010;88(1):31–8.
• Chandraharan E, Arulkumaran S. Acute tocolysis. Curr Opin Obstet Gynecol.
2005;17(2):151–156.
• Hole JW, Tressler TB. Management of preterm labor. J Am Osteopath Assoc. 2001;101:S14–
S18.
• National Guideline Clearinghouse. Management of preterm labor.
• www.acog.org/publications/patient_education/bp087.cfm. The American Congress of
Obstetrics and Gynecologists.
• www.guidelines.gov/content.aspx?id=3993.
• Cerebral palsy
• Vaginal delivery
CODES
ICD9
644.20 Early onset of delivery, unspecified as to episode of care or not applicable
ICD10
O60.00 Preterm labor without delivery, unspecified trimester
CLINICAL PEARLS
• Preterm birth occurs in 12% of pregnancies and is one of the leading causes of neonatal
morbidity and mortality.
• Tocolytics including magnesium sulfate, calcium channel blockers, prostaglandin synthetase
inhibitors, and beta-2-adrenergic agonists can be used to delay preterm delivery.
• Corticosteroid administration reduces neonatal morbidity associated with preterm birth.
• Magnesium sulfate administration prior to preterm delivery leads to a reduced incidence of
cerebral palsy.
• Beware of interactions of treatments for preterm labor and anesthetic techniques (e.g.,
excessive hypotension).
• Cesarean delivery is indicated for breech presentation of the preterm neonate.
PROPOFOL INFUSION SYNDROME (PRIS)
Jeremy Wong, MD
BASICS
DESCRIPTION
• Propofol infusion syndrome (PRIS) was first termed in 1998 to describe a clinical state
associated with propofol infusion in children. Patients demonstrated acute refractory
bradycardia that led to asystole in the presence of one or more of the following:
– Metabolic acidosis (base deficit >10 mmol/L)
– Rhabdomyolysis or myoglobinuria
– Lipemic plasma
– Clinically enlarged or fatty liver on autopsy
• A more recent definition of PRIS was published in 2009 and included:
– Metabolic acidosis
– Cardiac dysfunction
– One of the following:
Rhabdomyolysis
Hypertriglyceridemia
Renal failure
• To date, most of the information available on PRIS is based on case reports and
retrospective studies.
EPIDEMIOLOGY
Prevalence
• Large prospective study cited an incidence of 1.1% (11 of 1,017 patients)
• More than 80 case reports have been recorded.
• In a retrospective 2008 MEDWATCH analysis, 1,139 potential cases of PRIS were identified.
Morbidity
Severity ranges from minor laboratory abnormalities that resolve completely without
sequelae to multi-organ failure and death
Mortality
Reports range from 18–83%
• Large total cumulative propofol dose (>4 mg/kg/hr for longer than 48 hours)
• Severe head injury
• Airway infection
• High catecholamine and serum glucocorticoid levels
• Low carbohydrate intake/high fat intake
• Critical illness
• Young age
• Inborn errors of fatty acid oxidation
• Propofol is commonly used in the perioperative period for its sedative and hypnotic
properties. It can be utilized to induce and maintain general anesthesia (solely or in
combination with other agents) as well as for sedation during procedures, to reduce
intracranial pressure, provide neuroprotection, or to maintain sedation with mechanical
ventilation.
– Mechanism of action: Potentiates GABA receptor binding by attaching to the beta subunit
of the GABAA receptor. GABA is an inhibitory neurotransmitter that hyperpolarizes the
cell membrane (increases chloride conductance), thereby preventing depolarization and
neurotransmission.
– Cardiovascular effects: Capable of profound decreases in systolic BP from vasodilation of
the arterial and venous systems, as well as myocardial depression and bradycardia.
Propofol’s antagonist effect at beta-receptors and calcium channels is believed to result in
bradycardia and impaired myocardial contractility.
– Onset: 90–100 seconds or “one arm–brain circulation”
– Metabolism: Hepatic and extra-hepatic metabolism. The liver metabolizes propofol to
inactive water-soluble compounds (glucuronide, sulfate) that are renally excreted. The
lungs and kidneys are responsible for 30–60% of elimination; the urine and feces 3%.
• The pathophysiology of PRIS is complex, involving multiple simultaneous mechanisms but
has the common feature of cardiovascular collapse
• Impairment of ATP production: Propofol inhibits beta-oxidation of free fatty acids and the
mitochondrial electron transport chain. This results in a disruption of ATP production,
cellular hypoxia, and metabolic acidosis. The imbalance between cellular energy production
and utilization causes peripheral and cardiac muscle necrosis.
• Arrhythmias: Damage to the myocardial conduction system of the heart may result from:
– Direct effects of propofol on ion currents
– Indirect effects by increased free fatty acid levels, acidosis, and hyperkalemia
• Risk factors
– High levels of endogenous and exogenous catecholamines increase the cardiac output and
portal flow. This can increase propofol requirements and the potential for PRIS with
myofibrillar degeneration and stress cardiomyopathy.
– Mitochondrial myopathies result from defects in the mitochondrial respiratory chain.
When they are stressed with illness, infection, or starvation, they are unable to utilize
free-fatty acids for energy. This results in muscle cell breakdown and can be compounded
with propofol administration.
In the critically ill, consider maintaining an adequate carbohydrate supply, limiting excess
lipid loads, or using alternative methods of sedation.
• Patients with inadequate carbohydrate intake or children (with smaller carbohydrate stores)
may tend towards fat metabolism and thus increased circulating fatty-acid load, which may
predispose to PRIS.
• Evidence is mixed regarding the contribution of lipid load to PRIS. It is unclear whether or
not the lipid component of propofol is at least partly responsible for the development of
PRIS.
• Although no specific test is available, monitoring of pH, lactate, and CK levels are
recommended when unusually high doses or long infusion periods are unavoidable, or in
high-risk patients. It should be noted, however, that there have been reports of PRIS deaths
despite frequent laboratory monitoring and immediate cessation of propofol upon the
development of laboratory abnormalities.
• Presentation varies considerably, but practitioners should be aware of the signs that have
been described.
– Early signs can include unexplained lactic acidosis, lipemic serum, and cardiac
dysfunction or Brugada-like electrocardiogram changes.
– Later signs include cardiac failure, tachyarrhythmias or heart block, ventricular fibrillation
or ventricular tachycardia, rhabdomyolysis (elevated CPK and myoglobinuria),
hyperkalemia, renal failure, and fatty degeneration of the liver.
Consider other causes of lactic acidosis:
• Decreased oxygen delivery
– Hypotension (hypovolemia, cardiogenic shock, septic shock)
– Severe anemia
– Severe hypoxemia
– Carbon monoxide poisoning
– Ischemic tissue (bowel, extremity, etc.)
• Increased oxygen demand
– Exercise
– Seizures
– Shivering
– Malignant hyperthermia
• Disrupted oxygen utilization
– SIRS
– Malignancy
– TPN (with thiamine deficiency)
– Congenital lactic acidosis
– Mitochondrial myopathies
– Drugs/toxins (NRTIs, metformin, nitroprusside, alcohol, propylene glycol, salicylates)
TREATMENT
• PRIS is difficult to treat once it develops; efforts are mostly supportive.
• Discontinue propofol immediately.
• Cardiorespiratory support should be provided as needed.
• Hemodialysis/hemofiltration has been reported to be effective.
• Partial exchange blood transfusion (PEBT) has been recently reported in the treatment of
PRIS. A hemodynamically unstable 10-year-old boy on propofol for the treatment of status
epilepticus was successfully treated with PEBT as a bridge to continuous veno-venous
hemofiltration.
• IV fluids and inotropes are often ineffective.
• Cardiac pacing has shown some success in several case reports.
• ECMO has been reported in the successful treatment of 3 patients with PRIS. In a recently
published case report, a 17-year-old on propofol for status epilepticus developed PRIS.
Lactic acidosis improved with continuous hemofiltration, but cardiovascular collapse
developed. ECMO was successfully used until cardiac recovery ensued and was discontinued
5 days later.
REFERENCES
1. am PCA, Cardone D. Propofol infusion syndrome. Anaesthesia. 2007;62:690–701.
2. asile B, Rasulo F, Candiani A, et al. The pathophysiology of propofol infusion syndrome: A
simple name for a complex syndrome. Intensive Care Med. 2003;29:1417–1425.
3. Wysowski D, et al.Reports of death with use of propofol (Diprivan) for nonprocedural
(long-term) sedation and literature review. Anesthesiology. 2006;105(5):1047–1051.
4. Roberts R, et al.Incidence of propofol-related infusion syndrome in critically ill adults: A
prospective, multicenter study. Crit Care. 2009;13:R169.
ADDITIONAL READING
• Da-Silva SS, Wong R, Coquillon P, Gavrilita C, Asuncion A. Partial-exchange blood
transfusion: An effective method for preventing mortality in a child with propofol infusion
syndrome.Pediatrics.2010;125(6):e1493–e1499.Guitton J, et al.Propofol infusion syndrome
during refractory status epilepticus in a young adult: Successful ECMO resuscitation.
Neurocrit Care. 2010.
Lactic acidosis
CODES
ICD9
995.22 Unspecified adverse effect of anesthesia
ICD10
T88.59XA Other complications of anesthesia, initial encounter
CLINICAL PEARLS
• The infusion rate and duration of infusion are particularly important risk factors for the
development of PRIS. It is recommended that infusions >4 mg/kg/hr for longer than 48
hours be avoided.
• Early PRIS, however, has been shown to develop during high-dose, short-term infusions such
as those used in the practice of anesthesiology.
• Special care should be taken when patients receive high-dose infusions or prolonged
infusions, and in those who have risk factors that make the development of PRIS more likely
(such as mitochondrial disease or fatty acid oxidation defects, young age, critical illness of
the CNS or respiratory origin, exogenous catecholamine or glucocorticoid administration, or
inadequate carbohydrate intake).
• The monitoring of pH, lactate, and CK is recommended when unusually high doses or long
infusion periods are unavoidable.
• If prolonged or high-dose propofol administration is unavoidable, supplemental sedatives
can be used to decrease the amount of propofol necessary for the desired level of sedation.
Note, however, that a recent study in rabbits suggests that using an adjunct-like
remifentanil did not delay or prevent the development of PRIS despite reducing the
tolerance to co-administered propofol.
PROSTATECTOMY
BASICS
DESCRIPTION
General
• Prostatectomies are performed:
– Either to reduce the size of the prostate when causing bladder outlet obstruction, or to
remove the prostate secondary to tumor.
– Via open, laparoscopic, robotic assisted (RALRP), or trans-urethral (TURP) approaches.
• TURP is used for the treatment of bladder outlet obstruction from enlargement of the
prostate, but is not a treatment for prostate cancer. It is performed through a specialized
cystoscope (resectoscope) through which an electrocautery loop is passed and used to
reduce the impingement of the urethra caused by the prostate. Newer techniques use a laser
(PVP, greenlight) to vaporize the portion of the prostate that is causing obstruction. This is
associated with a nearly bloodless surgical field.
• Open procedures, radical perineal prostatectomy (RPP), or radical retropubic prostatectomy
(RRP) allow direct visualization and access. They are generally used for larger tumors or
significant intraperitoneal metastatic disease and are associated with increased blood loss,
and possibly longer hospital length of stay. However, this is largely dependent on an
individual surgeon’s practice and other patient factors. Some studies show a more favorable
oncologic outcome and improved urinary continence rates for open procedures but others
refute that finding (4).
• Robotic or laparoscopic techniques are generally used for patients with limited disease;
robotic procedures allow for increased dexterity. The data is conflicting with regards to
complication rate and oncologic outcomes compared to open procedures. There does seem
to be a higher rate of bowel injuries and fistula formation though, with a minimally invasive
approach (4).
Position
• TURP: Lithotomy, arms out
• Open abdominal: Supine, arms out
• Open RPP: Lithotomy, arms out
• Laparoscopic/RALRP: Lithotomy, arms tucked, steep Trendelenburg (up to 40°) (1).
Incision
• TURP: None, equipment inserted via penis
• Abdominal: Low midline or Pfannenstiel
• RRP: Perineal
• Laparoscopic/RARLP: 4–5 small incisions for trochar insertion
Approximate Time
• Surgical time will vary by institution and surgeon skill
• TURP: 1–2 hours; longer duration is associated with higher risk of TURP syndrome
• Open: 1–3 hours
• RPP: 3 hours
• RALRP: 2–4 hours
EBL Expected
• TURP: <500 mL
• Open simple: 500 mL
• RRP 200 mL–1500 mL (3)
• Robotic: 50–1,000 mL (3).
• Some patients with prostate cancer have a mild DIC that manifests perioperatively and can
result in higher than expected blood loss
Hospital Stay
• The majority of patients are discharged on the first postoperative day.
• TURP patients are often kept overnight to monitor for any significant postoperative
bleeding.
• Open procedures: 1–3 days
• TURP procedures require cystoscopy equipment and a fluid irrigation system
• For laser vaporization of the prostate, everyone in the OR, including the patient, must wear
protective eyewear to reduce the chance of injury if the laser fiber should break, causing
exposure to laser light.
• da Vinci® robotic surgical system for RARLP
EPIDEMIOLOGY
Prevalence
Benign prostatic hyperplasia will occur in >80% of men; surgical intervention is required in
∼20%.
Prevalence
There were approximately 2,276,112 men alive in the US with a diagnosis of cancer as of
January 1, 2007.
Morbidity
• Surgical complications include bleeding, infection, incontinence, impotence
• TURP: Significant intraoperative bleeding (10%), failure to void (6.5%), TURP syndrome (2–
5%), perforation of the bladder/urethra (<0.5%)
• Robotic/laparoscopic: Postoperative vision loss (ischemic optic neuropathy) is a rare but
devastating complication that may be influenced by prolonged surgical times in a steep
head-down position, hypotension, and pronounced hemodilution.
Mortality
Thirty-day mortality for TURP and open procedures is <1%.
• Although TURP and RALRP are minimally invasive procedures, the patients are often elderly
and have significant comorbidities that must be considered.
• The anaesthetist must be vigilant for signs of venous gas embolism during dissection of the
deep dorsal venous plexus.
• Appropriate fluid management during RALRP can positively impact outcomes. Minimizing
fluids given prior to dissection of the deep dorsal venous plexus and removal of the prostate
results in significantly decreased blood loss throughout the procedure (7).
SYMPTOMS
• BPH: Difficult urination, weak urinary stream, and waking at night to void.
• Advanced or metastatic disease: Bone pain, anemia, and renal failure.
History
• Inquire about common comorbidities such as COPD, CAD, and urinary retention/renal
failure.
• Patients with glaucoma, history of CVA, or cerebral aneurysm may be poor candidates for
robotic or laparoscopic procedures requiring steep Trendelenburg positioning.
Signs/Physical Exam
• A thorough physical examination including auscultation of heart and lungs and evaluation
of peripheral pulses should be performed.
• A standard airway examination.
• A neurologic examination can help identify pre-existing nerve injuries.
MEDICATIONS
• Chemotherapeutic agents
• Alpha-adrenergic antagonists
Labs/Studies
• Preoperative Hgb/Hct along with Type and Screen is appropriate for all radical
prostatectomies. Cross-matching of blood products should be considered on the basis of
patient factors and surgeon skill/expected blood loss.
• Coagulation studies and platelet count should be considered prior to a planned neuraxial
anesthetic, particularly if the clinical history suggests.
• Other tests (e.g., ECG, Echo, PFT) are based on comorbid conditions.
• Renal failure and azotemia can result from prolonged, severe, untreated prostatic
hypertrophy, and urinary obstruction.
• Metastatic disease to the brain, spine, or abdominal organs is possible.
TREATMENT
Premedications
• Caution should be exercised when using benzodiazepines in elderly patients as their effects
can be prolonged.
• Continue perioperative beta-blockade
• For RALRP, a discussion of the positioning and the risk of facial swelling, nerve palsies,
postoperative vision loss, and possible need for postoperative intubation (due to airway
edema) should occur.
• For neuraxial techniques, either as the sole anesthetic in TURP or for postoperative pain
management in open procedures, a discussion of the risks and benefits should be conducted.
• Antibiotic prophylaxis has been shown to reduce postoperative bacteriuria, bacteremia,
high-grade fever, and use of additional perioperative antibiotics (2).
• TURP
– Fluoroquinolone or TMP–SMX is the preferred antibiotic.
– Alternatively may use aminoglycoside +/− ampicillin or a first/second generation
cephalosporin.
• Open or laparoscopic
– First/second generation cephalosporin, aminoglycoside + clindamycin, or flagyl
preferred.
– Alternatively may use fluoroquinolone or ampicillin/sulbactam.
INTRAOPERATIVE CARE
• Open procedures: GETA +/− epidural
– Epidural analgesia may reduce the risk of postoperative DVT and ileus. There is some
weak evidence that with lower grade tumors, epidural analgesia is associated with
improved oncologic outcomes (6).
• TURP: General anesthesia (GA) or neuraxial (need T10 level). Considerations include:
– Allows for continuous monitoring of the patient’s mental status for signs of TURP
syndrome or fluid overload.
– Does not block the obturator reflex. The obturator nerve originates from L2–4 and runs
close to the prostatic urethra, bladder neck, and inferolateral bladder wall. Bladder
distention from irrigating fluid brings the nerve close to the lateral bladder wall; thus,
electrical currents can stimulate the nerve and cause an adductor muscle reflex of the
lower extremity. An obturator nerve block by the surgeon can prevent this (needs to be
blocked before it bifurcates into the anterior and posterior divisions).
• Laparoscopic/Robotic: General endotracheal anesthesia
Monitors
• Two large bore IVs for radical prostatectomy
• Urine output is often interrupted during the procedure and is unreliable as a monitor.
Hematuria is not unexpected.
• Arterial lines are sometimes used during robotic procedures because access to the patient is
severely limited when the robot is engaged.
Standard induction and airway management with alteration, as needed, depending on patient
comorbidities or physical examination (e.g., difficult airway).
Maintenance
• Any standard balanced maintenance technique is appropriate.
• During TURP, ensure an adequate depth of anesthesia to prevent movement that may cause
injury to the external urinary sphincter and lead to postoperative incontinence. Note: GA
without muscle relaxation does not prevent the obturator reflex from occurring. Fluids
should be judiciously administered, as absorption from the open prostatic venous plexuses
can result in hypervolemia.
• Muscle relaxation during a RALRP is critically important; patient movement while the robot
is engaged can lead to significant injury to the patient and damage to the equipment.
RALRP is associated with upper airway edema and an endotracheal tube occlusion test is
often performed prior to extubation to ensure airway patency.
FOLLOW-UP
BED ACUITY
Medical–Surgical unit, unless comorbid conditions warrant more advanced cardiac
monitoring.
ANALGESIA
• For open procedures, a combination of IV, oral and/or peridural analgesics are often used.
• For minimally invasive techniques, IV or oral analgesics are often sufficient.
COMPLICATIONS
• Postoperative erectile dysfunction: Regardless of technique, preservation of the
neurovascular bundles is critical in preserving potency.
• Obturator or peroneal nerve injury from lithotomy positioning
• Rectal injury
– Delayed bleeding
• Urinary incontinence is common initially but over 90% eventually regain good urinary
control.
• TURP
– Complications related to irrigant absorption (TURP syndrome, hypothermia, CHF, DIC,
blindness)
– Bacteremia/sepsis
– Bladder rupture
PROGNOSIS
• For BPH, prognosis is good once obstruction is removed.
• For organ-contained malignancies, the 10-year survival is 70–85% after prostatectomy. If
there is extracapsular extension of disease, the survival rate is 60% at 5 years and 30% at 10
years.
REFERENCES
1. Kalmar AF, et al. Influence of steep Trendelenburg position and CO(2) pneumoperitoneum
on cardiovascular, cerebrovascular, and respiratory homeostasis during robotic
prostatectomy. Br J Anaesth. 2010;104(4):433–439.
2. Wolf JS, et al. Best practice policy statement on urologic surgery antimicrobial prophylaxis.
J Urol. 2008;179(4):1379–1390.
3. Farnham SB, et al. Intraoperative blood loss and transfusion requirements for robotic-
assisted radical prostatectomy versus radical retropubic prostatectomy. Urology.
2006;67(2):360–363.
4. Nelson JB. Debate: Open radical prostatectomy vs laparoscopic vs robotic. Urol Oncol.
2007;25(6):490–493.
5. Sanda MG. Genetic susceptibility of benign prostatic hyperplasia. J Urol. 1994;152(1):115–
119.
6. Umbreit E, et al. Percutaneous nephrolithotomy for large or multiple upper tract calculi
and autosomal dominant polycystic kidney disease. J Urol. 2010;183(1):183–187.
• TURP syndrome
• Laparoscopy
CLINICAL PEARLS
• Patients presenting for prostatectomy are often elderly with multiple comorbid conditions.
• Acute septicemia may occur in up to 6–7% of patients undergoing TURP. This may manifest
as tachycardia, fever, and chills, however, severe cases may result in “septic shock” with
cardiovascular collapse.
• Patients undergoing RALRP should be gradually placed into the steep Trendelenburg
position to ensure adequate ventilation, hemodynamic stability, and stability of patient
position.
PROTEIN C
John B. Carter, MD
BASICS
DESCRIPTION
• Protein C has 2 functions:
– As an anticoagulant within the coagulation cascade
– Modulates the inflammatory response
• Homozygous Protein C deficiency is a rare, fatal thrombotic disease. Heterozygous disease
occurs more commonly and increases the risk of venous thromboembolism.
• Acquired deficiencies in Protein C can also be seen in sepsis, and its levels can serve as a
predictor of mortality.
• Protein C is a vitamin-K anticoagulant that is synthesized by the liver in an inactive form
(1).
• Anticoagulant functions
– Conversion of Protein C to activated protein C (aPC) by thrombin occurs on the
endothelial cell surface and involves 2 membrane receptors: Thrombomodulin, endothelial
protein C receptor (1,2).
– Thrombomodulin
– Endothelial Protein C receptor.
– The major action of aPC is to inactivate factors Va and VIIIa, as well as neutralize
plasminogen activator inhibitor; its overall effect is reduction of blood clotting.
Additionally, its actions are enhanced by protein S (1,2).
– These antithrombotic actions are especially important to the venous circulation as well as
the microcirculation.
• Anti-inflammatory and cytoprotective functions (3)
– Mediated through endothelial Protein C receptor and protease-activated receptor-1
– Inflammatory mediators are also down-regulated
• Hereditary deficiency is an autosomal dominant disorder. Heterozygous presentation has an
incidence of 1 in 200 to 1 in 500 in the population; it is higher in those with a history of
thromboembolism. Mutations can result in either quantitative or qualitative deficiencies (2).
– Type 1: Quantitative defect of Protein C (most common). This can result from a decrease
in production or half-life of Protein C.
– Type 2: Qualitative defect of Protein C, with normal levels. This can result from defects in
its interaction with thrombomodulins, factor V, and factor VIII.
– Venous thrombosis
Typically present after adolescence
Great deal of phenotypical variation
In heterozygotes, it most commonly occurs spontaneously (70%) but can also result
during pregnancy or in the postoperative arena (30%).
Has an increased incidence when associated with another deficiency such as protein S,
antithrombin III, or factor V Leiden.
Acute events are treated with heparin; long-term anticoagulation with warfarin or low
molecular weight heparin (LMWH) is frequently indicated.
Warfarin-induced skin necrosis. Because warfarin’s mechanism of action is via
suppression of vitamin K epoxide reductase, it not only decreases synthesis of coagulant
factors, but also Protein C. Additionally, Protein C levels are decreased prior to other
coagulant factors, thus causing a transient hypercoagulable state
Hematology consultation is necessary for management
Arterial thrombosis is not increased
Homozygous or double heterozygous fatality commonly occurs in infancy from neonatal
purpura fulminans. Administration of Protein C concentrate (Ceprotin; derived from
fresh frozen plasma) may be useful.
• Acquired protein C deficiency can result from:
– Disseminated intravascular coagulopathy (DIC)
– Severe liver disease
– Hemolytic uremic syndrome
– Thrombotic thrombocytopenic purpura
– Sepsis (4,5):
Critically ill patients often have systemic activation of both inflammation and
coagulation
Pro-inflammatory cytokines have been shown to impair anticoagulant pathways such as
the Protein C system.
Coagulation can also affect inflammatory activity. Activated coagulation proteases have
been shown to affect specific cellular receptors on inflammatory and endothelial cells,
thereby modulating the inflammatory response (1). This relationship appears to play a
major role in microvascular failure and subsequent organ failure (1).
Recombinant human aPC (drotrecogin alfa) and Xigris (Eli Lilly) have antithrombotic,
prothrombolytic, and anti-inflammatory effects. They have been FDA-approved in the
treatment of sepsis.
• Patients with Protein C deficiency are at increased risk of thrombosis and long-term
anticoagulation is frequently advised during pregnancy or after a deep venous thrombosis.
Perioperative anticoagulation management should be discussed and coordinated with the
surgeon and hematologist.
– Consider “bridging” with LMWH.
– Heparin SQ should be considered.
– Sequential compression devices should be started.
– In addition, anticoagulation should be re-instituted as soon as feasible.
• Regional anesthesia and anticoagulation
– See ASRA guidelines for specific recommendations.
– Neuraxial blocks: If the benefit (pain control, increased lower extremity blood flow,
reduced intraoperative bleeding, etc) is significant, then placement and catheter removal
should be considered and coordinated around anticoagulation issues.
– Peripheral nerve blocks: In general, anatomical landmarks are well defined or easily
visualized with ultrasound imaging and a developing hematoma can be easily accessed
and compressed. On the other hand, if infraclavicular brachial plexus blocks or deeper
blocks such as the posterior lumbar plexus block (especially with the use of continuous
catheter technique) are performed, bleeding complications may not be easily diagnosed or
treated.
• In the ICU, decreased Protein C levels have been associated with increased mortality,
multisystem organ failure, and/or sepsis.
REFERENCES
1. Levi M, van der Poll T. Inflammation and Coagulation. Crit Care Med. 2010;38(2
Suppl):S26–34.
2. Bick Rodger. Prothrombin G20210A mutation, antithrombin, heparin cofactor II, protein C,
and protein S defects. Hemotol Oncol Clin N Am. 2003;17:9–36.
3. Mosnier LO, Zlokovic BV, Griffin JH. The cytoprotective protein C pathway. Blood.
2007;109:3161–3172.
4. Brunkhorst F, Sakr Y, Hagel S, et al. Protein C concentrations correlate with organ
dysfunction and predict outcome independent of the presence of sepsis. Anesthesiology.
2007;107:15–23.
5. Marti-Carvajal A, Salanti G, Cardona AF. Human recombinant activated protein C for
severe sepsis. The Cochrane Database of Systematic Reviews. 2007;3:CD 004388.
6. Bernhard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human
activated protein C for severe sepsis. Massachusetts Medical Society. 2001.
• Sepsis
CLINICAL PEARLS
• Heterozygous Protein C deficiency is a relatively common disorder associated with an
increased incidence of thromboembolism. It may be considered if there is a family history of
venous thrombosis. The diagnosis and management are best performed by a hematologist.
• While mortality in sepsis is associated with decreased levels of Protein C, recombinant aPC
is not routinely prescribed. In the PROWESS trial, the 28-day survival was improved by
6.1%; however, there was an increased risk of bleeding. Other trials have not supported
these findings. There is weak evidence to support its use in patients with severe sepsis
(APACHE score > 25) and at a high risk of death. At this time, more randomized controlled
trials are needed. In addition, a Cochrane review in 2007 concluded that recombinant aPC
is not indicated in pediatrics (4,6).
PROTHROMBIN TIME (PT)
BASICS
DESCRIPTION
• The PT is a screening test for hemostasis, and is one of the most frequently ordered tests in
coagulation medicine.
• It is a measure of the integrity of the extrinsic and final common pathways of the
procoagulant cascade (Figure 1).
FIGURE 1. Schematic of coagulation cascade. HMWK = high-molecular-weight kininogen; PK = prekallikrein.
• PT represents the time (in seconds), for the patient’s plasma to clot after the addition of
calcium and an activator (tissue factor/factor III) of the extrinsic pathway
• The PT measures coagulation factors in the extrinsic and common pathways. These factors
(in order of their role in the coagulation cascade) are:
– Factor VII (extrinsic pathway)
– Factor V (common pathway)
– Factor X (common pathway)
– Factor II (common pathway)
– Fibrinogen (common pathway)
• The liver synthesizes Factor V and fibrinogen. Factors II, VII, and X are Vitamin-K-dependent
factors that are also synthesized in the liver.
• The normal range: Depends on the reagent and instrument combinations that each
laboratory uses. To that extent, the International Normalized Ratio (INR) is utilized to
standardize PT results. The tissue factor (TF) manufacturer provides an International
Sensitivity Index (ISI) that is derived from an international TF reference and utilized to
calculate INR values.
• Deficiencies or inhibitors of clotting factors within the extrinsic and final common pathways
result in prolongation of the PT. Etiologies can result from systemic disease, vitamin K
antagonists or deficiencies, congenital deficiencies, inhibitors, and artificial causes.
• Systemic disease:
– Liver disease: All coagulation factors are made in the liver except for vWF and a subunit of
factor XIII
– Connective tissue disease: Produces lupus anticoagulants
– Amyloidosis: Results in factor X deficiency
– Myeloproliferative disease: Results in factor V deficiency
– Disseminated intravascular coagulation and fibrinolysis
• Anticoagulation
– Warfarin inhibits vitamin K epoxide reductase which is responsible for the synthesis of
Factors II, VII, IX, and X (common, extrinsic, and intrinsic pathways). PT is the most
sensitive measure of factor VII and X activity.
– Heparin binds to antithrombin III, causing a conformational change that accelerates its
action 1000–3000-fold. Activated antithrombin III inactivates thrombin and Factor X
(common pathway). PTT is a more sensitive measure of heparin’s effects.
• Vitamin K deficiencies:
– Decreased nutritional intake
– Malabsorption
• Congenital coagulation factor deficiency:
– Factor II, V, VII, or X (autosomal inheritance)
• Presence of an inhibitor
– Specific factor inhibitors directed against specific clotting factors, (e.g., factor VIII or
factor V inhibitors).
– Nonspecific inhibitors (e.g., lupus anticoagulants)
• Artificial causes:
– Lipemic, icteric, or hemolyzed plasma samples (interferes with light transmission).
– High hematocrit (Hct) in patients with erythrocytosis (more plasma to anticoagulant
ratio).
– Even in the absence of the above conditions, the test needs to be repeated.
• In general anesthesia with an abnormal PT, consider avoiding:
– Nasal airway/intubation
– Esophageal and gastric instrumentation
– Central line placement in the thorax or neck. Adequate compression in the thorax is
difficult, but can be performed in the neck. If placement in the neck is attempted,
ultrasound may reduce inadvertent carotid artery puncture.
• In neuraxial anesthetic techniques, a prolonged PT can increase the risk of bleeding around
the spinal cord.
– Epidural hematoma is considered the most significant hemorrhagic complication in
regional anesthesia due to the catastrophic nature of bleeding into a fixed and
noncompressible space.
– Incidence: Actual incidence of neurologic dysfunction from hemorrhagic complications
associated with neuraxial blockade is unknown. Although the incidence cited in the
literature is estimated to be <1 in 150,000 epidural anesthetics, and <1 in 220,000
spinal anesthetics, recent epidemiologic surveys suggest that the frequency is increasing
and may be as high as 1 in 3,000 in some patient populations.
– Management: The decision to perform spinal or epidural anesthesia/analgesia and the
timing of catheter removal in a patient receiving antithrombotic therapy should be made
on an individual basis. The risk of a spinal hematoma must be weighed against the
benefits of regional anesthesia for a specific patient. If spinal or epidural needle/catheter
placement is performed, the patient’s coagulation status should be optimized during
placement, duration of epidural catheterization, and removal of the catheter.
• In plexus and peripheral nerve blockade, the associated risk of bleeding remains undefined.
– Neurologic deficits: The expandable nature of the peripheral site decreases the chance of
irreversible neural ischemia (unlike the epidural space).
– Massive hemorrhage: Bleeding into the neurovascular sheath (especially in plexus blocks)
may result in a significant decrease in the hematocrit.
– Incidence: Due to the rarity of the complications and lack of randomized studies, the
information available is based on case reports. The overall incidence of bleeding
complications associated with peripheral nerve blocks is low.
– Management: The decision to perform peripheral nerve or plexus block (single injection or
continuous catheter infusion) would be at the discretion of the anaesthetist weighing the
benefit of regional anesthesia against the risk of neural damage from hematoma or
bleeding complications. Generally, in superficial limb blocks, anatomical landmarks are
well defined or easily visualized with ultrasound imaging and a developing hematoma is
easily accessed and compressed. In deeper blocks (e.g., posterior lumbar plexus block,
infraclavicular brachial plexus block), bleeding complications may not be easily
diagnosed, especially with the use of continuous catheter technique.
• Warfarin therapy
– During the first few days of therapy, the PT reflects primarily a reduction of factor VII, the
half-life of which is ∼6 hours.
– After discontinuation of warfarin therapy, the coagulation status may not be adequate in
the first 1–3 days for hemostasis in spite of a decrease in the PT or the INR (indicating
return of factor VII activity).
– Warfarin therapy should have been stopped for 4–5 days before initiation of neuraxial
block in addition to normalization of the PT/INR.
– In urgent/emergent situations, the effects of warfarin may be reversed by oral or
intravenous of vitamin K and/or transfusion of fresh frozen plasma.
GRAPHS/FIGURES
FIGURE 2. Approach to a prolonged PT.
REFERENCES
1. amal AH, Tefferi A, Pruthi RK. How to interpret and pursue an abnormal prothrombin
time, activated partial thromboplastin time, and bleeding time in adults. Mayo Clin Proc.
2007;82(7):864–873.
2. uilenburg DJ, Singh A, Torzilli G, et al. Surgery in the patient with liver disease.
Anesthesiol Clin. 2009;27(4):721–737
3. orlocker TT, Wedel DJ, Rolingson JC, et al. Regional anesthesia in the patient receiving
antithrombotic or thrombolytic therapy. American Society of Regional Anesthesia and Pain
Medicine Evidence-Based Guidelines 3rd ed. Reg Anesth Pain Med. 2010;35(1):64–101.
4. Ho M, Ganapathy S. Is peripheral/plexus block safe in the anticoagulated patient?
Techniques in Regional Anesthesia and Pain Management. 2006;10:56–61.
• Cirrhosis
CLINICAL PEARLS
• There are no practice advisories or guidelines regarding routine coagulation testing. It is
generally performed when clinical or medication history suggests the potential for a
coagulopathy.
• It is important to recognize bleeding disorders that will not be detected by PT assays. These
disorders include:
– Qualitative and quantitative platelet defects, which require specialized platelet function
testing.
– von Willebrand disease, which requires assays for the von Willebrand factor
– Factor XIII deficiency, which requires specialized factor XIII screening or functional
assays.
– Deficiency of plasminogen activator inhibitor 1, which requires specific assays.
PULMONARY ARTERY CATHETER WAVEFORMS
Adam Thaler, DO
BASICS
DESCRIPTION
• Pulmonary artery catheters are flow-directed, balloon-tipped devices that can provide:
– Pressure measurements of the central venous/right atrium (RA), right ventricle (RV), and
pulmonary artery (PA); the left atrial and left ventricular end diastolic pressure can be
estimated by the pulmonary capillary wedge pressure (PCWP), also known as the PA
occlusion or wedge pressure.
– An assessment of the cardiac output/cardiac index
– Values to calculate the pulmonary vascular resistance (PVR) and the systemic vascular
resistance (SVR).
– Sampling of blood from the RA, RV, and PA; mixed venous oxygen saturation can be
determined.
• Pressure values are a surrogate for volume, and are dependent upon the chamber
compliance. To that extent, the use of echocardiography can provide a direct assessment of
volume.
• Several randomized clinical trials have not been able to convincingly demonstrate the
benefits of intervention on patient outcome in terms of morbidity and mortality in the ICU,
management of heart failure, or the perioperative period
• RA waveform: Consists of 3 positive (a, c, v waves) and 2 negative (x, y descents)
deflections.
– a wave reflects RA contraction near the end of ventricular diastole.
– c wave reflects bulging of the tricuspid valve into the RA during early ventricular systole.
– x descent corresponds to atrial relaxation and decreased RA pressure.
– v wave represents passive atrial filling during ventricular systole.
– y descent corresponds to tricuspid valve opening and filling of the RV in early ventricular
diastole.
– The numeric value represents the mean pressure and is a surrogate for preload.
• RV waveform:
– Systolic pressure is dramatically increased, with a prominent upstroke and downstroke.
– Diastole is characterized by a flattened upstroke as the RV rapidly fills with blood; this is
followed by a slow filling phase and then atrial systole (steeper slope).
– The numeric value is displayed as a systolic and diastolic value.
• PA waveform:
– Systolic pressure is similar to the RV pressure, but the diastolic pressure is increased
(represents the diastolic vascular tone).
– A dicrotic notch represents closure of the pulmonic valve.
• PCWP waveform:
– Reflects LA pressures, with a shape similar to the RA tracing, but with higher pressure
values and a more irregular tracing.
– a wave reflects LA contraction.
– c wave is often not seen, but reflects the mitral valve closure.
– x descent represents the decrease in LA pressure following the a wave.
– v wave represents the LA filling.
– y descent corresponds with decreased LA pressure following opening of the mitral valve
and filling of the LV.
– Numeric values are used to estimate the LV end diastolic pressure (LVEDP; surrogate for
LV preload) if no obstruction exists between the LA and the LV
• Respiratory cycle: Should be considered when interpreting pressure measurements.
– During spontaneous inspiration, the intrathoracic pressure decreases; whereas with
exhalation, it increases. In the intubated patient, positive pressure ventilation has the
reverse effect.
– Therefore, in order to minimize respiratory effects, measurements are made at end-
expiration, when the intrathoracic pressure is close to zero.
ANATOMY
• The standard, adult PAC is 7.0–9.0 FR and ∼110 cm in length. It has several lumens and
connections for transducing pressures. The lumens from proximal to distal are: Proximal
lumen (25 cm from the distal tip, lies in the RA); injectate lumen (∼20 cm from the distal
tip, lies in the RV); thermistor lumen (∼4 cm from the distal tip); distal lumen (tip of
catheter, lies in either the right or left side of the PA); balloon lumen (tip of catheter, can
inject 1.5 mL of air).
• Following the placement of a sterile introducer sheath into a central vein, the PA catheter is
inserted while monitoring the waveforms and pressures. After the catheter tip has entered
the RV, the distal balloon is inflated to “float” the catheter as blood is pumped toward the
LV; akin to a sail amongst waves. Proper positioning is determined by the pressure
waveform or fluoroscopic guidance.
• RA pressure reflects the central venous pressure (CVP), and is increased in RV failure, right-
sided valvular disease, and cardiac tamponade.
– Enlarged a waves are seen with tricuspid stenosis. “Cannon" a waves are seen with atrio-
ventricular dissociation (RA contracts against a closed tricuspid valve during ventricular
contraction).
– a waves may be absent in atrial fibrillation.
– Enlarged v waves are present with tricuspid regurgitation.
– Tamponade impairs venous return, decreasing the end-diastolic volume and cardiac
output, dramatically increasing filling pressures, and leading to the equalization of
pressures in all chambers at end-diastole.
• RV systolic pressure is increased in pulmonary hypertension, pulmonic stenosis, or
pulmonary embolism. RV diastolic pressure is increased in right heart failure and cardiac
tamponade.
• PA pressure elevations are seen in left heart failure, mitral valve disease, and primary
parenchymal lung diseases such as chronic bronchitis and emphysema. Pulmonary vascular
disease from pulmonary embolism and primary pulmonary hypertension also lead to
elevated pressures. Left-to-right cardiac shunts, as in atrial septal and ventricular septal
defects, are other potential causes.
• PCWP can be increased in left heart failure and mitral valvular disease.
– Enlarged a waves can be seen during mitral stenosis.
– Elevated v waves can be present with mitral regurgitation or ventricular septal defects.
• Complications with placement of the PAC.
– Arrhythmias are the most common complication
Transient PVCs: 68% of placements
Transient right bundle branch block: 5%. In patients with pre-existing left bundle branch
block, it can lead to a complete heart block
Persistent ventricular dysrhythmias: 3.1%
Atrial dysrhythmias: 1.3%
– Pneumothorax occurs with 0.5% of IJ cannulations, but is more common with subclavian
vein catheter placement.
– Infections can occur, with increased frequency in continuous monitoring and in patients
with pre-existing sepsis.
– Hemorrhage and damage to vascular structures can also occur. PA rupture is rare,
occurring in 0.02–0.2%, but has a mortality rate of 50%.
• Despite the widespread use of PA catheters in hemodynamically unstable patients, there are
many controversies that exist regarding appropriate indications for their usage. The
American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization
concluded that the placement of PA catheters should not be routinely used with low risk of
hemodynamic complications, and should be reserved for high-risk settings that depend on
the patient, surgery, and practice-setting variables. If clinical assessment or non-invasive
measures are not appropriate to determine the hemodynamic status, or if the use of the
catheter can change management, then its use is indicated.
– Indications for PAC in surgical patients include:
– Procedures that have a high-risk of complications from hemodynamic shifts (cardiac
surgery, aortic cross-clamping, liver transplantation).
– Patients with advanced cardiopulmonary disease.
– Shock. Can aid in the diagnosis, management, and measurement of therapeutic responses.
– Pulmonary edema to differentiate between the mechanisms (cardiogenic versus non-
cardiogenic).
EQUATIONS
• Normal pressure values
– RA: 1–5 mm Hg (mean)
– RV: 15–30/1–7 mm Hg
– PA: 15–30/4–12 mm Hg, mean 9–19 mm Hg
– PCWP: 4–12 mm Hg (mean)
• Cardiac output (CO) = 4.0–6.5 Liters/minute (normal)
– This is measured in a PAC by the thermodilution technique, where a known volume and
temperature of sterile solution is injected and the change in PA blood temperature is
measured by the thermistor.
• CO can also be calculated by Fick’s equation = (oxygen consumption)/(10 × arterio-venous
oxygen difference)
• SvO2 (mixed venous blood oxygenation) = SaO2 – (VO2/[CO × 1.36 × Hb])
– SaO2 = arterial Hb saturation (%)
– VO2 = oxygen consumption (mL O2/min)
– Hb = hemoglobin concentration (g/dL)
GRAPHS/FIGURES
REFERENCES
1. illy LS. ed. Pathophysiology of heart disease. Philadelphia, PA: Lippincott Williams &
Wilkins, 2003.
2. Roizen MF, Berger DL, Gabel RA, et al. Practice guidelines for pulmonary artery
catheterization: An updated report by the American Society of Anesthesiologists Task Force
on Pulmonary Artery Catheterization. Anesthesiology. 2003;99:988–1014.
3. Summerhill EM, Baram M. Principles of pulmonary artery catheterization in the critically
ill. Lung. 2005:183–209.
4. Shah MR, Hasselblad V, Stevenson LW, et al. Impact of the pulmonary artery catheter in
critically ill patients: Meta-analysis of randomized clinical trials. JAMA.
2005;294(13):1664–1670.
5. Sandham JD, Hull RD, Brant RF, et al. A randomized, controlled trial of the use of
pulmonary-artery catheters in high-risk surgical patients. N Engl J Med. 2003;48(1):5–14.
ADDITIONAL READING
• Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and
pulmonary artery catheterization effectiveness: The ESCAPE trial. JAMA.
2005;294(13):1625–1633.
• Harvey S, Harrison DA, Singer M, et al. Assessment of the clinical effectiveness of
pulmonary artery catheters in management of patients in intensive care (PAC-Man): A
randomised controlled trial. Lancet. 2005;366(9484):472–477.
• UptoDate: Pulmonary artery catheterization: Indications and complications; Pulmonary
artery catheterization: Interpretation of tracings
• Mitral valve stenosis
• Systole
• Diastole
• Pneumothorax
• Pulmonary hemorrhage
CLINICAL PEARLS
• PACs are useful tools in the measurement of hemodynamic parameters, such as cardiac
output, mixed venous oxygen saturation, and measurement of pressures in the right heart,
PA, and indirectly, the LA.
• It can enhance the assessment of hemodynamic status in patients further than clinical
assessment alone, and can help guide the administration and management of fluids and
vasoactive drugs.
• When compared to the echocardiogram, the PAC differs in that it measures pressures
(volumes are extrapolated), mixed venous oxygen saturation, and SVR can be calculated;
additionally, it can be left in place postoperatively.
PULMONARY ATRESIA
Nirvik Pal, MD
BASICS
DESCRIPTION
• Pulmonary atresia is a congenital heart defect with pulmonary valve (PV) “closure” that
precludes normal blood flow from the right ventricle (RV) to the pulmonary vasculature. It
requires some form of a “shunting” method in order to deliver blood to the lungs. There are
2 major categories:
– Intact ventricular septum (PA/IVS): Pathology is mostly proximal to the PV, with a small
RV and tricuspid valve (TV), as well as RV-dependent coronary blood flow.
– Ventricular septal defect (PA/VSD): Pathology is mostly distal to the PV, with
discontinuity between the RV and the PA, a misaligned large VSD, and large major aorto-
pulmonary collateral arteries (MAPCA) to the PA or directly supplying the lung lobes.
• Multiple staged surgeries are often needed depending on the morphology of the lesion;
patients often do not survive without definitive care.
EPIDEMIOLOGY
Prevalence
• Live births with PA/IVS: 0.07 per 1,000.
• PA/VSD accounts for ∼3.4% of all congenital heart defects.
Mortality
Without repair, neonates have a 50% risk and infants up to 6 months have an 85% risk.
• Lacks a familial association
• Intrauterine right ventricular outflow tract (RVOT) obstruction
• Trisomy 18 and 21 may be associated with PA/IVS
• Pulmonary atresia is characterized by a maldevelopment of the PV leading to obstruction in
normal blood flow from the RV to the lungs for oxygenation and ventilation. In intrauterine
life, oxygenation is provided by the mother/placenta, and pulmonary atresia is tolerated.
• PA/IVS is characterized by pathology mostly proximal to the PV. This includes a:
– Small but hypertrophied RV
– Small TV leading to limited blood flow and eventual hypoplasia of the RV.
– Tricuspid regurgitation (TR) often results from the structural defect or RV outflow
obstruction. If there is no, or minimal, TR, the RV chamber may be small, hypertrophic,
and have significant sinusoid formation. In moderate-to-severe TR, low RV pressures may
lead to reduced development of sinusoids and fistulae.
– Dilated right atrium
– Shunts: Atrial septal defect (ASD) and patent foramen ovale (PFO) are almost always
present. A patent ductus arteriosus (PDA) may also be seen.
– Blood flow: Sinusoids in the RV myocardium are present in over 50% of patients. The
number of sinusoids is increased with higher RV systolic pressures, smaller TV diameter,
smaller RV volume, and the absence of, or minimal, TR. There is a “dual” myocardial
blood supply from normal aorto-coronary flow and RV-coronary artery fistulae
(desaturated venous blood from RV sinusoids). This can result in chronic ischemia of the
myocardium.
• PA/IVS treatment goals:
– Minimize mortality
– Promote RV growth
– Limit non-definitive surgeries
• PA/IVS treatment options:
– Complete biventricular repair with closure of the ASD/PFO (40–60% of cases)
– Biventricular repair without closure of ASD/PFO
– “One-and-half” ventricle repair with cavopulmonary anastomosis
– “Single ventricle repair” with total cavo-pulmonary connection (Fontan)
– Heart transplantation
• PA/IVS surgical techniques are determined by the extent of RV and TV hypoplasia, TR, and
the extent of RV-dependent coronary circulation. These techniques include:
– RVOT patch annuloplasty with prostaglandin (PG) infusion to keep the PDA open.
– RVOT patch annuloplasty with systemic to PA shunt
– Pulmonary valvulotomy and systemic to PA shunt
• PA/VSD is often considered an “extreme” form of tetralogy of Fallot and the pathology is
mostly distal to the PV. There are 4 anatomic subtypes:
– (I) Simple valvular or infundibular atresia: Narrowing at the PV or the infundibulum.
Often accompanied by a patent PDA.
– (II) Absent main pulmonary artery (PA) although continuity of branches of the PA are
maintained by PDA-dependent flows. No communication between the RV and the PA
exists.
– (III) Hypoplastic true PA with multiple major aorto-pulmonary collateral arteries
(MAPCA).
– (IV) Total absence of a true PA with pulmonary blood flow entirely through MAPCAs. The
entire pulmonary blood flow is dependent on these multiple branches from the aorta.
• PA/VSD treatment goal is biventricular repair via:
– Reconstruction of the pulmonary vascular bed by combining all sources of pulmonary
blood supply
– Restoration of RV to PA continuity
– Closure of the VSD
• PA/VSD surgical techniques often are staged procedures and depend on individual
morphology:
– RV to PA conduit or aortopulmonary window or shunt
– Unifocalization or taking all MAPCAs and attaching to a single PA (single or multiple
surgeries)
– Definitive intracardiac repair of the VSD
• Excess flow through MAPCAs may lead to congestive heart failure (1,2).
• Avoid right ventricular decompression (low preload) in patients with RV to coronary blood
supply.
• Maintain ductal patency with PG infusion. There is an increase in apneic episodes with high
PG doses.
• The patient may need balloon dilatation of infundibular stenosis or MAPCA embolization in
cardiac catheterization suite prior to surgery.
SYMPTOMS
Congestive heart failure; edema, shortness of breath, tachypnea, hepatic congestion.
History
Cyanosis
Signs/Physical Exam
• Ductal flow murmur: Continuous flow murmur of the PDA.
• Single second heart sound
TREATMENT HISTORY
Staged procedures: See above.
MEDICATIONS
PG infusion to prevent PDA closure
Labs/Studies
• EKG: Right axis deviation, right atrial enlargement
• Chest radiography: Normal to low lung vascularity depending on ductal patency.
• Echocardiogram: Mainstay of diagnosis, both prenatal and postnatal.
• Cardiac catheterization: Confirmation of echocardiogram findings and ruling out of RV to
coronary fistulae.
Trisomy 18 or 21
Acute congestive heart failure
CLASSIFICATIONS
PA/IVS and PA/VSD: See Pathophysiology
TREATMENT
• Discuss the potential for postoperative intubation
• Blood transfusion consent
INTRAOPERATIVE CARE
• For unifocalization procedures, consider thoracic epidural/continuous intercostal nerve
block catheters
Monitors
• Arterial line
• Central venous line; PA catheters are not utilized due to the structural defects
• IV or inhalational technique.
• Unifocalization procedures often require lung isolation with bronchial blockers.
Maintenance
• MAPCA ligation may lead to desaturation. When this is anticipated, or if the patient has a
baseline SpO2 saturation <70%, cardiopulmonary bypass with moderate hypothermia and a
beating heart may be considered. In order to prevent cerebral hypoperfusion from
pulmonary run-off of oxygenated blood, the maximum possible number of MAPCAs should
be ligated before initiating CPB.
• After unifocalization procedures, a single cardiac output is perfused through the pulmonary
circuit. If the mean PAP is <30 mm Hg, VSD closure is performed. If the mean PAP is >30
mm Hg, a fenestrated closure may be attempted with delayed closure of the fenestration.
• Heparin infusions are started after shunt procedures, once surgical bleeding is controlled
(1,2).
The decision to extubate depends upon the baseline conditions, intraoperative course (e.g.,
cardiopulmonary bypass, blood loss), and standard extubation criteria (metabolic status,
pulmonary parameters).
FOLLOW-UP
BED ACUITY
ICU
• Gradual tapering of PG infusions
• Maintain O2 saturation above 70%
• Continue heparin
• Reduce RV preload with milrinone or dobutamine
• Watch for a “circular shunt”: Blood from the aorta to PA to PDA to RA to incompetent PV,
to LA to ASD and returning to the aorta, can result in high output cardiac failure.
COMPLICATIONS
• Shunt thrombosis
• Myocardial ischemia particularly in RV-dependent coronary circulation
• RV failure
• Intrapulmonary bleeding
• Reperfusion injury to the lung due to sudden increases in cardiac output
• Pulmonary hypertension post unifocalization
REFERENCES
1. Lake CL, Booker PD. Anomalies of pulmonary valves and right ventricular outflow tract.
Pediatric Cardiac Anesthesia, 4th ed. Lippincott Williams & Wilkins, 2005.
2. Andropoulos DB, Stayer SA, Russell IA. Anesthesia for right sided obstructed lesion.
Anesthesia for Congenital Heart Disease, 2nd ed. Wiley-Blackwell, 2009.
3. Bailey PD Jr, Jobes DR. The Fontan patient. Anesthesiol Clin. 2009;27(2):285–300.
4. Qu JZ. Congenital heart diseases with right-to-left shunts. Int Anesthesiol Clin.
2004;42(4):59–72.
5. Marcelletti CF, Iorio FS. Workshop on “one and one-half” ventricular repairs. Ann Thorac
Surg. 1998;66:615.
• Yuh DD, Reitz BA. Consensus approach to pulmonary atresia with intact ventricular septum
as described by the Congenital Heart Surgeons’ Society (CHSS). Congenital Cardiac Surgery.,
New York, NY: McGraw-Hill Inc, 2002 (99).
• Tricuspid atresia
CODES
ICD9
746.01 Atresia of pulmonary valve, congenital
ICD10
Q22.0 Pulmonary valve atresia
CLINICAL PEARLS
• A thorough understanding of the defect is necessary along with prior surgical “staging”
procedures that may have been performed; review studies and discuss with the surgical
team or cardiologist for any potential concerns or questions.
• In PA/IVS, the management is based upon the extent of the RV-dependent coronary blood
supply and RV development.
• In PA/VSD, the management is based upon the extent of MAPCAs and successful
unifocalization.
PULMONARY EMBOLISM
Carlos A. Puyo, MD
BASICS
DESCRIPTION
• Pulmonary embolism (PE) may manifest as a cardiovascular emergency secondary to
mechanical obstruction and the release of inflammatory mediators in the pulmonary arterial
system.
• The majority result from blood clots in the pelvic and deep veins of the lower extremities,
but can also occur with amniotic fluid, fat, air, and septic emboli.
• Intraoperative and postoperative PE can result from venous stasis and inflammatory
mediators related to surgery. Additionally, the choice of anesthetic technique (general
versus regional) may have an impact on perioperative hypercoagulability. Epidural and
spinal anesthesia have been shown to have a decreased incidence of deep venous
thrombosis (DVT).
• DVT/PE is regarded as an avoidable and preventable event. Thus, anesthesia providers play
a role in implementing and ensuring that preventative measures are performed.
EPIDEMIOLOGY
Prevalence
Annual incidence for DVT is estimated to occur in 23–69 cases per 100,000 surgical cases.
Prevalence
• Varies depending on the population studied and coexisting diseases.
• PE has been documented in 15–55% of cases after autopsy (death from all causes).
Morbidity
PE may occur in up to 50% of patients with DVT.
Mortality
• In the US: 300,000 deaths annually.
• If undiagnosed and untreated within 1 hour, 10% of patients may die.
• Acquired factors:
– Obesity
– Pregnancy and post-partum period
– Estrogen use
– Surgery: Orthopedic (hip or knee), GI, gynecological, cancer.
– Age 40 years and older
– Trauma: Fractures (hip or leg).
– Spinal cord injury
– Malignancy: Secondary to chemotherapy, hormone therapy.
– Prolonged immobilization: Travel, surgery
– Central venous catheters
– Antiphospholipid antibody syndrome
– Polycythemia vera
• Hereditary factors:
– Protein C and S deficiency
– Antithrombin III deficiency
– Factor V Leiden
– Prothrombin gene mutation
– Dysfibrinogenemia
– Plasminogen deficiency
• Other factors:
– History of DVT, heparin-induced thrombocytopenia (HIT), varicose veins.
– Medical conditions such as: Congestive heart failure (CHF), arrhythmia, respiratory
failure, and inflammatory disease (bowel, rheumatoid arthritis).
• Mechanical obstruction: PE may have various degrees of obstruction within the pulmonary
circulation depending on the number and location of emboli. This can result in:
– Dead space ventilation (ventilation without perfusion)
– Increased right ventricular afterload
– Pulmonary infarct
• Inflammatory mediators: Additionally, obstructive material may set off an inflammatory
cascade that releases vasoactive products and serotonin. The effect is a constellation of:
– Pulmonary edema
– Shunting (impaired alveolar ventilation secondary to atelectasis) and hypoxemia
– Increased airway resistance (wheezing)
– Increased minute ventilation
– Decreased vital capacity
– Decreased diffusing capacity
– Tachycardia and hypotension
• In severe cases, right ventricular dysfunction and respiratory collapse may result secondary
to an elevation in wall tension, ventricular dilation, and ischemia. Cardiogenic shock and
myocardial ischemia may occur.
• Avoid prolonged immobilization
• Heparin/low-molecular-weight heparin (LMWH) may be administered
preoperatively/postoperatively. Since most antithrombotic drugs are renally excreted,
caution must be observed when administering to patients with renal dysfunction. LMWH
has a better therapeutic profile than unfractionated heparin (UFH) and may provide
superior DVT prophylaxis in high-risk surgical groups (trauma, hip, and knee replacement).
• Intermittent pneumatic compression devices and elastic stockings applied during the
perioperative period have shown benefit in patients with a moderate risk for DVT or with a
known contraindication for anticoagulation.
• An inferior vena cava (IVC) filter is indicated if there is a recent diagnosis of DVT/PE and
the patient is unable to receive anticoagulation.
• Utilize adjuvant therapies for pain management such as intravenous analgesics (PCA) or
local regional techniques (nerve blocks, epidural, spinal, and wound infiltration). Regional
techniques may control acute pain for hours to days depending on the technique used.
Epidural and spinal anesthesia may decrease the rates of DVT, likely as a result of
sympathetic blockade with improvement in circulation and decrease in hypercoagulability.
• Fat emboli occurrence can be minimized with early treatment of the underlying cause:
Surgical repair of long bone fractures, careful monitoring of fat content in total parenteral
nutrition infusions, and surgical repair of cardiac wall defects (PFO).
• Septic emboli must be ruled out in patients with persistent fever and positive blood cultures.
A search for the embolic source (e.g., heart valves) is important in guiding therapeutic
decisions.
• The risk of PE is ∼15 times higher in the postpartum period than during pregnancy, and is
likely related to venous stasis, alterations in circulating clotting factors (I, II, VII, VIII, IX,
and X), declines in protein S, increased platelet activation, and elevated fibrin production.
The therapeutic approach is the same as the non-pregnant patient.
• Amniotic fluid emboli prevention requires avoidance of any uterine trauma (surgical and
nonsurgical) or spontaneous rupture.
• Clinical findings include tachycardia, tachypnea, calf pain or swelling, cough, hemoptysis,
chest pain/pleural rub, increased jugular pressure, or syncope (lacking sensitivity and
specificity)
• Location: Central vascular zones include the main pulmonary artery, left and right main
pulmonary arteries, anterior trunk, right and left interlobar arteries, left upper lobe trunk,
right middle lobe artery, and right and left lower lobe arteries. Peripheral vascular zones
include the segmental and subsegmental arteries of the right upper lobe, right middle lobe,
right lower lobe, left upper lobe, lingula, and left lower lobe.
• Extent: A PE is considered to be massive when it involves both pulmonary arteries or results
in hemodynamic compromise.
• Pre-test risk stratification is important for diagnosis and treatment. The Wells (2) and
Geneva (3) scores factor in risk factors and clinical findings and may aid in guiding further
diagnostic work-up.
• Computerized tomography (CT) scan. A spiral chest CT scan produces a 3-D image by
rotating the scanner around the body in a spiral and has a greater sensitivity (and is
quicker) than plain CT imaging (2-D). Contrast material may be injected to provide
delineation of the pulmonary vasculature and improve definition of nonvascular structures
(CT angiogram). However, contrast may be harmful to the kidneys.
• Pulmonary angiography use is reserved for cases requiring a catheter-based treatment.
• Ventilation-perfusion (V/Q) lung scanning is an alternative to CT angiography if contrast
dye is a concern. Highly sensitive in patients without cardiopulmonary disease.
• Compression ultrasonography can detect proximal DVT in 20% of patients with PE; they
have a high sensitivity and specificity for proximal DVT of the lower extremities (evidence
grade A).
• Chest radiography is useful to rule out acute conditions such as hemothorax and
pneumothorax.
• Echocardiography is an alternative if the patient is too unstable for transport. TEE has a
sensitivity of 60–80% and specificity of 95–100%. TTE is useful in detecting right
ventricular dysfunction. Findings include abnormalities in ventricular wall motion,
ventricular dilation, paradoxical septal motion, tricuspid insufficiency, elevated pulmonary
artery pressure, and IVC congestion.
• PA catheter may be considered for management and differential diagnosis purposes.
• ECG may have an S1, Q3, T3 pattern consistent with acute cor pulmonale. Right bundle
branch block (RBBB) and right axis deviation may also be present. ECG findings in PE are
neither specific nor sensitive. Helpful in MI diagnosis during an acute hemodynamic crisis.
• Arterial blood gas analysis is useful to evaluate hypoxemia, hypercarbia, and can aid with
the differential diagnosis of PE.
• D-dimer levels: If there is a low pre-test probability, a negative test can be useful to rule out
a PE (strong negative predictive value).
TREATMENT
• Intravenous anticoagulation:
– Heparin enhances the activity of antithrombin III, which inhibits thrombin and other
factors such as Xa, IXa, XIa, and XIIa. Thrombin also inhibits factors V, VIII, and
thrombin-induced platelet activation. Initial treatment of PE and DVT consists of a heparin
bolus (80 U/Kg) with a maintenance dose (18 U/Kg); aPTT levels should be titrated to
1.5–2.5 times normal levels or a plasma concentration of 0.3–0.7 IU/L within 24 hours.
Current evidence suggests treatment for 5–6 days in combination with oral therapy
(evidence level A).
– LMWH are derived from heparin after chemical and enzymatic depolymerization to create
shorter compounds that have a decreased ability to combine with other molecules.
Enoxaparin 1 mg/kg SQ q12 hours or 1.5 mg/kg SQ QD can be used for the treatment of
PE and DVT (has been shown to be as effective as heparin for PE, and more effective for
DVT). LMWHs have the benefit of SQ administration, lower rates of HIT, and do not
require routine laboratory monitoring. If monitoring is necessary (obesity, pregnancy,
renal failure), anti-factor Xa levels are checked.
• Oral anticoagulation:
– Warfarin inhibits the enzymes that convert vitamin K epoxide to reduced vitamin K. The
initial dose for PE and DVT treatment is 5–10 mg daily with individual factors requiring
dose adjustments. INR levels should be titrated to a level of 2.0–3.0 for venous
thromboembolism (VTE) for 2 consecutive days prior to the discontinuation of heparin.
Treatment for 3 months is recommended for PE due to reversible causes (evidence level
A).
• Thrombolytic therapy (urokinase, streptokinase, alteplase) is indicated in proven cases of PE
with cardiogenic shock. They rapidly dissolve thrombus, but carry significant risk of
intracranial bleeding. It has the greatest benefit if used within 48 hours of the onset of
symptoms.
• Thrombin inhibitors: If HIT is suspected, consider therapy with argatroban, lepirudin, or
bivalirudin.
• Catheter-based pulmonary embolectomy and local intraembolic thrombolytic therapy can be
lifesaving. Surgical embolectomy can be considered in patients with free-floating thrombi in
the right atrium.
FOLLOW-UP
• Acute intraoperative PE should be suspected in any patient with a strong preoperative

history suggestive of DVT.
• Intraoperative TEE (transesophageal echocardiogram) may be helpful with the diagnosis of
PE.
REFERENCES
1. Konstantinides S. Clinical practice. Acute pulmonary embolism. N Engl J Med.
2008;359:2804–2813.
2. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside
without diagnostic imaging: Management of patients suspected of pulmonary embolism
presenting to the emergency department by using a simple clinical model and D-Dimer.
Ann Intern Med. 2001;135:98–107.
3. Le Gal G, Righini M, Roy PM, et al. Prediction of pulmonary embolism in the emergency
department: The revised Geneva score. Ann Intern Med. 2006;144:165–171.
4. Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008;358:1037–1052.
5. Hirsch J, Guyatt G, Albers GW, et al. Antithrombotic and thrombolytic therapy: American
College of Chest Physicians (ACCP) Evidence-Based Clinical Practice Guidelines Executive
Summary. Chest. 2008;133:71S–105S.
• Dead space
• D-dimer
CODES
ICD9
415.19 Other pulmonary embolism and infarction
ICD10
I26.99 Other pulmonary embolism without acute cor pulmonale
CLINICAL PEARLS
• Diagnosis and treatment of PE requires a high index of suspicion and rapid risk
stratification.
• Hemodynamically unstable patients require immediate evaluation to exclude sepsis,
hypovolemia, and new onset arrhythmia. If the initial assessment is negative, they are
regarded as high risk for PE.
• Prevention is essential in hospitalized patients with the use of heparin, LMWH, warfarin,
and/or sequential compression devices.
PULMONARY FUNCTION TESTS
BASICS
DESCRIPTION
• Pulmonary function tests (PFTs) measure lung volumes, airflow, and diffusing capacity of
gas across the alveolar–capillary membrane (DLCO).
• Lung volumes and capacities refer to the volume of air associated with different phases of
the respiratory cycle.
FIGURE 1. Lung volumes and capacities.
• Lung volumes are directly measured. They include:

– Tidal volume (TV), inspiratory reserve volume (IRV), expiratory reserve volume (ERV),
and residual volume (RV).
• Lung capacities are composed of one or more lung volumes. They include:
– Inspiratory reserve capacity (IRC), vital capacity (VC), total lung capacity (TLC), and
functional residual capacity (FRC).
• Forced expiratory spirometry measures expiratory flow and volume while the patient
forcefully exhales after maximal inhalation.
FIGURE 2. Forced expiratory spirometry.
• TV: Volume of air inspired with passive breathing.
– Normal TV: ∼6–8 mL/kg
– TV decreases with decreased lung compliance and/or reduced ventilatory muscle strength.
• IRV: Maximal volume of air that can be additionally inspired after a normal tidal
inspiration.
– Normal IRV: ∼1.9–3.3 L
• ERV: Maximum volume of air forcibly expired after a normal tidal expiration.
– Normal ERV: ∼0.7–1 L
• RV: Volume of air remaining in the lungs after forceful expiration. It cannot be exhaled, and
hence cannot be measured on routine spirometry.
– Normal RV: ∼1 L
• Inspiratory capacity (IC): Volume of air inspired with maximum lung expansion after resting
expiration.
– IC = IRV + TV (normal ∼2.5 − 3.5 L)
– Reduced IC can signify extrathoracic airway obstruction.
• FRC: Volume of gas remaining in the lungs after passive expiration.
– FRC = ERV + RV (normal ∼1.8 − 2.3 L)
– FRC influences the ventilation–perfusion relationship within the lung.
– Reduced FRC leads to an increase in venous admixture and arterial hypoxemia.
– Indirect determination of FRC (because RV cannot be measured on spirometry).
Equilibration method: FRC is calculated by the equilibration of a tracer gas (helium) in a
closed-circuit system. Using a spirometer and starting at FRC, the patient breathes a
given concentration of helium and oxygen. Helium equilibrates between the patient’s
lungs and the spirometer. Since the system is closed, FRC can be determined by
(Concentration1 × Volume1) = (Concentration2 × Volume2).
Washout method: FRC is calculated from the washout of a tracer gas (nitrogen) within
the lungs. The patient breathes 100% oxygen for several minutes to “wash out” alveolar
nitrogen. Nitrogen fractional concentration and expired volume is measured over 7
minutes. The initial and final alveolar nitrogen fractional concentrations and the
nitrogen concentration in the collected expirate are used to calculate FRC.
Plethysmography: The patient sits in a box with a pressure transducer and breathes
through a mouthpiece. The mouthpiece is connected to an electronic shutter and a
differential pressure pneumotachometer. Mouth pressure and box pressure changes are
measured during tidal breathing and panting maneuvers. The differential pressures are
used to calculate thoracic gas volume and FRC.
• VC: The maximum volume of air that can be exhaled after maximal inspiration.
– VC = IRV + TV + ERV (normal ∼60 mL/kg)
– VC correlates with the ability for deep breathing and effective coughing.
• TLC: The volume of air within the lungs after maximum inspiratory effort.
– TLC = IRV + TV + ERV + RV (normal ∼ 5 L)
• Forced vital capacity (FVC): The volume of air exhaled with maximal expiration after
maximal inspiration.
– FVC normally equals VC.
– FVC measurements are dependent on patient effort and cooperation.
• Forced expiratory volume in 1 second (FEV1): The volume of air exhaled forcefully in the
first second of an FVC maneuver.
– Measure of flow (volume expired over time).
– Dependent on patient effort. Low FEV1 may be a result of inadequate effort, not lung
disease.
• FEV1/FVC: Normalizes FEV1 measurements to the patient’s individual lung volume.
– Normal FEV1/FVC ≥ 0.75; the volume of air that is expired in 1 second should be 75% of
the forced vital capacity.
• Forced midexpiratory flow rate (FEF25-75%): Exhaled volume between 25% and 75% of FVC.
– Formerly called the maximum midexpiratory flow rate (MMFR).
– Less effort dependent than FEV1 or FVC, but may be reduced by submaximal inspiration
(decreased FVC) or markedly decreased expiratory effort.
– Normal values vary widely due to the dependence on FVC. Both the absolute value
(normal ∼ 2–5 L/sec) and the percentage of predicted value (normal ∼ 100% ± 25%)
are recorded.
• Diffusing capacity (DLCO): Measures the diffusion of carbon monoxide (CO) across the
alveolar–capillary membrane. Diffusion capacity is determined by measuring the partial
pressure difference between inspired and expired CO.
– DLCO reflects the diffusing capacity of physiologic gases, such as oxygen and carbon
dioxide.
• Maximum voluntary ventilation (MMV): Largest volume that can be breathed in 1 minute by
voluntary effort.
– MMV records the patient breathing as rapidly and deeply as possible for 10 seconds by a
pneumotachograph and the results are extrapolated to 1 minute.
– Best indicator of ventilatory muscle endurance.
• Obstructive lung disease: Asthma, chronic bronchitis, emphysema, bronchiolitis, and chronic
obstructive pulmonary disease (COPD).
– Diminished expiratory airflow from collapse of small airways.
Decreased FEV1/FVC and FEF25-75%.
– Airway collapse during expiration causes air trapping with subsequent hyperinflation.
Increased TLC, FRC, RV.
• Restrictive lung disease: Intrinsic and extrinsic pulmonary processes.
– Intrinsic (loss of alveolar airspace): Pulmonary fibrosis, sarcoidosis, or pneumonia.
– Extrinsic (reduction of lung space): Scoliosis, disorders of thoracic cage, pleural effusion,
pneumothorax, or neuromuscular disorders.
– Smaller lung volumes along with normal or decreased expiratory flow (decreases to a
lesser extent than volume).
Normal or increased FEV1/FVC and FEF25-75%
– Reduction of all lung volumes, especially TLC, VC, and RV.
• Compromise of alveolar capillary unit: Loss of lung parenchyma (emphysema or COPD),
thickening of the alveolar–capillary membrane (interstitial lung disease or pulmonary
fibrosis), or pulmonary vascular disease.
– Reduction of DLCO
• Patients undergoing general anesthesia and surgical procedures (particularly thorax and
upper abdomen) develop changes in pulmonary function that may contribute to
– VC is reduced up to 25–50% of preoperative values after open thorax or upper abdominal
procedures and remains depressed for 10–14 days.
– FRC decreases by 10–15% in the supine position.
• The primary goal of preoperative PFTs is to recognize patients at high risk of postoperative
pulmonary complications.
– Reduced FVC values (<15 mL/kg) are associated with postoperative pulmonary
complications (1).
Most commonly seen in quadriplegics or severe neuromuscular disease.
Reduced FVC is associated with ineffective cough and development of atelectasis.
• PFTs provide some predictive benefit in patients undergoing lung resection.
– Predicted postoperative FEV1 calculated by multiplying the preoperative FEV1 by the
percentage of lung tissue expected to remain after resection. An increased risk of
perioperative pulmonary morbidity is associated with a predicted postoperative FEV1
<30% (2).
EQUATIONS
• IC = TV + IRV; where IC is inspiratory capacity, TV is tidal volume, and IRV is inspiratory
reserve volume
• FRC = ERV + RV
• VC = IRV + TV + ERV; where VC is vital capacity, ERV is expiratory reserve volume, and
IRV is inspiratory residual volume
• TLC = VC + RV; where TLC is total lung capacity, VC is vital capacity, and RV is residual
volume
REFERENCES
1. Qaseem A, Snow V, Fitterman N, et al. Risk assessment for and strategies to reduce
perioperative pulmonary complications for patients undergoing noncardiothoracic surgery:
A guideline from the American College of Physicians. Ann Int Med. 2006;144(8):575–580.
2. Bapoje SR, Whitaker JF, Schulz T, et al. Preoperative evaluation of the patient with
pulmonary disease. Chest. 2007;132(5):1637–1645.
3. Task force on preanesthetic evaluation. Practice advisory for preanesthesia evaluation: A
report by the American Society of Anesthesiologists. Anesthesiology. 2002;96(2):485–496.
ADDITIONAL READING
• Stock MC. Respiratory Function in Anesthesia. In: Barash PG, ed. Clinical Anesthesia. 5th ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2006:804–807.
CLINICAL PEARLS
• Preoperative PFTs help clinicians diagnose previously unknown lung diseases and allow the
assessment of the severity of known lung diseases.
• While PFTs are well established in the preoperative workup of patients undergoing
pulmonary resections, it is not recommended for routine preoperative evaluation (3).
• PFTs should not be used in isolation to determine if a patient is ineligible for surgical
intervention. Rather, it should be utilized in conjunction with other assessments of
cardiopulmonary functions such as history, physical examination, exercise testing, arterial
blood gas analysis, chest radiography, ventilation–perfusion scintigraphy, and split-lung
function studies as indicated.
PULMONARY HEMORRHAGE
Gerard R. Manecke Jr., MD
BASICS
DESCRIPTION
• Pulmonary hemorrhage is a life-threatening emergency characterized by severe, acute lung
bleeding. It may cause gas exchange problems, airway obstruction, and hemodynamic
compromise.
• In the perioperative period, it:
– May be present as a medical emergency in which an anesthesia provider is asked to assist
airway management.
– May occur intraoperatively as an acute process or complication (surgery, pulmonary
artery catheterization, airway management).
EPIDEMIOLOGY
Prevalence
Rare complication that is reported in <1% of anesthetics
Prevalence
• Ongoing pulmonary hemorrhage is very rare (it either resolves, is treated successfully, or the
patient succumbs to it).
• Conditions predisposing to it, such as fungal infection or tuberculosis (TB) are rare, with the
prevalence dependent upon the specific population.
Morbidity
• Blood or clot in the airway may cause airway/endotracheal tube obstruction.
• Blood loss may cause hypovolemia or hemorrhagic shock.
Mortality
High and can exceed 50% depending upon the etiology as well as the timeliness and
effectiveness of treatment.
• Pulmonary infection
– Cavitary TB (“Rasmussen’s aneurysm”)
– Fungal infection
• Bronchiectasis
• Wegener’s granulomatosis: A vasculitis affecting the nose, ears, kidneys, and lungs.
• Goodpasture’s syndrome: An autoimmune disease affecting the kidneys and lungs.
• Hydrostatic gradient bleeding
– Negative pressure in airway obstruction (1)[C]
– Severe acute pulmonary hypertension
• Pulmonary vessel trauma
– Thoracic trauma
– Pulmonary artery catheter (PAC) placement
• Diffuse pulmonary hemorrhage results from:
– Infectious processes with widespread pulmonary capillary or arterial breakdown (e.g.,
capillaritis).
– Large pulmonary capillary–alveolar hydrostatic gradient (severe pulmonary hypertension,
negative pressure from airway obstruction).
• Localized bleeding usually results from trauma, with the exception of cavitary infections
such as TB.
– Pulmonary artery rupture
– Complication of pulmonary thromboendarterectomy (2)[C]
• PACs must be used with care.
– “Wedge” the catheter only for good reason.
– Withdraw the catheter 1–2 cm prior to inflating the balloon.
– Remove the catheter gently, as there have been case reports of accidental suturing to the
PA wall during cardiac surgery. General rule: If something is not easy to remove, do not
use force!
• Blood appears in the airway
– Dark blood usually indicates pulmonary arterial bleeding.
– Bright red blood usually indicates bronchial (systemic) arterial bleeding.
• History and records may reveal:
– History of fungal or tuberculous infection
– Recent chest trauma
– Recent PAC placement
– Difficult removal of a double lumen endobronchial tube after pneumonectomy (may have
been accidentally sutured in place during surgery)
– Difficult pulmonary thromboendarterectomy with disruption/perforation of a pulmonary
artery (2)[C]
• Fiberoptic bronchoscopy (FOB) is recommended to determine the source of bleeding (diffuse
vs. lobar process, left vs. right). It may be necessary to perform a rigid bronchoscopy when
the flexible scope is inadequate.
• Pulmonary edema with severe capillary leak may have a hemorrhagic component.
• GI bleeding (hematemesis)
• Nasopharyngeal or oropharyngeal bleeding
TREATMENT
• Supportive modalities:
– Control the airway with placement of an endotracheal tube. Use the largest ETT feasible to
allow for effective suctioning and bronchoscopy.
– Provide oxygen and ventilation.
– Positive airway pressure (e.g., PEEP) may help tamponade bleeding.
– Consider lung isolation to keep the bleeding localized and preserve gas exchange in
uninvolved lung segments (maintain V/Q matching).
Double lumen endobronchial tubes are excellent for lung isolation. However, suctioning
and FOB may be difficult because of the smaller lumens. In addition, if an endotracheal
tube is already in place, it should only be removed with great caution; airways may be
edematous and intubation may become difficult or impossible, even with exchange
catheters.
Bronchial blocker (ArndtTM, UniventTM, Fogarty catheter). However, it is not feasible to
maintain lung isolation while performing a bronchoscopy or suctioning.
– Correct coagulopathy if it is present.
– Transfuse red blood cells as necessary
• Therapeutic modalities
– Consider topical vasoconstrictor; can be delivered either via an endotracheal tube or
locally via FOB.
Vasopressin (2 U/mL, 20 mL)
Phenylephrine (100 mcg/mL, 20 mL)
Epinephrine (5 mcg/mL, 20 mL)
– Embolization of the bleeding bronchial artery or balloon occlusion of the pulmonary
artery may be performed by interventional radiologists (4)[C].
– Consider lung resection or pneumonectomy for localized bleeding refractory to other
treatments.
FOLLOW-UP
• After bleeding resolves, the assistance of the anaesthetist may be required for:
– Removal of the bronchial blocker
– Exchange of double lumen tube with a single lumen endotracheal tube
– Weaning from mechanical ventilation and extubation
CLOSED CLAIMS DATA
• Since it is rare, there are few closed claims data on pulmonary artery hemorrhage during
anesthesia.
– 2 cases of pulmonary artery rupture from PAC out of a total of 3,533 claims in the ASA
Closed Claims Database: http://depts.washington.edu/asaccp/ASA/index.shtml
REFERENCES
1. Dolinski SY, MacGregor DA, Scuderi PE. Pulmonary hemorrhage associated with negative-
pressure pulmonary edema. Anesthesiology. 2000;93:888–890.
2. Manecke GR Jr, Kotzur A, Atkins G, et al. Massive pulmonary hemorrhage after pulmonary
thromboendarterectomy. Anesth Analg. 2004;99:672–675.
3. Huang GS, Wang HJ, Chen CH, et al. Pulmonary artery rupture after attempted removal of
a pulmonary artery catheter. Anesth Analg. 2002;95:299–301.
4. Dopfmer UR, Braun JP, Grosse J, et al. Treatment of severe pulmonary hemorrhage after
cardiopulmonary bypass by selective, temporary balloon occlusion. Anesth Analg.
2004;99:1280–1282.
5. Carron H, Hill S. Anesthetic management of lobectomy for massive pulmonary
hemorrhage. Anesthesiology. 1972;37:658–659.
ADDITIONAL READING
• Manecke GR Jr, Kotzur A, Atkins G, et al. Massive pulmonary hemorrhage after pulmonary
thromboendarterectomy. Anesth Analg. 2004;99:672–675.
CODES
ICD9
786.30 Hemoptysis, unspecified
ICD10
R04.89 Hemorrhage from other sites in respiratory passages
CLINICAL PEARLS
• Pulmonary hemorrhage is life-threatening; asphyxia is the most common cause of death.
• The most common causes are infection and pulmonary vessel trauma.
• Impaired gas exchange leading to hypoxia and hypercarbia along with airway obstruction is
common.
• Diagnosis often involves FOB to localize the source of bleeding.
• Treatment often involves tracheal or endobronchial intubation, continuous airway pressure,
topical vasoconstrictors, and bronchial blockade.
PULMONARY HYPERTENSION
Nirvik Pal, MD
Anand Lakshminarasimhachar, MBBS, FRCA
BASICS
DESCRIPTION
• Pulmonary hypertension (PH) is defined as a mean pulmonary artery pressure > 25 mm Hg.
Pulmonary artery hypertension is also defined as pulmonary vascular resistance (PVR) > 3
Wood units (240 dynes s/cm5) (1). It can result from chronic disturbances or diseases in
pulmonary venous and arterial pressures, cardiac output, or left atrial pressures.
– Primary PH: Due to intrinsic pathology of reactive pulmonary vasculature.
– Secondary PH: As a result of some other primary pathology of lung, heart, or systemic
diseases.
• The pulmonary vasculature is often responsive to hypoxia, hypercarbia, acidosis, and
noxious stimuli such as airway instrumentation or suctioning; in PH, it may be
hyperreactive. Increased pulmonary artery pressures can result in RV dysfunction, ischemia,
and failure, as well as systemic hypotension, and cardiac arrest.
EPIDEMIOLOGY
Prevalence
• New cases of primary PH in the US: ∼300/year
• New cases of secondary PH in the US: ∼1,000/year
Prevalence
• Primary PH in the US: 1:906,666
• Secondary PH in the US: 1:272,000
Morbidity
Increased incidence of prolonged intubation, ICU stay, and length of hospital stay
Mortality
Higher perioperative mortality in both cardiac and non-cardiac surgeries due to the increased
incidence of pulmonary embolism, heart failure, deep vein thromboses, ARDS, etc.
See classifications
• Resistance = pressure/flow (1)
– Therefore, PVR = (PAP − LAP)/CO
– Alternatively, PAP = LAP + (CO * PVR), where PVR is pulmonary vascular resistance,
PAP is pulmonary artery pressure, LAP is left atrial pressure, CO is cardiac output
• Depending upon the etiology, PH may result from a rise in the left atrial pressure, right
heart blood flow, pulmonary vascular resistance, or a mix of these conditions.
• Increased left atrial pressure (as may be seen with left ventricular failure, long-standing
mitral stenosis, or severe mitral regurgitation) increases the “afterload” of the pulmonary
vasculature.
• Increased right heart blood flow, from “shunting” or “mixing” cardiac lesions (atrial septal
defect, ventricular septal defect) increases flow through the pulmonary vasculature with a
resultant increase in pulmonary pressure.
• Increased PVR or pulmonary arterial hypertension (PAH) can result from vasoconstriction,
cellular proliferation, thrombosis, and apoptosis in pulmonary arteries. At a molecular level,
this is often mediated by nitric oxide, endothelin, prostacyclin, serotonin pathways, or
genetic constitution like BMPR2, ALK-1, or 5-HTT mutations.
• With time, PH results in right ventricular hypertrophy or dilation, followed by dysfunction
or failure due to:
– High RV afterload
– RV ischemia from hypoperfusion during systole (normally RV perfusion happens both in
systole and diastole) due to elevated PA pressure
– Systemic hypotension from interventricular septal shifting of the dilated RV that leads to
restricted LV filling
• The anaesthetist needs to be aware of the underlying pathophysiology and severity of the
disease, as well as assess if the patient is currently optimized. The RV status should be
determined and the use of pulmonary vasodilators may be necessary.
• Perioperative goals include avoidance of hypoxia, hypercarbia, coughing, and bucking
during induction or emergence; in addition, appropriate volume status, cardiac output, and
systemic BP need to be maintained.
• In PH, TPG = mPAP – PCWP; where TPG is transpulmonary gradient, mPAP is mean
pulmonary artery pressure, and PCWP is pulmonary capillary wedge pressure. If the TPG
>12 mm Hg, PH may be due to high PVR; if the TPG <12 mm Hg, PH may be due to left
heart failure.
SYMPTOMS
• Fatigue, weakness
• Dyspnea
• Angina can result from an imbalance in oxygen supply and demand
History
• Palpitations from arrhythmias
• Syncopal events from hypotension or arrhythmias (due to dilated heart chambers)
Signs/Physical Exam
• Edema from RV or LV failure
• Jugular venous distension
• Clubbing may indicate congenital heart disease or chronic lung disease
• Cyanosis
TREATMENT HISTORY
• Medication pump installed to continuously deliver pulmonary vasodilators
• Lung transplantation (or awaiting one)
MEDICATIONS
• Anticoagulation: Perioperative management should be discussed with the surgeon and
primary physician. In addition, it may preclude neuraxial anesthesia.
• Diuretics can affect electrolytes and volume status
• Contraception: Severe PH is considered unsafe for labor and delivery.
• Calcium channel blockers provide systemic and pulmonary vasodilation; may be useful in
reversible PH
• Phosphodiesterase inhibitors (PDE-5i)
• Endothelial receptor antagonist (ETRA)
Labs/Studies
• Autoantibody tests: Scleroderma, SLE, RA, vasculitis
• Liver function tests: May be elevated from hepatic congestion
• Chest radiograph: May show emphysema or prominent lung vasculature
• EKG: RV enlargement, right axis deviation, right heart strain pattern
• Echocardiogram: Right ventricular function, congenital heart disease
• Pulmonary function tests: Chronic lung disease
• Sleep study: Obstructive sleep apnea
• V/Q scan: Chronic thromboembolic disease
• Right heart catheterization can reveal the status of the RV function, PA pressures, and
congenital heart lesions.
• Left heart catheterization for LV function and transpulmonary gradient. Vasodilator tests can
show the reversibility of PH and is performed during catheterization using inhaled
prostaglandin or nitric oxide; utilized to help plan subsequent therapy.
• Liver dysfunction
• Left heart disease
• Arrhythmias from dilated chambers
Acute RV ischemia, dysfunction, or failure
CLASSIFICATIONS
• World Health Organization classification of PH (Venice, 2003) (2):
– (I) Pulmonary hypertension: Idiopathic, familial, associated with diseases (congenital
heart disease, collagen vascular disease, portal hypertension, HIV, drugs, toxins)
– (II) PH secondary to left heart disease: Left-sided hypertension or ventricular heart
disease.
– (III) PH secondary to lung disease with or without hypoxemia: Interstitial lung disease,
chronic obstructive pulmonary disease, sleep-disorders, alveolar hypoventilation disease,
chronic exposure to altitude
– (IV) PH secondary to thrombotic or embolic disease: Thromboembolic obstruction of the
proximal or distal pulmonary arteries
– (V) Miscellaneous: Sarcoidosis, histiocytosis X
TREATMENT
Premedications
• Sedation can result in hypoxia or hypercarbia and exacerbate PH; if used, judicious
administration, supplemental oxygen, and pulse oximetry is recommended.
Postoperative intubation should be discussed
INTRAOPERATIVE CARE
• Sedation
• Regional: Platelet inhibition may result from systemic pulmonary vasodilators like
prostacyclin
Monitors
• Arterial line placement for beat-to-beat BP monitoring and frequent ABGs; consider placing
pre-induction
• Central line placement for measurements of central venous pressures that can reflect
changes in PAP, RV, or LA pressures
• Pulmonary artery catheter may be indicated in severe disease, or when the underlying cause
is due to left heart disease
• TEE depending on the complexity of surgery
• Sedation should implement supplemental oxygen via nasal cannula, face mask, or non-
rebreather as appropriate.
• Regional techniques should implement supplemental oxygen if sedation is given; neuraxial
techniques can result in sympatholysis and should be dosed appropriately. Epidural
catheters allow for slow bolusing and time to treat hemodynamic changes. Balance the need
for preoperative fluid boluses with the potential for CHF.
• General anesthesia: A laryngeal mask airway (LMA) may be used, but has the potential for
hypercarbia; consider pressure support modes to maintain volumes. Endotracheal tube
(ETT) allows for greater control of ventilatory parameters, and is often chosen.
• Avoid hypotension with induction; consider etomidate (avoid ketamine), high dose narcotic
technique, concurrent inotropic or vasopressor treatment. Avoid hypercarbia with adequate
bag mask ventilation. Avoid hypoxia by appropriately pre-oxygenating, limiting duration of
laryngoscopy. Avoid noxious responses to airway instrumentation by ensuring that the
patient is adequately induced prior to any airway instrumentation. Avoid nitrous oxide as it
can increase pulmonary vascular resistance.
Maintenance
• Ventilation strategy is aimed at avoiding hypoxia, hypercarbia, and increased thoracic
pressures (3).
– Tidal volumes: Maintaining ventilation at optimal functional residual capacity is essential.
Tidal volumes that are too high or too low may lead to increased PVR either due to
compression of overdistended alveoli or atelectasis.
– PaCO2: Maintain at normal or mild alkalosis by increasing RR or TV; weigh against the
potential to increase mean pulmonary pressures
– PaO2: Increase FIO2, PEEP to reduce atelectasis (need to balance PEEP levels against the
increase in thoracic pressures).
• Inhaled pulmonary vasodilators (nitric oxide, prostacyclin [PGI2]) are often preferred to
systemic vasodilators as these agents have the added benefit of maintaining hypoxic
pulmonary vasoconstriction. Since they are delivered via the inhalation route, they only
vasodilate vessels that are perfusing ventilated alveoli; which prevents desaturation by
avoiding pulmonary blood flow to non-ventilated areas of the lung.
• Maintain systemic BP for adequate RV perfusion.
• Careful monitoring of RV function; reductions may require the use of inotropic drugs such as
phosphodiesterase inhibitors that bestow inotropy with afterload reduction (e.g., milrinone).
Dobutamine and dipyridamole may also be utilized.
• Prevent and treat metabolic acidosis.
• Maintain an adequate level of anesthesia and analgesia to blunt sympathetic or stress
responses.
• Fluid administration needs to be monitored as excess fluid may precipitate ventricular
failure and pulmonary edema.
Coughing, bucking, bearing down can result in excessive pulmonary pressures. Deep
extubation with continued ventilatory support via bag mask may be considered to avoid this.
FOLLOW-UP
BED ACUITY
• Bedside telemetry at a minimum is usually needed.
• ICU/HDU care may be necessary in severe disease, intraoperative events, inotropic support,
or pulmonary vasodilator treatment.
• Pulmonary and/or cardiology consult; consider having a discussion with the patient’s
specialist who is managing their disease prior to the procedure to discuss any
recommendations and establish good follow-up.
• Inhaled vasodilators (nitric oxide or prostacyclin)
REFERENCES
1. ritts CD, Pearl RG. Anesthesia for patients with pulmonary hypertension. Curr Opin
Anesthesiol. 2010;23:411–416.
2. McLaughlin V, McGoon M. Pulmonary artery hypertension. Circulation. 2006;114:1417–
1431.
3. Blaise G, Langleben D, Hubert B. Pulmonary arterial hypertension: Pathophysiology and
anesthetic approach. Anesthesiology. 2003;99:1415–1432.
4. Farber H, Loscalzo J. Pulmonary artery hypertension. N Engl J Med. 2004;352:1655–1665.
5. Hoeper MM, Barbera JA, Channick RN, et al. Diagnosis, assessment and treatment of non-
pulmonary arterial hypertension pulmonary hypertension. J Am Coll Cardiol.
2009;54(suppl 1):S85–S96.
6. Memtsoudis SG, Ma Y, Chiu YL, et al. Perioperative mortality in patients with pulmonary
hypertension undergoing major joint replacement. Anesth Analg. 2010;111(5):1110–1116.
7. Ramakrishna G, Sprung J, Ravi BS, et al. Impact of pulmonary hypertension on the
outcomes of noncardiac surgery. J Am Coll Cardiol. 2005;45(10):1691–1699.
8. Reich DL, Bodian CA, Krol M, et al. Intraoperative hemodynamic predictors of mortality,
stroke, and myocardial infarction after coronary artery bypass surgery. Anesth Analg.
1999;89:814–822.
9. Van Wolferen S, Marcus JT, Boonstra A, et al. Prognostic value of right ventricular mass,
volume, and function in idiopathic pulmonary arterial hypertension. Eur Heart J.
2007;28:1250–1257.
CODES
ICD9
• 416.0 Primary pulmonary hypertension
• 416.8 Other chronic pulmonary heart diseases
ICD10
• I27.0 Primary pulmonary hypertension
• I27.2 Other secondary pulmonary hypertension
CLINICAL PEARLS
• A thorough understanding of the underlying pathophysiology, severity, and current
treatment of PH.
• Maintain systemic BP.
• Reduce pulmonary artery pressure.
• Monitor right ventricle function.
PULMONARY VASCULATURE
Ali Salehi, MD
BASICS
DESCRIPTION
• The pulmonary vasculature is a vascular bed that delivers non-oxygenated blood from the
right ventricle to the lungs, facilitates gas exchange at the alveolar level, and delivers
oxygenated blood to the left atrium.
• It is a high-flow, low-pressure system. Pulmonary vascular endothelium is exposed to the
whole cardiac output (CO) and has a surface area of 200 m2. Compared to the systemic
circulation, its resistance is lower secondary to a higher compliance of peri-capillary
pulmonary arterioles (thinner media, fewer smooth muscle cells). Normal pulmonary artery
pressure (PAP) is 1/5th that of systemic arterial pressure (SBP).
• Histologically, like all other vessels, pulmonary vessels consist of 3 layers: Intima
(endothelium), media (smooth muscle), and adventitia.
• Oxygenation: Although gas exchange can theoretically occur in any pulmonary vascular
wall, under normal conditions, little O2 and CO2 exchange occurs before the true pulmonary
capillaries. As blood enters the capillary bed, it loses velocity because of a sudden increase
in the overall surface area from arterioles (1 m2) to capillaries (50–70 m2), though it is still
pulsatile due to the low vascular resistance. The capillary network has considerable length,
crossing several alveoli of the terminal respiratory unit before forming a venule. The length
of the capillary network, together with the large surface area of the pulmonary capillary
bed, provides reasonable transit time (~0.5–1 seconds) for the red blood cells. This allows
sufficient time for equilibrium between oxygen and carbon dioxide tensions to occur in the
alveoli and the capillary bed.
• Reservoir: Functions as a reservoir between the right and left heart. There is sufficient blood
volume in the pulmonary vascular bed to enable moderating the changes in right
ventricular output over 2–3 beats.
• Blood filter: 75% of the circulating blood is in the venous system; the pulmonary
microvasculature is the first vascular bed that blood flows through. A moderate amount of
microemboli have no detectable effect on the pulmonary vascular bed due to the presence
of multiple parallel pathways in the microcirculation.
• Physiologic factors:
– CO: Increases in the CO recruit previously closed vessels and distend open vessels with a
resultant increase in the overall pulmonary vascular surface area and decrease in the PVR.
– Ventilation: PVR is at its maximum with small lung volumes (constriction of extra-alveolar
vessels) as well as large lung volumes (compression of alveolar vessels). PVR is at its
minimum at the functional residual capacity (FRC). This results in a “U”-shape
relationship between PVR and lung volumes.
– Alveolar oxygen: Increases in alveolar oxygenation result in pulmonary vasodilatation,
whereas alveolar hypoxia results in pulmonary vasoconstriction (hypoxic pulmonary
vasoconstriction; HPV). HPV serves to divert blood flow from poorly ventilated areas of
the lung to the better ventilated areas, which improves the ventilation/perfusion
matching.
– CO2 and pH: CO2 exerts no direct effect on the pulmonary vasculature, but increases the
hydrogen ion concentration. Decreasing the pH results in pulmonary vasoconstriction and
increased PVR.
– Autonomic nervous system: Pulmonary vasculature shows less vasomotor response to
autonomic stimulation than the systemic vasculature.
• Pulmonary vasodilators: Pulmonary vascular endothelium mediates smooth muscle tone,
pulmonary vascular resistance (PVR), and PAP in response to different stimuli through
vasodilator and vasoconstrictor activity. Vasodilators include:
– Nitric oxide (NO) synthase activity converts L-arginine to L-citrulline and releases NO. NO
diffuses to pulmonary vascular smooth muscle where it increases the activity of guanylate
cyclase which converts guanosine triphosphate (GTP) to cyclic guanosine monophosphate
(cGMP) and increases the cytoplasmic levels of cGMP. cGMP mediates relaxation of
vascular smooth muscle and vasodilatation. Phosphodiesterase-5 (PDE-5) catalyzes the
breakdown of cGMP, thus limiting the duration of vasodilatation.
– Activation of cyclooxygenase enzyme results in the production of prostacyclin (PGI2) from
arachidonic acid. PGI2 diffuses to smooth muscles (SMCs) and upregulates the activity of
adenylate cyclase and conversion of adenosine triphosphate (ATP) to cyclic adenosine
monophosphate (cAMP). cAMP mediates relaxation of vascular smooth muscle (SM) and
vasodilatation.
– Phosphodiesterase-3 (PDE-3) catalyzes the breakdown of cAMP and limits the time of
vasodilatation. It has been shown that PDE-3 is inhibited by cGMP.
– Cyclic nucleotides activate specific protein kinases which decrease the influx of Ca++ into
the SM and decrease the sensitivity of the SM contractile apparatus to Ca++.
• Pulmonary vasoconstriction is mediated via several mechanisms: Prostaglandin F2α and
Prostaglandin A2; endothelin stimulates production of growth factors; serotonin promotes
smooth muscle proliferation and hyperplasia; angiotensin binds AT1 receptors, increasing
intracellular calcium and stimulating protein kinase C (7).
ANATOMY
• The main pulmonary artery divides at the level of the sternal notch to the left and right
branches entering the relative hilum. Each pulmonary artery then divides into lobar arteries
which accompany the corresponding bronchi. Subsequently, the lobar arteries and bronchi
branch into segmental arteries and bronchi followed by arterioles and end in alveolar
capillaries.
• The alveolar capillaries are lined with non-fenestrated endothelial cells. The overall surface
area of the capillary endothelium is 130 m2. Water and solutes pass through the capillary
bed through receptor-mediated uptake or transcellular transport. The latter is usually
restricted by tight junctions.
• Two pulmonary veins (superior and inferior) on each side carry the oxygenated blood from
the lungs to the left atrium. They run independently of the arteries and the bronchi in the
lungs.
• Due to high PVR in utero, only 5–10% of the right ventricular CO goes through the lungs and
the remainder is diverted into the systemic circulation through the patent ductus arteriosus
(PDA). After birth and the first breath, NO and PGI2 are released in response to increased
oxygen levels and the productions of ATP from the oxygenated red blood cells. This results
in a rapid drop in PVR and a 10-fold increase in pulmonary blood flow along with the
closure of the patent foramen ovale (PFO) and the PDA.
• Pulmonary edema occurs when fluid enters the alveoli faster than it is removed and can
result in impaired gas exchange and hypoxemia. The Starling equation cites the factors that
govern fluid transit in the lungs. The driving force for fluid filtration in the lungs is the
balance between the transmural hydrostatic pressures (Pc–Pi) and the colloid osmotic
pressures (πc–πi). The actual amount of filtrate that is produced depends on the integrity of
the barrier to filtration (Lp) and reflection (σd) coefficients. The safety factors that protect
the lungs from edema include the lung lymphatic system, resorption into blood vessels,
drainage into the mediastinum and pleural space, and active transport by alveolar and distal
airway epithelial cells.
– Pulmonary edema results from increases in driving pressures (increased pressure edema),
barrier conductance (increased permeability edema), or both. Barrier permeability
differentiates the two and is normal in increased pressure edema and abnormal in
increased permeability edema.
– Increased lung microvascular hydrostatic pressure can result from left ventricular
dysfunction, mechanical obstruction of left atrial outflow (mitral stenosis), volume
overload, pulmonary venous hypertension, or increased lymphatic outflow pressure.
– Re-expansion pulmonary edema can be seen in patients with a collapsed lung
(pneumothorax, hemothorax) after placement of chest tube and removal of air and fluid,
or in patients undergoing thoracic surgery and lung isolation. This is thought to be due to
the generation of negative intrathoracic pressure and ischemia-reperfusion injury. Upon
reperfusion, not only are free radicals and inflammatory mediators released, which
increase the permeability of the basement membrane, but PVR also shifts more toward the
postcapillary venules and increases hydrostatic pressure in the capillary bed.
• Endothelial dysfunction: Inflammation, acidosis (in the setting of infection), hypoxemia,
increased CO (pregnancy, anemia, hyperthyroidism), and elevated pressures (left ventricular
failure, mitral stenosis/regurgitation, pulmonary venous occlusion) can lead to endothelial
dysfunction. It can result in a decrease in endothelium-derived NO, and prostacyclin as well
as an increase in thromboxane and endothelin-1 with resultant pulmonary vasoconstriction,
SM proliferation, and platelet aggregation. Platelet aggregation leads to in situ thrombosis
and release of serotonin and plasminogen activator inhibitor (decrease in fibrinolytic
activity) which exacerbate pulmonary vasoconstriction and rise in PVR. Endothelin and
serotonin cause fibroblast proliferation, collagen deposition in the adventitia, and
hyperplasia and hypertrophy of the pulmonary vascular smooth muscle. If the underlying
condition is not treated and controlled, it will lead to pulmonary hypertension.
• Patients with a risk of pulmonary edema (congestive heart failure, renal failure, liver
failure) should be carefully evaluated and optimized prior to surgery. Excess fluid can be
removed with the use of diuretics or dialysis. Perioperative volume administration should
be performed with caution to provide adequate preload but to avoid volume overload and
pulmonary congestion.
• Patients undergoing thoracic procedures with lung isolation are at a higher risk for re-
expansion pulmonary edema.
• Negative pressure pulmonary edema can be seen during extubation (more common in young
healthy patients). The generation of large negative intrathoracic pressures with concurrent
upper airway obstruction result in either “pulling” of fluids from the pulmonary capillary
bed into the alveoli (Starling forces) or injury to the pulmonary microvascular membranes
from severe mechanical stress that results in capillary “leaking” of fluid.
• Persistent hypoxemia can result in a sustained rise of PAP and vascular remodeling. PVR
rises as the PaO2 decreases below 60 mm Hg. Hence, supplemental oxygen is a cornerstone
of management of patients with pulmonary hypertension.
• During mechanical ventilation in patients with pulmonary hypertension or other pulmonary
pathology, attention to the “U”-shape relationship between lung volumes and PVR is
important in selecting appropriate tidal volumes. Optimal tidal volume is closer to FRC,
which results in the lowest PVR and avoids intrapulmonary shunting (small tidal volume)
and decreased pulmonary perfusion (large tidal volumes).
– NO, prostacyclin analogs (Epoprostenol, Iloprost), endothelin inhibitors (Bosentan), PDE-3
antagonists (milrinone, amrinone) and PDE-5 antagonists (sildenafil) are the cornerstones
of management of patients with pulmonary hypertension based upon the mechanisms
discussed before. Most of these drugs are used in the perioperative management of these
patients.
– Patients with pulmonary hypertension should be closely monitored. All attempts should be
made to prevent any sudden rise in PVR and PAP which can lead to RV failure. These
include adequate oxygenation, hyperventilation (in intubated patients with close attention
to tidal volume and respiratory rate) with a goal end-tidal CO2 of 35–40 mm Hg,
correction of acidosis (respiratory/metabolic), adequate pain control (to attenuate
sympathetic response), maintenance of normothermia and euvolemia.
EQUATIONS
• Starling equation for microvascular barrier: Jv = LpS [(Pc − Pi) − σd (πc − πi)]
– Jv is net fluid filtration rate across the microvascular barrier
– Lp is the hydraulic permeability of the barrier
– S is the surface area of the barrier
– Pc is pulmonary capillary hydrostatic pressure
– Pi is interstitial hydrostatic pressure
– πc is the capillary (microvascular) plasma colloid osmotic (or oncotic) pressure
– πi is the interstitial (perimicrovascular) fluid osmotic pressure
– σd is the average osmotic reflection coefficient of the barrier (a measure of how effective
the barrier is in hindering the passage of solutes from one side of the barrier to the other).
REFERENCES
1. Rubinfire M, Bayram M, Hector-Word Z. Pulmonary hypertension in the critical care
setting: Classification, pathophysiology, diagnosis, and management. Crit Care Clin.
2007;23(4):801–834.
2. Fischer LG, Van Aken H, Bürkle H. Management of pulmonary hypertension: Physiological
and pharmacological considerations for anesthesiologists. Anesth Analg. 2003;96(6):1603–
1616.
3. Brimioulle S, Vachiery JL, Brichant JF, et al. Sympathetic modulation of hypoxic
pulmonary vasoconstriction in intact dogs. Cardiovasc Res. 1997;34(2):384–392.
4. Wojciak-Stothard B, Haworth SG. Perinatal changes in pulmonary vascular endothelial
function. Pharmacol Ther. 2006;109(1–2):78–91.
5. MacKnight B, Martinez EA, Simon BA. Anesthetic management of patients with pulmonary
hypertension. Semin Cardiothorac Vasc Anesth. 2008;12(2):91–96.
6. effner JE. Mechanisms underlying ischemia/reperfusion injury of the lung. In: Matthay MA,
Ingbar D, eds. Pulmonary edema. New York, NY: Marcel Dekker; 1998:379–341.
7. Higuchi S, Ohtsu H, Suzuki H, et al. Angiotensin II signal transduction through the AT1
receptor: Novel insights into the mechanisms and pathophysiology. Clin Sci.
2007;112(8):417–428.
ADDITIONAL READING
• Mason: Murray and Nadel’s textbook of Respiratory Medicine, 5th ed. Volume 1, Chapter 1:
Anatomy of the Lungs, Pulmonary Circulation.
• Mason: Murray and Nadel’s textbook of Respiratory Medicine, 5th ed. Volume 2, Chapter
55: Pulmonary Edema and Acute Lung Injury.
CLINICAL PEARLS
• The pulmonary vasculature is an active bed that is under the control of numerous mediators
and physiologic functions. In addition, if functions as a blood reservoir, filtration system,
and metabolizes several drugs.
PULMONARY VENTILATION–PERFUSION MATCHING
Ana Maria Manrique-Espinel, MD
Todd M. Oravitz, MD
BASICS
DESCRIPTION
• Ventilation is defined as the mechanism of gas flow through the lungs that allows exchange
of oxygen into and carbon dioxide out of the system.
• Perfusion is defined as the mechanism of blood flow through the lungs that allows uptake of
oxygen into red blood cells and simultaneous removal of carbon dioxide; it functions to
transport gases from tissue to lung and vice versa.
• The relationship between ventilation (V) and perfusion (Q) determines gas exchange. The
ideal V/Q ratio is 1; however, there are physiologic regional differences and the average
V/Q ratio is 0.8 (4 liters/minute compared to 5 liters/minute).
– Upper lung areas receive more ventilation relative to perfusion; therefore V > Q and V/Q
> 1
– Lower lung fields receive more perfusion relative to ventilation; therefore V < Q and V/Q
< 1
• Matching: Under physiologic states, ventilation and perfusion are not equally distributed
within the lung.
– Ventilation: Minute ventilation (MV) is the product of tidal volume and respiratory rate; in
the average adult, MV is ∼4 L/min.
– Perfusion: The lungs accept the entire cardiac output (CO). Thus, blood flow to the lungs
is equal to stroke volume multiplied by heart rate; in the average adult, CO is ∼5 L/min.
– Regional differences in V, Q, and hence matching, exist normally in the lungs as a result of
gravitational and non-gravitational factors.
• Gravitational forces.
– Ventilation: Gas more readily distributes to the apex of the lungs; the alveoli are bigger
and there is less resistance to inflow.
– Perfusion: Blood more readily distributes to the base of the lungs secondary to gravity.
• Non-gravitational forces.
– Ventilation: Intrinsic anatomic variation of the airways, lung volumes, or airway
resistance which are dependent upon pleural hydrostatic gradients, regional compliance,
and bronchial anatomy.
– Perfusion: Dependent upon differences between the arterial pulmonary pressure, arterial
venous pressure, and interstitial and alveolar pressures. Studies suggest that hydrostatic
forces are the most important influence on V/Q and result in more central flow compared
to peripheral flow. Mapping of the lung has shown an “onion distribution” of the
perfusion; perfusion is greatest at the hilum and decreases towards the periphery.
• Zones: 4 areas of ventilation/perfusion distribution have been described:
– Zone 1: Apex of the lung. The alveolar pressure is greater than both pulmonary arterial
and venous pressures.
– Zone 2: Middle of the lung. Pulmonary arterial pressure exceeds alveolar pressure. Blood
flow will depend on the difference between arterial and alveolar pressures and, in fact, is
independent of venous pressure (unless it is higher than alveolar pressure).
– Zone 3: Base of the lung. Arterial and venous pressures are higher than alveolar. Blood
flow is continuous and will increase with increases in the hydrostatic pressure.
– Zone 4: Describes a physiologic zone, not an anatomic zone, where the vessels are
decreased in diameter and there is increased resistance to blood flow. Occurs at high and
low lung volumes as well as increased interstitial pressures.
• Oxygen and carbon dioxide: The oxygen content and composition of the gases follow the
mass conservation law in which the total oxygen content of the blood is equal to the sum of
the pulmonary capillary oxygen content and the oxygen content in the shunt. Variations in
V/Q determine the composition of the gases at each level of the lung, as well. Arterial
oxygen pressure (PaO2) is higher in the apex and the arterial carbon dioxide (PaCO2) is
lower. The oxygen uptake is higher in the lower base of the lung because this is the area
where there is more flow (most efficient).
• Measuring V/Q: The gold standard is the multiple inert gas elimination technique “MIGET."
Most recently single-photon emission computed tomography has been used “SPECT”
ANATOMY
• Regional flow
– Blood flow is higher in the dorso-caudal areas of the lung compared with ventrocephalad
areas.
– “Onion distribution” describes the preferential perfusion to the hilum of the lung,
decreasing toward the periphery.
– The right lung receives more ventilation and perfusion in the upright and supine position
than the left lung.
• Regional ventilation:
– Apices have bigger alveoli. Lower zones of the lung have smaller, more compliant alveoli
that facilitate air entry.
– Gas exchange is better in the dependent areas of the lung regardless of the position.
– The shape of the thoracic cavity is also an important influence in the differences in the
regional ventilation.
• Dead space refers to areas of the lung that are ventilated but have no blood flow. V/Q =
V/0 = ∞
– Anatomical dead space: Volume of gas occupying the conducting airways where there is
no gas exchange; it may be affected by the size of the subject, age, posture, and position of
the neck. Normal dead space is ∼150 mL (∼2 mL/kg).
– Alveolar dead space: Volume of gas that passes through the alveoli but does not perform
effective exchange. This may occur due to a lack of perfusion to the alveoli. The alveolar
dead space can increase significantly when there is low CO, pulmonary embolism, or
inadequate settings for mechanical ventilation in the lateral position.
– Physiologic dead space (VD) is the sum of all parts of the tidal volume that do not
participate in gas exchange (anatomical plus alveolar dead space). Normally, this
comprises ~30% of the tidal volume; in pediatrics it reaches close to half of the tidal
volume.
– Aging produces an increase in the vascular resistance of the small capillaries and fibrosis
of the interstitium that interferes with gas exchange;as a consequence, elderly patients
have increased heterogeneity of ventilation and perfusion of the lung. Also the decreased
elastic recoil in some areas produces collapse of alveoli and decreased ventilation.
• Shunt
– Physiologic shunt: Describes blood that travels through the pulmonary vasculature but
does not contact ventilated alveoli (atelectasis concept). V/Q = 0/Q = 0. In pediatrics,
the physiologic shunt is increased ~10%.
– Anatomic shunt: Describes blood that bypasses the lungs through an anatomic channel
such as the bronchial veins, Thebesian veins, and right- to-left shunts (ventricular septal
defect).
• General anesthesia:
– Spontaneous ventilation: The diaphragm function is impaired and there are increases in
physiologic shunting (decreased FRC).
– Mechanical ventilation and muscle relaxation: Ventilation is greater in the upper portions
of the lung (less resistance to flow); whereas, the blood flow is greater in the dependent
portions of the lung.
• Position: In the awake, spontaneously ventilating patient, distribution of ventilation in the
upright lung was shown to vary somewhere between 6–24%. When supine, the variation
through the lung derived from the gravitational forces is small. Under general anesthesia:
– Supine: Cephalad movement of the diaphragm and abdominal contents results in
decreased FRC; there is decreased ventilation to the base of the lung, while perfusion
continues.
– Trendelenburg: Accentuated cephalad movement of the diaphragm and abdominal
contents; decreased ventilation to the base of the lung, with continued but decreased
perfusion (secondary to gravitational forces).
– Reverse Trendelenburg: Gravity results in caudal displacement of the diaphragm and
abdominal contents with resultant improvement to ventilation in this area. Perfusion to
the base is increased due to gravitational forces
– Lateral: Both ventilation and perfusion are greater in the dependent lung.
• Hypoxic pulmonary vasoconstriction (HPV): Occurs in normal lung, under hypoxemic
conditions to decrease shunting. Low oxygen pressures are sensed in the pulmonary
endothelium, causing the release of calcium from the sarcoplasmic reticulum, which results
in vasoconstriction. There is evidence of inhibition of HPV from inhaled anesthetics. Thus,
hypoxic or poorly ventilated alveoli will continue to be perfused.
• Pulmonary disease: The effects of general anesthesia and mechanical ventilation may have a
significant impact in ventilation/perfusion matching. Patients should be carefully assessed
preoperatively for risk stratification and implementation of maneuvers that may decrease
• One lung ventilation (OLV): Changes depend on:
– Awake and breathing spontaneously: Ventilation is dominant in the dependent (lower)
lung, along with perfusion.
– General anesthesia and mechanical ventilation: Following clamping (onset of OLV),
ventilation will be directed to the dependent lung, with the non-dependent or operative
side compressed. Perfusion will follow the hydrostatic pressure, being more prominent in
the dependent lung. However, a significant right- to- left shunt is created in the non-
dependent lung, because it continues to be perfused.
EQUATIONS
• Alveolar ventilation equation: VA = f (VT - VD); where VT is tidal volume, VD is dead space
ventilation, and f is the frequency of breaths.
• Alveolar gas equation: PAO2 = PIO2 – PaCO2/R; where PAO2 = partial pressure of oxygen
in the alveoli PIO2 = partial pressure of oxygen in the inspiratory gas; PaCO2 = partial
pressure of carbon dioxide in the artery; and R = the respiratory exchange ratio or
VCO2/VO2.
• Ventilation/perfusion ratio equation: VA/Q = 8.63R
• (CaO2 − CvO2) / PaO2; where CaO2 = arterial oxygen content; CvO2 = venous oxygen
content.
REFERENCES
1. Evans AM, Hardie DG, Peers C, et al. Hypoxic pulmonary vasoconstriction: Mechanisms of
oxygen-sensing. Curr Opin Anaesthesiol. 2011;24(1):13–20.
2. opkins SR, Arai TJ, Henderson AC, et al. Lung volume does not alter the distribution of
pulmonary perfusion in dependent lung in supine humans. Physiol. 2010;588(Pt 23):4759–
4768.
3. Taylor BJ, Johnson BD. The pulmonary circulation and exercise responses in the elderly.
Semin Respir Crit Care Med. 2010;31(5):528–538.
4. King GG, Harris B, Mahadev S. V/Q SPECT: utility for investigation of pulmonary
physiology. Semin Nucl Med. 2010;40(6):467–473.
5. Salome CM, King GG, Berend N. Physiology of obesity and effects on lung function. J Appl
Physiol. 2010;108(1):206–211.
6. Glenny RW. Determinants of regional ventilation and blood flow in the lung. Intensive Care
Med. 2009;35(11):1833–1842.
ADDITIONAL READING
• Pulmonary physiology. Michael G. Levitzky. 7th ed. McGraw Hill 2007 Chapter 5
Ventilation–Perfusion relationships. 113–129.
• Respiratory Physiology. John B west. 8th ed. Lippincott 2008 – Chapter 5 Ventilation–
Perfusion relationships—How matching of gas and blood determines gas exchange. 55–74.
• Dead space
CLINICAL PEARLS
• Changes in mechanical ventilation settings, position of the patient, and hemodynamics are
factors that can be manipulated to achieve adequate ventilation–perfusion matching.
PULSE OXIMETRY
BASICS
DESCRIPTION
• The pulse oximeter noninvasively estimates the percentage of hemoglobin–oxygen
saturation in the arterial blood.
• Expressed as SpO2%.
• Functions as a measure of how much oxygen is bound to hemoglobin, as a percentage of the
maximum carrying capacity.
• The two-part probe is applied over a reasonably translucent site with good blood flow, such
as the finger or ear lobe.
• Comprised of an emitter that produces light on one end and a photodetector on the other
end; the tissue lies in between.
• Delivery of oxygen to the tissues by the blood is dependent on: The total oxygen-carrying
capacity of blood, cardiac output, and blood flow to the tissues. Almost all of the oxygen
carried in the blood is bound to hemoglobin. Only a small amount is present in the
dissolved form due to the low solubility coefficient (0.003 mL of oxygen per dL of blood per
mm Hg PaO2). Conversely, each gram of hemoglobin carries 1.34 mL of oxygen when
completely saturated. Note: The percent oxygen saturation of hemoglobin is in equilibrium
with and dependent on the PaO2 of blood.
• Oxyhemoglobin curve: Used to describe the relationship between the PaO2 and oxygen
saturation. Some important numbers to remember include:
– PaO2 760 mm Hg = SpO2 100%
– PaO2 100 mm Hg = SpO2 97.4% Increasing the PaO2 > 100 mm Hg will not significantly
increase the oxygen-carrying capacity.
– PaO2 70 mm Hg = SpO2 93%
– PaO2 28 mm Hg = SpO2 50% (known as the P50)
• Sigmoidal shape: The hemoglobin molecule favors oxygen loading in the lungs and
unloading to the tissues.
– The upper part of the curve is almost flat; thus, the PaO2 in the lungs (alveoli) has to drop
<70 mm Hg before a significant change in the hemoglobin saturation of oxygen can
occur. This provides a margin of safety.
– The steep portion between a PaO2 of 10–40 mm Hg represents how a small change in the
PaO2 will result in larger changes in oxygen saturation. This serves a critical physiologic
function in peripheral tissues where the PaO2 is very low. Thus, slight changes in the PaO2
will result in greater unloading of oxygen to the tissues.
See Table
• P50: Describes the PaO2 at which the hemoglobin saturation is 50%. The binding and
dissociation of oxygen to hemoglobin can be affected by several factors including: pH,
PaCO2, temperature, and 2,3 diphosphoglycerate (2,3 DPG). These changes result in right
and left shifting of the oxy-hemoglobin curve.
– Right shifting refers to a decreased oxygen affinity to hemoglobin; a greater PaO2 is
required to saturate the hemoglobin molecule. Physiologic conditions include acidosis, as
well as, higher PaCO2 levels, temperatures, and 2,3 DPG levels; such conditions are
prevalent in peripheral tissues and facilitate the unloading of oxygen. The relatively flat
upper portion of the curve is less affected, thus minimizing the impact on the loading of
oxygen in the lungs.
– Left shifting refers to an increased oxygen affinity to hemoglobin; a smaller PaO2 is
required to saturate the hemoglobin molecule. Physiologic conditions include alkalosis, as
well as decreases in PaCO2, temperatures, and 2,3 DPG.
• The principle of pulse oximetry is based upon the differential light absorption characteristics
of oxygenated and deoxygenated hemoglobin.
– Oxyhemoglobin absorbs more infrared light at wavelength of 840 nm.
– Reduced deoxyhemoglobin absorbs more red light at a wavelength of 680 nm.
– Transmission method: The emitter and photodetector are on opposite sides from each
other. The transmitted red (R) and infrared (IR) signals are received at the photodetector,
and the R/IR ratio is calculated and converted into a SpO2% value.
– Arterial pulsations result in a momentary increase in blood volume across the measuring
site and enhance light absorption. An algorithm differentiates absorbance between static
tissue components (e.g., venous flow, bone, skin, muscle, etc) and dynamic arterial flow.
• Limitations in pulse oximeters can result in false readings, false alarms, data drop outs, and
missed desaturations from:
– Motion artifacts
– Irregular heart rhythms
– Electrocautery interference
– Intense ambient light interference
– Poor signals during low perfusion or poor perfusion states
– Vasopressor use
– Cold periphery
– Some types of nail varnishes
ANATOMY
• The optically shielded probe is usually applied to finger tips or ear lobes. Occasionally, it
can also be applied to the buccal mucosa or ala of the nares in situations of poor perfusion.
• These probes contain light emitting diodes applied on one side of the finger and a sensor on
the opposite side. The probes may get significantly warmed and need to be changed in
vulnerable populations: preemies or neonates.
• Decreased cardiac output: Results in decreased oxygen delivery to the tissues (causes include
reduced cardiac preload, heart failure, and shock). With anemia, pulse oximeter SpO2% may
be normal; however, there may be decreased oxygen delivery to the tissues.
• Hypoxia: Mechanisms may be broadly categorized as due to low inspired oxygen
concentration, hypoventilation, ventilation–perfusion mismatch, shunt, and low cardiac
output. Various medical conditions such as pneumonia, pneumothorax, and pulmonary
embolism cause hypoxia often by a combination of the above-mentioned mechanisms.
• Dyshemoglobins: Can affect the accuracy of the conventional two wavelength pulse
oximeter readings.
– Methemoglobin will read at 85% oxygen saturation regardless of actual levels. Pulse
oximeters measure two wavelengths of light: 660 nm (red, oxyhemoglobin) and 940 nm
(infrared, deoxyhemoglobin). Methemoglobin absorbs equal amounts of these
wavelengths; a ratio of pulsatile and nonpulsatile absorbances equal to 1 corresponds to a
hemoglobin saturation of 85%. Normal methemoglobin levels are <1%.
– Carboxyhemoglobin and oxyhemoglobin have similar absorption characteristics. Its
presence will give falsely elevated readings and therefore is clinically significant.
Carboxyhemoglobin does not carry oxygen and also affects dissociation of oxygen to the
tissues. Usual carboxyhemoglobin levels are <1.5% in non-smokers, and higher in city
dwellers, and can be as high as 3–15% in smokers.
– Fetal hemoglobin will not affect the accuracy of estimation of hemoglobin saturation. HgF,
however, does cause a shift in the oxyhemoglobin dissociation curve to the left (binds
oxygen more tightly resulting in higher saturations at lower PaO2 levels). Consequently,
there is decreased “off-loading” of oxygen at peripheral tissues.
– Effects of sickle cell hemoglobin are controversial with some studies showing large errors
and others minimal.
• Pulse oximetry allows for the immediate recognition of hypoxia and has contributed to the
safety of modern anesthesia and intensive care management. It is a routinely used monitor
in most clinics, every operating room, and perioperative and intensive care unit across the
US and the western world.
– Shows excellent correlation with the measured co-oximeter hemoglobin SpO2 above 75%.
– Used during patient transport as well as in procedure rooms where sedation is
administered.
– Used during intrapartum monitoring of the fetus, neonatal resuscitation, and premature
neonates to limit pulmonary oxygen toxicity and retrolental fibroplasia.
• Specialty sensors
– Congenital heart disease: Sensors have been developed that show greater correlation with
saturations as low as 60%.
– Parameters such as the pleth variability index (PVI), have been derived from the variation
in the plethysmographic waveform during ventilation. This may be helpful in the goal-
directed administration of intravenous fluids during perioperative management.
– Newborn sensors have been developed that can measure the high pulse rate, as well as
provide maximum sensitivity that allows for quick application of monitor information.
– Specialized monitors exist to detect carbon monoxide poisoning in the field by firefighters
and emergency medical technicians (EMT), as well as diagnosis and monitoring of
treatment in the emergency rooms.
EQUATIONS
Delivery of O2/min = CO (mL/min) × (hemoglobin concentration in gm/dL × 1.34 ×
SpO2) + (0.003 × PaO2 in mm Hg).
REFERENCES
1. arker SJ, Badal JJ. The measurement of dyshemoglobins and total hemoglobin by pulse
oximetry. Curr Opin Anaesthesiol. 2008;21:805–810.
2. Wukitsch MW, Petterson MT, Tobler DR, et al. Pulse oximetry: Analysis of theory,
technology, and practice. J Clin Monit. 1988;4:290–301.
3. Pedersen T, Moller AM, Hovhannisyan K. Pulse oximetry for perioperative monitoring.
Cochrane Database Syst Rev. 2009;7(4):CD002013.
4. Chapman KR, Liu FL, Watson RM, Rebuck AS. Range of accuracy of two wavelength
oximetry. Chest. 1986;8(4):540–542.
5. Josten KU. Oximetry. Br J Anaesth. 1986;58(2):248–249.
6. May WS Jr. Respiratory monitoring. Int Anesthesiol Clin. 1986;24(1):159–169.
ADDITIONAL READING
• Barrett KE, Barman SM, Boitano S, Brooks H, “Chapter 36. Gas Transport & pH in the Lung”
(Chapter). Barrett KE, Barman SM, Boitano S, Brooks H: Ganong’s Review of Medical
Physiology, 23e.
• Oxygen-carrying capacity
CLINICAL PEARLS
• The pulse oximeter will only reveal hemoglobin’s oxygen saturation; it does not provide
PaO2 values. Therefore, pulse oximetry should be interpreted with caution, where
monitoring of the PaO2 is critical (e.g., fetal or neonatal monitoring).
• The SpO2% does, however, provide an indirect measure of the PaO2 when the partial
pressure is <100 mm Hg.
• Pulse oximeter readings may be normal, but the oxygen-carrying capacity of blood may be
severely reduced in the presence of anemia.
PULSELESS ELECTRICAL ACTIVITY
J. Scott Bluth, BS
BASICS
DESCRIPTION
• Pulseless electrical activity (PEA), previously known as electromechanical dissociation
(EMD), is defined as electrical depolarization of the heart in the absence of synchronous
cardiac myocyte shortening. New evidence suggests that it is a heterogenous clinical
condition with varying levels of BP and cardiac activity:
– Pseudo PEA: Severe hypotension, no clinically detectable pulses, residual cardiac activity.
– True PEA: BP and cardiac wall motion are completely absent.
• Treatment requires initiation of advanced cardiac life support (ACLS) with concurrent
diagnosis and treatment of the underlying cause; this approach has not evolved in decades.
Recent increases in the incidence of PEA have aroused interest and the development of
animal models to better understand the pathogenesis in order to improve therapies and
survival.
• Anaesthetists must be aware of potential, common perioperative events that could incite
PEA such as hypoxia, hypovolemia, potassium abnormalities, hypothermia, acidosis, and
concomitant beta-blocker and calcium-channel blocker use; as well as pulmonary embolism,
hypoglycemia, cardiac tamponade, tension pneumothorax, and coronary artery thrombosis.
EPIDEMIOLOGY
Prevalence
• Comprises ∼35–40% of all in-hospital cardiac arrests
• Comprises ∼22–30% of all out-of-hospital cardiac arrests
• Pseudo-PEA data not available
Morbidity/Mortality
• In-hospital PEA cardiac arrests: 11% survival, of which 62% had good neurologic outcomes.
• Out-of-hospital arrests: 2.5% survival to discharge.
• Outcomes following PEA were slightly better than those following asystole.
PEA and other forms of cardiac arrest are often caused by a set of reversible conditions
conveniently referred to as the “H’s” and “T’s.” These factors should be considered and
corrected as quickly as possible while life-saving efforts are being performed.
• Hypoxia (common perioperative cause)
• Hyperkalemia or hypokalemia
• H+ ions (acidemia)
• Hypovolemia (common perioperative cause)
• Hypothermia
• Hyperglycemia
• Tamponade
• Tension pneumothorax
• Thrombosis, coronary
• Thrombosis, pulmonary
• Toxins (poisoning)
• Trauma
• Electrical depolarization is typically followed by mechanical contraction and blood ejection
from the ventricles. This sequence is fast and elegant; however, there are several clinical
conditions that can impede it.
• The H’s and T’s involve cardiac, respiratory, and metabolic disturbances with a common
end-point: Electrical activity without a meaningful pulse. The exact pathogenesis remains
unclear; however, evidence suggests that myocardial ischemia is the common
pathophysiologic insult, either by decreased preload or cardiac contractility.
– Decreased preload may result from hypovolemia, tension pneumothorax, tamponade, or
pulmonary thrombosis.
– Decreased cardiac contractility may result from hypoxia, hypothermia, potassium
abnormalities, acidosis, or coronary thrombosis.
• Global myocardial ischemia can consequently result in hypoxia, acidosis, and increased
vagal tone. These disturbances are believed to cause depolarization and the uncoupling of
excitation and contraction with resultant PEA.
– Hypoxia results in anaerobic metabolism and lactic acidosis, with resultant hyperkalemia.
It has negative inotropic effects.
– Intracellular acidosis from hypoxia and the build-up of metabolic by-products may be
responsible for impairing calcium affinity to troponin C. It has negative inotropic effects.
– Increased vagal tone can reduce heart rate and BP.
• Animal studies have suggested that calcium uptake following reperfusion may be involved
in, or is the result of, PEA. A significant uptake of calcium into myocardial cells is followed
by swelling, damage to mitochondria and myofibrils, and deposits of intramitochondrial
calcium phosphate. The increased calcium uptake has been postulated to impair voltage-
gated calcium ion channels, calcium stores in the sarcoplasmic reticulum, and affinity of
calcium to troponin C (1).
• Beta-blocker and calcium-channel blocker use has been associated with an increased
incidence of PEA and a concomitant decrease in ventricular fibrillation. The etiology has
been attributed to their negative inotropic effects (2).
Avoidance of the “H’s” and “T’s” of PEA
• The history should provide information regarding possible etiologies (drug overdose,
diabetes, coronary artery disease, trauma, intubation, insertion of central venous catheter,
etc.)
• Physical examination should include a palpation for a pulse, temperature, assessment for
tracheal shifting, breath sounds, distended jugular veins.
• Diagnostic procedures/Other
– Blood sugar
– Potassium level
– Arterial blood gas
– Echocardiogram to assess for cardiac tamponade, hypovolemia
– Handheld Doppler to rule out pseudo-PEA
• Monitors
– Pulse oximetry, BP cuff, and arterial line indicate the lack of a pulse or mechanical
contraction.
– Tachycardia and hypertension often precede onset; however, perioperatively, this lacks
specificity (surgical stimulation, light anesthesia, ephedrine, etc.).
– EKG can demonstrate suggestive etiologies prior to the onset of PEA (usually applicable
for intraoperative events).
Peaked T waves: Consider hyperkalemia
Inverted T waves (U waves): Consider hypokalemia
ST segment changes: Consider cardiac thrombosis (myocardial infarction)
Wide QRS: Consider myocardial injury, hyperkalemia, hypoxia
Wide QRS and slow: Consider drug overdose from tricyclic antidepressants, beta-
blockers, calcium-channel blockers
Narrow QRS: Consider hypovolemia, pulmonary embolus, cardiac tamponade
• Pseudo-PEA
• Implantable pacemaker firing in asystole
TREATMENT
• ACLS for PEA.

– The goal during resuscitation is to maintain perfusion to vital organs during cardiac arrest
and simultaneously diagnose and treat any underlying causes until return of spontaneous
circulation (ROSC) occurs.
• In the operating room, begin CPR, administer or increase oxygen delivery, attach
defibrillator.
• PEA is not a shockable rhythm; therefore its algorithm differs from that of ventricular
fibrillation and tachycardia (3).
– Perform chest compression and ventilation for 2 minutes. The provider performing chest
compressions should switch every 2 minutes.
– Administer epinephrine (1 mg IV every 3–5 minutes) or vasopressin (40 U IV) to replace
the first or second dose of epinephrine.
– Note that atropine is no longer recommended for routine use in PEA/asystole.
– Check for shockable rhythm after 2 minutes.
– If shockable, follow the appropriate algorithm
– If not shockable, check for pulse. If pulse is present, begin post-resuscitation care. If
absent, continue chest compressions and rhythm evaluation.
• Airway management should also be addressed during the ACLS algorithm.
– In the perioperative setting, the patient’s airway may already be secured; proper
placement should be confirmed.
– If the patient is undergoing monitored anesthetic care (MAC), mask ventilation or
intubation should be performed
– In the scenario where a supraglottic device is being utilized, consider converting to an
endotracheal tube to provide positive pressure ventilation if appropriate.
– The key is to minimize interruptions in chest compressions during airway placement.
• Differential diagnosis: While performing CPR, providers should review the potentially
reversible “H’s” and “T’s” as possible causes and correct them when possible (4).
– Hypoxia should be treated with oxygen at a FiO2 100%.
– Hyperkalemia can be treated with a combination of calcium, bicarbonate, glucose, and
insulin to stabilize myocardial cells and shift potassium intracellularly. Administer
furosemide to enhance potassium excretion.
– Hydrogen ion excess (acidemia) may be treated with IV bicarbonate and hyperventilation.
– Hypovolemia can be corrected with IV fluid hydration or blood transfusion in cases of
severe hemorrhage.
– Hypothermia can be corrected with active internal warming techniques.
– Tamponade can be treated with thoracotomy in cases of trauma or pericardiocentesis
guided by echocardiography when possible.
– Tension pneumothorax should be treated with needle decompression and chest tube
placement.
– Thrombosis, coronary: Thrombolytic therapy, coronary reperfusion, and emergency
cardiopulmonary bypass should be considered.
– Thrombosis, pulmonary: Consider fibrinolytic therapy when pulmonary infarction is
suspected or known.
– Toxins: Activated charcoal is indicated in many instances of drug overdose. Some toxins
require specific correctional measures but ACLS guidelines should always be followed.
Urgent toxicology consultation is recommended when ROSC occurs, if there are no other
obvious causes.
– Trauma involving the head and neck requires C-spine stabilization. The jaw-thrust
maneuver should be used to establish an airway.
FOLLOW-UP
• Intraoperative arrests with ROSC: The decision to proceed with the surgery depends on
whether the initiating event has been resolved (or will recur) and the level of
urgency/emergency of the procedure. Postoperatively, patients should be admitted to an
intensive care unit for surveillance and ongoing therapy as indicated.
• Out of OR arrests with ROSC: Patients should be transferred to an intensive care unit for
further stabilization and ongoing treatment, as indicated. Unresponsive patients should be
considered for transfer to a facility that can provide a comprehensive care plan that includes
rigorous cardiac, neurologic, and metabolic monitoring (5).
• Avoid hyperventilation. Hyperventilation also increases intrathoracic pressure and inversely
lowers cardiac output (5).
• Induced hypothermia may be considered for neural and visceral protection
• Coronary angiography and PCI are indicated when necessary and may be helpful even in
comatose patients who do not show signs of ST segment elevation on ECG (5).
REFERENCES
1. arabee TM, Paradis NA, Bartsch J, et al. A swine model of pseudo-pulseless electrical
activity induced by partial asphyxiation. Resuscitation. 2008;78(20):196–199.
2. oungquist ST, Kaji AH, Niemann JT. Beta-blocker use and the changing epidemiology of
out-of-hospital cardiac arrest rhythms. Resuscitation. 2008;288:3308–3013.
3. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life support:
emergency cardiovascular care. Circulation. 2010;122(18 suppl 3):S729–S767.Paradis NA,
Halperin HR, Kem K. Cardiac arrest: The science and practice of resuscitation medicine.
Cambridge University Press.Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: Post-
cardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary
resuscitation and emergency cardiovascular care. Circulation. 2010;122(18 suppl 3):S768–
S786.ACLS algorithmDesbiens NA: Simplifying the diagnosis and management of pulseless
electrical activity in adults: A qualitative review. Crit Care Med. 2008;36(2):391–396
• Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: Cardiac arrest in special situations:
emergency cardiovascular care. Circulation. 2010;122(18 suppl 3):S829–S861.
• Hyperkalemia
• Pneumothorax
• Hypothermia
• ACLS anesthesia management
CODES
ICD9
ICD10
• I46.9 Cardiac arrest, cause unspecified
• I46.8 Cardiac arrest due to other underlying condition
CLINICAL PEARLS
• PEA refers to a heterogenous group of cardiac rhythm disorders; all characterized by
pulselessness in the presence of some types of electrical activity other than VT or VF.
• Treatment involves institution of the ACLS algorithm with concurrent diagnosis and
treatment of the inciting cause.
• Although the causes vary greatly, there appears to be a shared pathophysiologic cascade.
Following an initial global myocardial ischemic event, hypoxia, acidosis, and increased
vagal tone ensue. The pathogenesis is not completely understood at this time; however,
there appears to be a renewed interest, given the increased incidence of PEA in cardiac
arrests. A greater understanding may improve therapy and prognosis.
PYLORIC STENOSIS
Jinlei Li, MD, PhD
BASICS
DESCRIPTION
• Pyloric stenosis, also known as infantile hypertrophic pyloric stenosis (IHPS), is the most
common cause of intestinal obstruction in infants. It typically presents in infants between
the ages of 5 days to 5 months, with the average age being 3 weeks.
• Intractable, non-bilious projectile vomiting of ingested food is characteristic.
• The classic/traditional treatment is an open pyloromyotomy via a Ramstedt RUQ transverse
incision. More recently, circumumbilical laparoscopic approaches have supplanted the open
repair, with cosmetic benefits and lower rates of wound infections (1,2).
EPIDEMIOLOGY
Prevalence
In the US: 3:1,000 infants
Prevalence
More common in those of Northern European descent, less common in Africans, and rare in
Asians
Morbidity
• Dehydration
• Metabolic derangements
Mortality
Rare
• Male to female infant ratio 4:1
• First born
• Caucasians
• Macrolide antibiotics (oral erythromycin)
• Etiology unknown and probably multifactorial
• A hypertrophied pyloric sphincter muscle in the newborn causes functional obstruction and
blocks the passage of stomach contents into the small intestine.
• Contents of the small intestine do not reflux back into the stomach; thus bile is not present
in the vomitus unlike other GI tract obstructions that occur below the pylorus.
• Gastric acid is comprised of 0.5% hydrochloric acid (HCl), and large quantities of potassium
chloride (KCl) and sodium chloride (NaCl). Thus vomiting depletes sodium, potassium,
chloride, and hydrogen ions. This results in a hypochloremic, hypokalemic metabolic
alkalosis.
• Initially, chloride ion loss inhibits the excretion of bicarbonate in the kidneys (to maintain
electroneutrality) with a resultant metabolic alkalosis. In severe dehydration, the renin–
angiotensin–aldosterone system is activated by hypovolemia. Hyperaldosteronism leads to
retention of sodium and paradoxic excretion of potassium and hydrogen ions resulting in
aciduria. In the body’s effort to maintain physiologic pH, a compensatory respiratory
acidosis and hypoventilation ensue.
• Pyloric stenosis is a medical, not surgical, emergency. Optimize fluid status, correct acid–
base disturbances and electrolyte derangements prior to surgery.
• Assume that the patient is a “full stomach”; a rapid sequence induction or awake intubation
should be performed after gastric suctioning in the supine, lateral, and prone positions (3).
SYMPTOMS
• Projectile non-bilious vomitus, belching, abdominal pain
• Constant hunger, failure to thrive
• Dehydration, manifested by depressed fontanelles, dry mucous membranes, or poor skin
turgor
History
Age: Typically diagnosed between 3 weeks and 6 months of age.
Signs/Physical Exam
• Palpation of an olive-sized mass in the right epigastric region.
• Indirect hyperbilirubinemia and jaundice may exist in a small group of patients, possibly
due to starvation. These typically resolve after surgery.
TREATMENT HISTORY
• The patient should remain NPO
• IV fluids: Initial resuscitation in dehydrated patients should start with a 0.9% NaCl bolus of
20 mL/kg. Patients with normal laboratory values should have 1.5–2 times maintenance
rates of a fluid such as 5% dextrose in water (D5W) or 0.25–0.45% NaCl.
• Since lactate is metabolized to bicarbonate, lactated Ringer’s should be avoided.
• Electrolyte replacement: Potassium can be added to fluid as needed after urine output is
normalized.
• A nasogastric tube may be placed prior to surgery to suction the stomach and prevent (or
reduce) aspiration.
MEDICATIONS
• H2-blockers and antacids have not traditionally been used, as patients are routinely kept
NPO as well as suctioned orally or nasally both preoperatively and prior to extubation.
• Bicarbonate, in general, is not indicated even in patients with metabolic acidosis. The acid–
base imbalance is the direct result of severe dehydration and hypoperfusion and therefore
efforts should be directed to correct the underlying pathology.
• Limited data is available for nonsurgical treatment. There is some evidence that IV or oral
atropine can cause regression or decreased severity of obstruction. However, surgical
correction is the standard of care and medical management should only be considered if the
patient is a poor surgical candidate or whose parents are opposed to surgery (4).
Labs/Studies
• Generally accepted values for surgical readiness:
– Serum [Cl-] <100 mEq/L
– Serum [HCO3-] <28 mEq/L
– Urine output 0.5–1 mL/kg/hr
• Ultrasound, has a 95% sensitivity and 100% specificity; it has largely replaced the historical
oral contrast barium swallow test as the standard diagnostic tool
Rare
CIRCUMSTANCES/CONDITIONS TO DELAY
Correction of volume deficit and electrolyte disturbances with IV fluids must be done prior to
surgical repair. This can usually be accomplished in 24–48 hours.
TREATMENT
Premedications
• Premedication with narcotics and benzodiazepines are generally avoided to prevent
hypoventilation (respiratory acidosis) in the setting of metabolic alkalosis.
• Atropine is routinely administered prior to gastric suction tube placement and
succinylcholine injection to prevent bradycardia. Infants have stiff ventricles and are
dependent on their heart rate to maintain adequate cardiac output; thus, bradycardia is
poorly tolerated.
Risk of pulmonary aspiration
INTRAOPERATIVE CARE
General anesthesia with an endotracheal tube
Monitors
• One IV catheter is adequate (22 gauge)
• Invasive monitors such as arterial lines are generally not indicated in a fluid-resuscitated
patient without other comorbidities.
• Patients may present with a nasogastric tube. If not, gastric contents should be removed
with an orogastric tube prior to induction. Several passes in different positions may be
necessary.
• A rapid sequence IV induction with cricoid pressure is traditionally performed to reduce the
• An awake intubation is indicated if there are concerns for a difficult airway or high risk for
aspiration. Viscous lidocaine can be used to topicalize the oropharynx.
• Although succinylcholine is generally contraindicated in children, it may be considered in
pyloric stenosis surgery; atropine is administered to prevent bradycardia. When
succinylcholine is contraindicated, intubation without muscle relaxant or with rocuronium
can be performed.
• Propofol and pentothal have been successfully used. Etomidate can result in adrenal
suppression.
• The choice of ETT size should be based on the baby’s age and weight. In this patient
population, a cuffed or uncuffed 3.5–4.5 ETT is usually appropriate. A size 3.5 cuffed or
uncuffed tube can typically be used. Although uncuffed tubes are routinely utilized to avoid
subglottic stenosis, in this clinical scenario, cuffed tubes are appropriate (5).
Maintenance
• Inhalational agents or IV technique.
• Narcotics should be used cautiously, if at all, secondary to existing metabolic alkalosis and
subsequent ventilatory suppression. The surgical team routinely infiltrates the wound with
local anesthetics at the end of the procedure. Acetaminophen is usually sufficient for
postoperative pain control.
• Oxygen should be minimized as tolerated to avoid oxygen toxicity and retinopathy of
prematurity, especially in preterm patients. Nitrous oxide is generally avoided in
laparoscopic procedures, at least during insufflation.
• In laparoscopic surgery, there may be hypercapnia secondary to CO2 absorption.
Hyperventilation should be avoided to prevent apnea. Abdominal insufflation can result in
decreased venous return, reduced functional residual capacity, and increased airway
pressure; this should be anticipated and treated accordingly.
• Normothermia should be maintained. Infants have a relatively larger body surface area from
which heat can radiate to the cooler environment. In addition, temperature regulatory
mechanisms have not fully developed. Severe hypothermia can lead to metabolic acidosis
and coagulopathy.
• Awake extubation is recommended, given the risk of aspiration, hypoventilation, and apnea.
• If a non-depolarizing muscle relaxant has been used, check twitch monitor and adequately
dose reversal agents as appropriate.
• Stomach and oral secretions should be thoroughly cleared prior to extubation.
FOLLOW-UP
BED ACUITY
Regular floor bed; observation for 12 hours is needed to assess for postoperative apnea and
hypoventilation.
This age group is prone to hypoglycemia and glucose levels should be checked especially
when dextrose-containing maintenance fluids are ceased.
COMPLICATIONS
• Duodenal perforation
• Incomplete myotomy with recurrent vomiting
• Dehiscence
• Hernia
REFERENCES
1. Bissonnette B, Sullivan PJ. Pyloric stenosis. Can J Anesth. 1991;38(5):668–676.
2. Hulka F, Harrison MW, Campbell TJ, et al. Complications of pyloromyotomy for infantile
hypertrophic pyloric stenosis. Am J Surg. 1997;173:450–452.
3. Cook-Sather SD, Tulloch HV, Cnaan A, et al. A comparison of awake versus paralyzed
tracheal intubation for infants with pyloric stenosis. Anesth Analges. 1998;86:945–951.
4. Yamataka A, Tsukada K, Yokoyama-Laws Y, et al. Pyloromyotomy versus atropine sulfate
for infantile hypertrophic pyloric stenosis. J pediatr surg. 2000;35(2):338–342.
5. Lichtor JL, Shiveley TJ, Wallace EC. Images in anesthesiology: pyloric stenosis.
Anesthesiology.. 2010;112:1270.
ADDITIONAL READING
• Malhotra V, Sharma A. Pyloric Stenosis. In: Yao FF, ed. Yao and Artusio’s anesthesiology
problem-oriented patient management. 6th edition. Philadelphia, PA: Lippincott Williams &
Wilkins; 2008:514–526.
• Alkalosis metabolic
• Hypokalemia
• Hypoglycemia
CODES
ICD9
• 537.0 Acquired hypertrophic pyloric stenosis
• 750.5 Congenital hypertrophic pyloric stenosis
ICD10
• K31.1 Adult hypertrophic pyloric stenosis
• Q40.0 Congenital hypertrophic pyloric stenosis
CLINICAL PEARLS
• Pyloric stenosis is a medical, not surgical, emergency. Fluid and electrolyte abnormalities
should be optimized prior to surgical repair.
• Patients are considered to have a “full stomach” and require gastric decompression followed
by a rapid sequence induction or awake fiberoptic intubation.
• Judicious use of respiratory depressants such as narcotics and benzodiazepines.
• Postoperative hypoventilation or apnea can occur with intraoperative hyperventilation or an
alkalotic CSF.
QT PROLONGATION
BASICS
DESCRIPTION
• The QT interval (QT) refers to the time between the start of ventricular depolarization to the
end of repolarization; normally between 0.3 and 0.44 seconds.
• A prolonged QT interval is affiliated with ventricular arrhythmias, particularly the
development of Torsades de Pointes. This condition is otherwise known as long QT
syndrome (LQTS) and can be either congenital or “acquired.”
• Surgical stimulation and several perioperative medications can have adverse effects on
patients with LQTS.
EPIDEMIOLOGY
Prevalence
US: 1:1,100–5,000 people
Morbidity
Although some patients present initially with syncope to the emergency department, for
many patients there is no pre-morbid state prior to collapse and out-of-hospital cardiac arrest.
Mortality
US: 4,000/year
Risk Factors
• Increased sympathetic tone can precipitate Torsades de Pointes.
• Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia)
• Drugs (see Table 1)
• Anorexia nervosa (severe starvation)
• Hypothermia
Table 1 Medications that affect the QT interval
• Normal ventricular depolarization: After the sinoatrial (SA) node spontaneously depolarizes
(sodium channel influx), the signal is spread via 3 accessory conduction tracts in the atrium
to the atrioventricular (AV) node. Adjacent myocardial cells depolarize in a domino fashion.
Electrical depolarization is followed by mechanical contraction of the atrium, with blood
being pumped into the ventricles. The conduction fibers from the atrium are connected to
those in the ventricle via the bundle of His (preceded by the AV node); in the ventricles, the
signal is then transmitted along the left and right bundle branches onto the Purkinje fibers.
In the same manner, the adjacent muscle cells are depolarized in a domino fashion, and
depolarization is followed by ventricular contraction and blood ejection.
• Normal early myocardial repolarization in the ventricle begins with a rapid, transient efflux
of potassium. Potassium efflux continues via slowly activating (iKs) and rapidly activating
(iKr) delayed rectifier channels. However, this process is counteracted by an influx of
calcium and sodium that prolongs repolarization and allows time for mechanical
contraction and systolic ejection of blood. The complex interactions between these ions and
their respective channels dictate the duration and characteristics of repolarization.
• Heterogenous rate of repolarization: The rate of repolarization is not equal between the
epicardium, mid-myocardium, and endocardium. The mid-myocardial cells have less iKs
channels and more iNa channels; therefore, the rate of repolarization is slower than the
other 2 layers. This causes a transmural dispersion of repolarization (TDR).
– EKG: The peak of the T wave represents epicardial cell repolarization and the end of the T
wave represents mid-myocardial cell repolarization (where repolarizatoin is slowest).
– TDR is manifested on the EKG by the interval between the peak of the T wave to the end
of the T wave (Tp-e).
• The QT interval represents the time period during which ventricular depolarization and
repolarization occur. It is rate-dependent; bradycardia has longer intervals whereas
tachycardia has shorter intervals. Thus, its assessment and interpretation must factor in, and
be corrected for, heart rate. The corrected QT (QTc) is calculated using Bazett’s formula,
QTc = [QT/(R–R)]. R−R is the R-to-R interval in seconds.
• LQTS is caused by the malfunction of cardiac ion channels. Any condition that qualitatively
or quantitatively decreases the iK channel function or increases the iNa channel function
will prolong the QT interval, exaggerate the TDR, and prolong repolarization. This
heterogeneity of repolarization leads to an increased potential for self-sustaining re-entrant
circuits and early after-depolarizations (EADs), which can degenerate into Torsades de
Pointes.
– Prolonged QT is defined as a corrected QT interval (QTc) >0.45–0.47 seconds in males
and 0.47–0.48 seconds in females.
• “Acquired” LQTS is thought to occur in silent gene carriers until symptoms manifest after
being exposed to a provoking drug or sympathetic stimulation.
• Preoperative assessment of the patient may reveal historical and/or ECG characteristics
diagnostic for LQTS. It is necessary to correct for heart rate; most modern EKG machines
provide a QTc value.
• Anesthesia in patients with untreated LQTS carries a very high risk for malignant ventricular
arrhythmias. They should be optimized prior to surgery and should be on a maintenance
beta-blocker regimen.
• Avoidance of sympathetic outflow is necessary as this predisposes to re-entrant ventricular
arrhythmias and Torsades de Pointes.
SYMPTOMS
• 60% of patients are asymptomatic until a presenting syncopal or pseudoseizure episode
(usually in childhood or early adulthood).
• Occasionally, the first symptom may present as Torsades de Pointes under anesthesia.
History
• In patients without known LQTS, some “red flags” to watch out for are syncope with or
without stress, unexplained sudden cardiac death before age 30 in immediate family
members, and family members with known LQTS. It will often manifest as a child or in
early adulthood. If concern for LQTS is raised in an elective case, referral to a cardiologist
should be made for a possible electrophysiology study.
• Patients with a known history of LQTS should be on scheduled beta-blockers that are
continued perioperatively. Serum electrolytes should be within normal limits.
Signs/Physical Exam
• Often nonspecific physical examination
• Adequately beta-blocked patients should (ideally) not have any change in QT interval during
a Valsalva maneuver.
MEDICATIONS
Beta-blockers help reduce the incidence of cardiac events, but they are not entirely effective
for preventing sudden death.
Labs/Studies
• ECG: Prolonged QTc, T wave alternans, notched T wave in 3 leads
• Serum electrolytes should be assessed and abnormalities should be corrected.
• If a pacemaker or ICD is present, follow appropriate perioperative management.
• In Jervell and Lange-Nielsen syndrome, patients also have congenital deafness.
• In Andersen syndrome (LQT7), patients have periodic paralysis.
• Inadequate beta-blockade
• Abnormalities in electrolytes can delay repolarization (hypokalemia, hypomagnesemia, and
hypocalcemia).
CLASSIFICATIONS
• Acquired LQTS: It is now thought that these cases have common nucleotide polymorphisms
that alter ion channel repolarization behavior in the presence of drugs, electrolyte
abnormalities, or in certain disease states.
• Congenital LQTS: 8 different genotypes (LQT1-8) have been identified. Romano–Ward
syndrome is the most common presentation of congenital LQTS and is inherited in an
autosomal dominant manner. Jervell and Lange-Nielsen syndrome is autosomal recessive
and is associated with deafness.
TREATMENT
Premedications
• Consider preoperative sedation when appropriate. Limiting anxiety and sympathetic outflow
is crucial.
• Avoid abrupt and loud noises; may trigger Torsades de Pointes.
INTRAOPERATIVE CARE
Epidurals, spinals, and general anesthetics have all been administered safely; there is no
evidence that one mode is safer than the other.
Monitors
• Low threshold for intra-arterial monitoring
• Low threshold for central venous access, as it can facilitate transvenous pacing.
• Midazolam, fentanyl, morphine, and propofol appear to be benign in LQTS. Thiopental
prolongs the QT interval but may reduce dispersion of depolarization and has been safely
used in congenital LQTS. Ketamine should be avoided.
• Succinylcholine may prolong the QT interval.
• Laryngoscopy, intubation, suctioning, and cold-inspired gases can cause a sympathetic
outflow; these potent stimuli may be attenuated by a short-acting opioid and/or esmolol.
• Consider topical anesthesia to vocal cords prior to intubation.
• Total IV anesthesia with a propofol and remifentanil infusion may provide excellent
attenuation of sympathetic outflow throughout induction, intraoperative maintenance, and
emergence; with the advantage of a short context sensitive half-life.
Maintenance
• Avoid sympathetic stimulation by maintaining normocarbia, normothermia, normoglycemia,
normovolemia, and normoxia.
• Volatile anesthetics prolong the QT interval, but isoflurane and sevoflurane have been used
safely in congenital LQTS.
• Keep patient “deep” or adequately anesthetized; otherwise innocuous stimuli can result in
increased sympathetic outflow.
• High ventilatory pressures should be avoided as this may cause QT prolongation.
• Pancuronium has vagolytic properties and should be avoided.
• Avoid sympathomimetic drugs such as ephedrine.
• Droperidol should be avoided in LQTS. Ondansetron is considered a medication with
possible risk for prolonging the QT interval.
• Consider “deep” extubation while the patient is in a surgical plane of anesthesia, if
appropriate.
• Neostigmine, edrophonium, atropine, and glycopyrrolate should be avoided because each
may cause QT interval prolongation.
FOLLOW-UP
BED ACUITY
• Will need postoperative ECG monitoring, as the perioperative period may exacerbate QT
prolongation.
• Good pain control can avoid sympathetic stimulation.
COMPLICATIONS
• Torsades de Pointes:
– Some episodes will be short and self terminating.
– Can occur at any point in the perioperative period.
– Can manifest in hemodynamic instability and degenerate into ventricular fibrillation.
• Treatment consists of:
– If unstable, ACLS should be instituted immediately with early chest compressions,
asynchronous defibrillation, and magnesium sulfate (30 mg/kg).
– Magnesium dose can be repeated after 15 minutes, followed by an infusion of 3–20
mg/min if arrhythmias persist.
– If resistant to magnesium, Torsades can be treated with pacing to accelerate the heart rate.
REFERENCES
1. Kies SJ, Pabelick CM, Hurley HA, et al. Anesthesia for patients with congenital long QT
syndrome. Anesthesiology. 2005;102:204–210.
2. Hunter J, Sharma P, Rathi S. Long QT syndrome. Continuing education in anaesthesia.
Critical Care and Pain. 2008;8(2):67–70.
3. Schwartz PJ, Moss AJ, Vincent GM. Diagnostic criteria for the long QT syndrome: An
update. Circulation. 1993;88:782–784.
ADDITIONAL READING
• www.torsades.org
• ACLS anesthetic management
• 12-lead EKG
• Magnesium
• Defibrillation
CODES
ICD9
• 426.82 Long QT syndrome
• 794.31 Nonspecific abnormal electrocardiogram [ECG] [EKG]
ICD10
I45.81 Long QT syndrome
CLINICAL PEARLS
• LQTS is a significant cause of sudden death in young people, and is probably
underdiagnosed.
• For a significant number of patients with LQTS, their first manifestation may be under
anesthesia.
• Avoid stimuli that evoke sympathetic outflow including hypothermia, pain, hypoxia,
excessive ventilatory pressure, and hypovolemia.
• For patients with known LQTS, ensure that they are not hypokalemic, hypocalcemic, or
hypomagnesemic. Ensure that they are adequately beta blocked.
RADIATION SAFETY
Bradley T. Dollar, MD
BASICS
DESCRIPTION
• Medical exposure to irradiation typically comes from three major sources: Diagnostic
radiologic examinations, the use of radiopharmaceuticals in nuclear medicine, and
therapeutic applications of radiation. We will focus on radiologic examinations.
• Anesthesia providers are exposed to increasing amounts of radiation as the intraoperative
use of fluoroscopy and other radiologic techniques increase.
• Anesthesiology pain practitioners increasingly use fluoroscopy to facilitate proper needle
placement for nerve blocks.
• Perspective: Radiation exposure occurs daily in the form of cosmic rays from outer space
(higher during airplane travel) and naturally occurring radioactive materials (e.g., radon
gas). Persons living at higher altitude or at the north and south poles have higher exposure
to cosmic radiation than persons at sea level or nearer the equator.
• Factors affecting the dose of radiation with x-ray include patient size, beam angle, type of
fluoroscopy, and acquisitions.
• Patient size:
– Radiation is attenuated by 1/2 for every 5 cm of soft tissue. For example, a patient with
10 cm of extra tissue requires four times the dose to maintain the same image quality.
– Dose increases in a fluoroscopy unit are automatically controlled so the operators do not
perceive these differences.
• Beam angle:
– Directing the beam through the patient at an oblique angle will raise the radiation dose
due to increased tissue thickness.
• Type of fluoroscopy:
– Continuous fluoroscopy allows real time visualization of dynamic activity using low x-ray
tube currents.
– Pulse fluoroscopy acquires frames that are less than real time (e.g., 7.5 or 15 frames per
second) thereby reducing patient dose.
– Pulsed – High (30 f/s) approaches continuous dose rate.
– Photospot images (e.g., acquisitions) are obtained utilizing the same imaging chain as
fluoroscopy but the x-ray tube current increases from 1 to 5 mA to ∼300 mA. Photospot
images are of diagnostic quality required for most clinical diagnosis.
• Increased magnifications:
– Dose increased in order to maintain image brightness
– Not a substantial effect on patient or operator.
• Collimation: The process of restriction and confinement of an x-ray beam to focus only on
the area of interest.
– Decreases area of skin and volume of tissue exposed and makes it easier to distribute the
skin dose
– Less scatter to personnel
– Improved image quality from less scatter
– Increases automatic brightness control that increases entrant skin dose
ANATOMY
• Tissue weighting factors refer to the different probabilities for the occurrence of stochastic
radiation effects. Higher values reflect an increased probability of detrimental effects to that
organ system from radiation exposure.
See Table
• Additional anatomical considerations:
– Eyes. Excessive exposure can lead to premature cataracts (left eye most common for c-arm
operators due to usual location of beam).
– Developing fetus during pregnancy can be affected (especially during organogenesis in the
first trimester).
– Patient skin. Varying the entry point of the radiation beam, when practical, will spread
the radiation over more skin and reduce the likelihood that any one area will be
overexposed. The image intensifier should be lowered as close as practical to the patient’s
skin to minimize scatter and maximize the gap between the x-ray tube and the skin. Even
for a fixed fluoroscopy unit (tube fixed under the unit’s table so that the tube to skin
distance is fixed) lowering the image Intensifier will lower the skin dose.
• Cells that survive radiation exposure may be subsequently modified. This can occur as
carcinogenenesis or hereditary effects, both of which are stochastic effects.
• Stochastic effects (cancer and genetic damage) have an increased risk of occurrence with
increased radiation dose; they occur many years after exposure. There is no threshold or
certainty that they will occur, only an increased risk (stochastic effects are also known as
the “linear-no threshold theory”). Furthermore, the severity of that disease is independent of
the dose once the disease is present.
• Nonstochastic effects (deterministic effects). Unlike stochastic effects, they have a clear
relationship between the exposure and the effect. Nonstochastic effects often result from
very large dosages in a short period of time and manifest within hours or days. Examples
include erythema, skin and tissue burns, sterility, and radiation sickness.
• Genetic mutations leading to hereditary effects. Any dose of radiation has the potential to
cause a mutation in the DNA that can be passed on genetically. Females are born with all of
the eggs that they will have for their lifetime. Proper shielding should occur to minimize the
risk.
• Early effects of ionizing radiation. These are dose-dependent stochastic effects of total body
radiation that occur in the following sequence:
– Hematologic (bone marrow syndrome)
– GI syndrome
– CNS syndrome (highest doses of exposure).
– Local tissue damage (skin, gonads, extremities)
– Hematologic depression
– Cytogenic damage
• Late effects:
– Leukemia
– Malignancies (bone, lung, breast, etc.)
– Local tissue damage (skin, gonads, eyes)
– Shortened life span
– Genetically significant dose
• Effects on fetus:
– Lethal effects can occur before or immediately after implantation of the fertilized ovum in
the uterine wall or at any time during intrauterine development. It can be expressed as
prenatal or neonatal death.
– Congenital malformation is expressed after birth as a result of radiation exposure during
organogenesis (multiple organ systems may be affected, but is most commonly seen in the
CNS, skeletal, and ocular systems).
– Childhood malignancies (leukemia)
– Diminished growth and development (intrauterine or after birth)
– Atomic bomb survivors exposed in utero most commonly presented with microcephaly and
mental retardation defects.
• Radiation reduction can be accomplished by
– Reducing the gap between the patient and the image intensifier (less scatter)
– Minimizing beam time
– Collimating (with fluoro OFF)
– Using the lowest possible fluoro pulse rate (high-dose settings deliver 10 times the dose).
– Minimizing acquisition (use last image hold and cine hold).
– Using lowest frame rate acquisition as needed (and variable frame rate).
– Changing beam angle to vary skin dose to avoid patient skin burns (collimation helps).
– Using the least magnification possible.
– Positioning the C arm fluoroscopy field of view on the opposite side of the practitioner
(reduces the exposure of the upper body).
– During cross table x-rays, if the image intensifier side is positioned over the patient,
dosing can be reduced by 1/5th (scatter occurs as the beam contacts the patient).
• Reducing provider dose:
– Lead apron. During fluoroscopy, a 0.5 mm lead equivalent apron can attenuate 95% of the
scattered radiation to the shielded torso; a 0.25 mm apron attenuates 80%. Wear a wrap-
around apron if the back will be to the source.
– Thyroid shield
– Custom lead protective glasses: A 5 mm thick lens will block 92% of the radiation and a
10 mm thick lens will block 99%. Regular glass lenses of 5 and 10 mm thickness block
30% and 50% of radiation, respectively.
– Table skirt
– Overhead shield
– Lead gloves provide minimal protection and may cause a false sense of security – Holding
hands with lead-lined gloves in x-ray beam causes fluoroscopy unit to adjust to increase
the dose delivered (don’t place hands in primary beam).
– Stand at least 6 feet from beam if possible.
• Monitoring provider radiation dose:
– Over apron dosimeter is placed at the thyroid collar to monitor exposure to eyes, thyroid,
and head.
– Under apron dosimeter to monitor exposure to the rest of the body.
– For practitioners near the beam, a finger ring dosimeter to monitor exposure to hands.
– Pregnant providers should be provided an additional dosimeter to be worn under the lead
apron at waist level to monitor fetal exposure and should strongly consider a wrap around
lead apron that provides coverage from exposure from behind. Usual precautions should
be utilized as well.
• Recommended dose limits. The International Commission on Radiological Protection
recommends an effective dose limit of 20 mSv/year (mSv = millisievert) averaged over 5
years to limit the probability of stochastic effects. In addition, the effective dose should not
exceed 50 mSv in any given year. Pregnant females should have a supplementary equivalent
dose limit of 2 mSv applied to the surface of the abdomen to reduce the risk of fetal effects.
EQUATIONS
• Equivalent doses = sum of the weighted absorbed doses; does not take into account the
differing susceptibilities of radiation to different organs.
• Effective dose = sum of the weighted equivalent doses in all tissues and organs of the body.
Accounts for the “tissue weighting factor” that represents the relative contribution of that
organ to the total detriment due to those effects resulting from uniform radiation of the
whole body.
• Rule of thumb – One step back from tableside: Cuts exposure by a factor of 4.
GRAPHS/FIGURES
Radiation units – There are a number of units to measure radiation dose and exposure:
• rad: Radiation absorbed dose
• rem: Roentgen-equivalent-man
• Roentgen (R, r) (rent-gen, rent-chen).
• sievert (Sv) (see-vert). The most pertinent unit for measuring ionizing radiation effective
dose, which accounts for relative sensitivities of different tissues and organs exposed to
radiation. The radiation quantity measured by the sievert is called the effective dose. A mSv
is one-thousandth of a sievert.
• Comparative patient radiation doses of different studies:
– Dental x-ray – 0.005 mSv
– Chest x-ray – 0.1 mSv
– Mammogram – 0.4 mSv
– CT abdomen/pelvis – 15 mSv
– CT abdomen/pelvis with and without contrast – 30 mSv
– Fluoroscopic-guided procedures – Difficult to measure due to operator variability and
fluoroscopy time differences.
REFERENCES
1. Mettler FA, Upton AC. Medical Effects of Ionizing Radiation, 3rd ed. Philadelphia: WB
Saunders Company, 2008.
2. Norris TG. Radiation safety in fluoroscopy. Radiol Technol. 2002;73(6):511–536.
3. Schueler BA, Vrieze TJ, Bjamason H, et al. An investigation of operator exposure in
interventional radiology. RadioGraphics. 2006;26:1533–1541.
4. Seeram E. Radiation Protection. Philadelphia: Lippincott-Raven, 1997.
5. Tremains MR, Georgiadis GM, Dennis MJ. Radiation exposure with use of the inverted-c-
arm technique in upper-extremity surgery. J Bone Joint Surg. 2011;83:674–678.
• Infectious disease exposure in the health care worker
CODES
ICD9
990 Effects of radiation, unspecified
ICD10
• T66.XXXA Radiation sickness, unspecified, initial encounter
• T66.XXXD Radiation sickness, unspecified, subsequent encounter
• T66.XXXS Radiation sickness, unspecified, sequela
CLINICAL PEARLS
• Minimizing provider exposure includes the use of shielding, increasing distance from the
source of radiation, and reducing exposure time.
• Ultrasound uses acoustic radiation and no known risk is associated with this type of
imaging.
• MRI. The patient and provider are exposed to rapidly changing magnetic fields as well as
electromagnetic radiation. Although thought to be safe, there is a potential for undiscovered
biological effects. Known hazards may occur in providers with pacemakers, defibrillators, or
other implantable devices. In addition, ferrous materials in the vicinity can become
hazardous projectiles.
• Standard set-up for a C-arm is the x-ray tube in the down position (near the floor) and the
image intensifier in the up position. These devices are occasionally inverted. It is important
to recognize the configuration so that the practitioner is able to minimize provider exposure
and also in order to properly shield the patient.
• Lead aprons should be hung and not folded. Folding leads to cracks in the lead that can
cause decreased effectiveness in the barrier.
• Routine maintenance of equipment should be performed to ensure proper functioning and
safety.
• X-rays done in patient settings that have multiple patients (postanesthesia care unit) should
be avoided to minimize unnecessary exposure of other patients to radiation.
• Anesthesia providers are occasionally asked to care for critically ill patients in the CT
scanner. Recall that radiation doses for CT scans are much higher and the provider should
maintain as many safety measures as possible (time, distance, and barriers).
• There is significantly increased x-ray tube current to obtain a photo spot (acquisition)
image: 1 photo spot image is approximately equivalent to 20–25 seconds of fluoroscopy
time (though significant variation can exist secondary to technique).
RADICAL NECK DISSECTION
BASICS
DESCRIPTION
General
• Performed to remove primary and metastatic cancer from the head and neck. The close
proximity of several structures, including lymph nodes in the neck, facilitates spread to
nearby tissues.
• Traditional radical neck dissection (RND) is defined as the exploration and systematic
removal of lymph nodes from all five levels of the neck as well as an en bloc resection.
– Neck levels describe and identify lymph nodes in the neck. Level I begins cephalad to the
submental and submandibular triangles. Subsequent levels progress caudally down the
neck with level 5 including the spinal accessory nerve and transverse cervical artery.
– En bloc resection describes the removal of the sternocleidomastoid muscle, internal jugular
(IJ) vein, and spinal accessory nerve (CNXI) contained within those neck levels (1)[C].
• Modified RND removes lymph nodes from all five levels but is “modified” to preserve the
sternocleidomastoid muscle, IJ vein, and/or CN XI.
Position
• Supine; often with a shoulder roll to improve neck extension and exposure
• Head laterally rotated to opposite side of the surgery
• Arms often tucked to allow surgeons to stand closely
• Head of bed often rotated 180° from the anesthesia machine
Incision
Varies based on patient characteristics and surgeon preference (e.g., wine glass, apron access,
McFee). Typically, a horizontal skin incision with vertical extension along the neck allows for
good exposure.
Approximate Time
Variable. Usually takes 2–4 hours but may take significantly longer if a free flap
reconstruction is involved. Pathological evaluation of lymph nodes during surgery may
increase anesthetic time with very little surgical stimulation to the patient.
EBL Expected
• Typically 100–300 mL
• Blood loss may be increased in patients who have received preoperative radiation therapy,
require primary tumor resection in addition to lymphadenectomy, or require flap
reconstruction.
• It may be prudent to type and screen all patients undergoing RND and crossmatch those
with anemia or at an increased risk for blood loss.
Hospital Stay
2–5 days; recent evidence for <24-hour stay has been reported in patients who had no
primary site resection and no oral resection (2)[B].
• Nerve monitoring via direct nerve stimulation for the spinal accessory nerve (CN XI),
hypoglossal nerve (CN XII), and marginal mandibular branch of the facial nerve are
common. The marginal mandibular branch of the facial nerve aids in smiling (supplies
muscles of lower lip and chin); it is a small nerve and is at higher risk of injury.
• Difficult airway equipment may be needed to secure the airway, including surgical
tracheostomy equipment.
EPIDEMIOLOGY
Prevalence
In the US, ∼ 5,000–10,000 neck dissections/year
Prevalence
Dependent on primary cancer source (e.g., squamous cell, melanoma, thyroid, and salivary
gland)
Morbidity
Ranges from 3–30% and includes bleeding and infection. Risk increases based on the nature
of dissection (radical, modified), ASA class, and duration of anesthesia (3)[B].
Mortality
Low
• Patient population often has a history of longstanding tobacco use with resultant
cardiovascular and pulmonary comorbidities.
• Airway management may be challenging given the location and amount of tumor burden in
the neck as well as a previous history of radiation or surgery on the head or neck for
primary tumor.
• Nerve monitoring precludes the use of intermediate and long-acting muscle relaxants.
• Fluid and hemodynamic management may be challenging if free flap reconstruction is
employed; need to balance the maintenance of anesthesia, combined with low surgical
stimulation and the need to avoid vasopressors (may jeopardize perfusion of the free flap).
SYMPTOMS
• Common symptoms include dysphagia, odynophagia, and neck/jaw pain that can result in
weight loss and malnutrition.
• Some patients may be asymptomatic and metastatic tumor is found on serial follow-up
exam.
History
Carefully question the patient about previous anesthetics and history of past intubation
attempts. Many patients have a history of previous head and neck surgery or radiation
therapy to the neck, which can complicate airway management. Evaluation of old anesthetic
records, if available, may be invaluable.
Signs/Physical Exam
• Auscultation of the heart and lungs, at a minimum, is necessary for each patient.
• Careful airway exam given the potential for a difficult airway (Mallampati score, mouth
opening, thyromental distance, neck mobility, tracheal palpation, and cervical range of
motion).
MEDICATIONS
• Chemotherapeutic agents
• Bronchodilators, steroids
• H2 blockers or proton pump inhibitors
Labs/Studies
• Type and screen is usually warranted for all patients.
• Further preoperative lab testing is based on individual patient comorbidities.
• Preoperative lymph node biopsies may be performed by the surgeon prior to RND.
• Radiographic studies such as neck CT or head/neck MRI are often performed preoperatively
to assess for involvement of nearby structures (e.g., vasculature). PET scan may be
completed to evaluate for further metastatic disease. Anaesthetist may consider reviewing
films to assess for tumor invasion or edema of the trachea.
• Barium swallow may be performed preoperatively to evaluate patients at high risk for
swallowing difficulty/malnutrition.
• Cerebrovascular disease, coronary artery disease, and COPD are common if the patient is
elderly and has a significant history of tobacco use.
• Thyroid disease/dysfunction may be evident if the patient has a history of primary thyroid
cancer.
TREATMENT
Premedications
• Patient specific: Related to patient comorbidities (e.g., beta-blockers, albuterol, and
nonparticulate antacids)
• Airway topicalization, anticholinergics, and anxiolytics may be necessary for patients
requiring awake fiberoptic intubation.
Consent for anesthesia should include a discussion of special airway management (e.g., need
for awake fiberoptic), the possibility of blood transfusion if the patient is at a higher risk for
blood loss, the possibility of tracheostomy, and postoperative mechanical ventilation.
• Broad spectrum, third-generation cephalosporin such as cefazolin can protect against skin
flora.
• Ampicillin/sulbactam if the surgery involves the parapharyngeal cavity or free flap
reconstruction.
• Clindamycin is a reasonable alternative for the penicillin-allergic patient.
INTRAOPERATIVE CARE
• Typically general anesthesia with an ETT
• Consider a combination of regional anesthesia (superficial or deep cervical plexus blocks for
postoperative pain management) and general anesthesia in select patient populations.
Regional anesthesia as the sole anesthetic is limited by patient willingness, anaesthetist’s
experience, surgical time, and surgical site involvement.
Monitors
• Two large bore IVs
• Arterial line may be considered in patients with known heart dysfunction and moderate-to-
severe lung dysfunction, or in patients undergoing concomitant free flap reconstruction.
• Flow-volume loops for patients with moderate to severe lung dysfunction.
• Central line is rarely required unless the patient has moderate-to-severe left ventricular
dysfunction or poor existing IV access. CVC sites are typically limited to the contralateral
IJ/subclavian (or femoral veins if the patient is undergoing bilateral RND).
• Brain function monitors such as a BIS may be helpful if total IV anesthesia is employed or if
muscle relaxants are avoided due to nerve monitoring.
• Special airway management should be considered based on the preoperative airway
assessment, history of previous anesthetics, history of radiation therapy, recent radiographic
studies, and discussion with surgical ENT colleagues to delineate potential difficulties with
intubation.
• If a standard IV general induction is to be performed, have difficult airway equipment and
assistants readily available for a potential difficult airway.
• Awake tracheostomy may be necessary if the airway is severely compromised.
• If surgical nerve monitoring is planned, avoid intermediate and long-acting muscle relaxants
to facilitate intubation.
Maintenance
• A balanced technique based on the anaesthetist’s preference, use of nerve monitoring, and
length of procedure
• Total intravenous anesthesia (TIVA). Propofol TIVA is usually well-tolerated by patients. It
results in rapid emergence and has been shown to reduce postoperative nausea/vomiting; it
may be combined with another sedative or opioid as part of a balanced technique. May see
hypotension at general anesthetic doses; decreases in BP with propofol TIVA may be
associated with decreased surgical blood loss.
• Volatile agents. Easy to use, well tolerated by patients.
• Narcotics. Free flap reconstruction may be associated with significant postoperative pain.
However, opioids can result in sympatholysis and potential hypotension that is compounded
during times of minimal surgical stimulation. Balance the titration or infusion of narcotics
intraoperatively against the potential for hypotension, or consider starting titration toward
the end of the procedure.
• Free flap perfusion may be enhanced by the avoidance of vasopressors and keeping the
patient warm. Vasoconstrictors may reduce flow; hypothermia results in vasoconstriction.
• If surgical nerve monitoring used, avoid muscle relaxants.
• IV and breathing circuit extensions may be necessary when the bed is turned
• Standard extubation criteria apply. Try to avoid coughing/bucking on the ETT; control BP
during emergence to avoid bleeding from the wound.
• Extubation in patients who were difficult to intubate, have undergone long procedures with
free flap reconstruction and/or tracheostomy placement, or are at high risk for pharyngeal
or laryngeal edema, should only be performed with extreme caution, if at all. Consider
postoperative mechanical ventilation and intensive care unit (ICU) transport.
FOLLOW-UP
BED ACUITY
For uncomplicated RND, a floor bed is usually adequate. ICU monitoring is often necessary
for patients who have undergone free flap reconstruction and recent tracheostomy placement.
ANALGESIA
• IV narcotics, including patient-controlled analgesia, are typical.
• Superficial or deep cervical plexus nerve blocks may be considered in patients with chronic
pain or other unique conditions.
COMPLICATIONS
• Intraoperative complications include
– Hypotension/bradycardia due to carotid sinus irritation
– Prolonged QT interval due to interruption of the cervical sympathetic innervation of the
heart in patients undergoing right RND
– Air embolism if the IJ is opened or sacrificed
– Airway trauma/edema due to a difficult airway or prolonged intubation
– Pneumothorax if dissection is low in the neck
– Massive hemorrhage and/or stroke if the carotid is injured (4)[C].
• Postoperative complications include
– Hypertension due to carotid sinus denervation (5)[B]
– Airway compromise due to tight dressing/possible hematoma or postoperative
oropharyngeal/laryngeal edema
– Diaphragm dysfunction if the phrenic nerve is injured
– Facial edema if the IJ is sacrificed
– Winged scapula and shoulder dysfunction if the spinal accessory nerve is sacrificed
– Facial droop if the facial nerve is injured
– Carotid blow-out (rare but carries 50% mortality) (4)[C].
• Preoperative malnutrition and history of neck radiation increases the risk of a postoperative
wound infection and poor wound healing.
PROGNOSIS
Overall good, but ultimately based on the type and extent of metastatic disease and the
ability to completely resect disease burden.
REFERENCES
1. obbins KT, Shaha AR, Medina JE, et al.Consensus statement on the classification and
terminology of neck dissection. Arch Otolaryngol Head Neck Surg. 2008;134(5):536–538.
2. Tracy JC, Spiro JD. Short hospital stay following neck dissection. Arch Otolaryngol Head
Neck Surg. 2010;136(8):773–776.
3. Ferrier MB, Spuesens EB, Le Cessie S, et al. Comorbidity as a major risk factor for mortality
and complications in head and neck surgery. Arch Otolaryngol Head Neck Surg.
2005;131:27–32.
4. Kerawala CJ, Heliotos M. Prevention of complications in neck dissection. Head Neck Oncol.
2009;12:1–35.
5. Celikkaat S, Akyol MU, Koc C, et al. Postoperative hypertension after radical neck
dissection. Otolaryngol Head Neck Surg. 1997;117:91–92.
ADDITIONAL READING
• Lalwani AK. Current Diagnosis and Treatment in Otolaryngology: Head and Neck Surgery.
McGraw-Hill Medical, USA, 2008.
• Tracheostomy
• Cervical block
• Carotid sinus
CLINICAL PEARLS
• RND is a common surgical procedure for cervical metastasis from head and neck cancer.
• Most patients now undergo a modified version of the classical RND that allows sparing of
important vascular and nervous structures and in turn reduces overall morbidity and
mortality.
• GETA is usually employed intraoperatively; be prepared for a potential difficult airway.
• Nerve monitoring may prohibit the use of neuromuscular blockers.
• Damage to major vascular structures in the neck is rare but potentially life-threatening.
RAYNAUD’S PHENOMENON
Edward Kosik, DO
BASICS
DESCRIPTION
• Raynaud’s phenomenon (RP) is an exaggerated and reversible vasospasm of digital arteries
in response to cold or stress. It is classified as either monophasic, biphasic, or triphasic
based upon the presence of
– Pallor
– Cyanosis
– Rubor (hyperemia)
• Primary Raynaud’s describes vasospasm not caused by an underlying disorder. It classically
affects all fingers and is also known as Raynaud’s disease or idiopathic Raynaud’s.
• Secondary Raynaud’s describes vasospasm associated with another disorder, such as an
autoimmune disorder (e.g., scleroderma, systemic sclerosis). It generally has an asymmetric
distribution and is also known as Raynaud’s syndrome and is usually more severe than
primary Raynaud’s.
EPIDEMIOLOGY
Prevalence
• The exact prevalence is not known because of differences in diagnostic criteria. (0.5% to
>20%)
• Females > males
• Primary > secondary
Morbidity
• Primary Raynaud’s rarely results in digital ulcers or gangrene.
• Secondary Raynaud’s has variable morbidity that is related to the known cause.
• Primary Raynaud’s
– Age <30 years
– Exposure to vinyl chloride
– Use of vibrating tools such as jackhammers
– Use of certain medicines (vinblastine, cisplatin, beta-blockers, and migraine drugs)
– Living in a cold climate
– Smoking (controversial)
– Thoracic outlet syndrome
• Secondary Raynaud’s
– Age >30 years
– Immunologic diseases: Scleroderma, systemic sclerosis, CREST syndrome
– Pulmonary hypertension
• The pathophysiology is not fully understood and multiple theories/explanations exist. The
most widely accepted mechanism includes vascular, neural components, and the
coagulation system. There is excessive vasoconstriction relative to vasodilation and the
neural component affects vascular tone and circulating mediators:
– Vasoconstrictors: Increased levels of endothelin-1, neuropeptide Y, and platelet
thromboxane A2; increased activity of α2C-adrenoreceptor expression can be increased in
some instances by estrogen (may play a role in primary Raynaud’s disease in women).
– Vasodilators: Decreased levels of nitric oxide; and prostaglandins, which have vasodilating
properties, could also be responsible for inhibition of platelet aggregation (coagulopathy)
and increase in fibrinolytic activity.
– Neural components: Calcitonin-gene-related peptide is a vasodilator released by nerve
endings and is diminished in both primary and secondary RP.
– Coagulation system activation may be secondary to vascular obstruction, platelet
thromboxane A2.

• Keep the patient normothermic, paying close attention to distal extremities.
• Avoid hypotension and hypovolemia.
• If an arterial line is needed, consider placing a femoral arterial line, if possible.
• IV administration of vasoconstrictors should be avoided if possible. Alternatively, use
smaller doses and with great caution, as well as consider inotropes and (warmed) fluid
administration, as appropriate
• Avoid the use of epinephrine and phenylephrine in regional blockade.
• Continue perioperative medications such as calcium channel blockers
SYMPTOMS
• Pain and stiffness in extremities when exposed to cold. Determine if the patient experiences
pallor, cyanosis, or rubor.
• Collect information that pertains to the underlying immunological cause.
History
• Identify primary versus secondary
• Frequency of vasospastic episodes
• Collect information related to underlying immunological cause
Signs/Physical Exam
Color change in digits to pale, cyanotic, or hyperemic.
TREATMENT HISTORY
• Sympathectomy may be performed for severe disease. It is performed by removing the nerve
attachments at the extremities and has variable success.
• Nerve blocks to sympathetic nerves may be effective, but likely need to be repeated.
• Amputation may be necessary if there is necrotic or gangrenous tissue (very rare).
MEDICATIONS
• First line treatment
– Calcium channel blockers (nifedipine, amlodipine, and fenoldipine) provide vasodilation
in the extremities, thus decreasing the frequency and severity of attacks, as well as
possibly aid with the healing of skin ulcers.
– Alpha receptor antagonists counteract the effects of endogenous norepinephrine (prazosin,
doxazosin).
• Second-line treatment
– ACE inhibitors, angiotensin receptor blockers
– Nitroglycerin paste can be applied topically for digital ulcers
– Sildenafil
– Fluoxetine
– Prostaglandins
Labs/Studies
None in particular; order as needed for specific causes
There is some evidence that Raynaud’s patients are at increased risk for CVA.
TREATMENT
Premedications
• Calcium channel blockers; consider having the patient take a regular or reduced dose of
their home regimen with a small sip of water.
• Administer anxiolytics as appropriate; anxiety has been known to exacerbate some types of
Raynaud’s.
INTRAOPERATIVE CARE
• General and regional anesthesia are both acceptable techniques.
• Regional blocks should not contain epinephrine or phenylephrine as they may cause an
exaggerated vasoconstrictive response.
• Use of tourniquets is controversial.
Monitors
• Use a noninvasive BP cuff (as opposed to a radial arterial line), if possible
• Be prepared to perform special airway management techniques in patients with small mouth
openings (scleroderma) or limited neck mobility (rheumatoid arthritis).
• Rapid sequence induction should be considered if the patient exhibits signs of esophageal
dysmotility or gastric reflux.
Maintenance
• Ensure that the patient is euvolemic to avoid hypotension and maintain perfusion to digits.
• Vasopressors should be used with caution due to the possibility of an exaggerated response.
• Position patients with care to maintain optimal blood flow to the extremities (e.g., caution
should be used with elevation of the hand in the lateral position).
• Maintain normothermia
– Warm the room to decrease radiation of heat from the patient into the cooler environment
– Convection warming blankets reduce radiation of heat into the cooler environment as well
as actively warm the patient. Consider implementing in the preoperative holding area
– Warm IV fluids
– In patients with advanced disease, use gloves and socks on their extremities.
– Use reflective coverings
– Hat covering
No special concerns unless systemic disease affects the respiratory system; otherwise use
normal extubation criteria.
FOLLOW-UP
BED ACUITY
Determined by underlying disease, surgical procedure, and intraoperative events
• Analgesia
– Consider that pain may be from extremity vasoconstriction
COMPLICATIONS
Digital ischemia and/or gangrene
REFERENCES
1. Baumhäkel M, Böhm M. Recent achievements in the management of Raynaud’s
phenomenon. Vasc Health Risk Manag. 2010;6:207–214.
2. Cooke JP, Marshall JM. Mechanism of Raynaud’s disease. Vasc Med. 2005;10:293–307.
3. Herrick AL. Pathogenesis of Raynaud’s phenomenon. Rheumatology. 2005;44:587–596.
4. NIH. Raynaud’s Phenomenon
http://www.niams.nih.gov/HealthInfo/RaynaudsPhenomenon/default.asp. Published April
2009. Accessed 9/19/2011.
5. Suter LG, Murabito JM, Felson DT, et al. The incidence and natural history of Raynaud’s
phenomenon in the community. Arthritis. 2005;52(4):1259–1263.
• Hypothermia
• Scleroderma
• Rheumatoid arthritis
CODES
ICD9
443.0 Raynaud’s syndrome
ICD10
I73.00 Raynaud’s syndrome without gangrene
CLINICAL PEARLS
• Keep the patient warm!!!
• When an arterial line is indicated, assess the risks versus the benefits of placement in the
radial artery; consider other proximal sites
• Use IV vasoconstrictors with great caution
• Avoid beta-blockers (especially nonselective) as they can cause unopposed alpha
constriction.
RECOMBINANT ACTIVATED FACTOR VII (RFVIIA)
Keyvan Karkouti, MD, FRCPC, MSc
BASICS
DESCRIPTION
• Recombinant activated factor VII (rFVIIa; Novo Nordisk A/S, Bagsvaerd, Denmark) is similar
to human plasma-derived activated factor VII.
• It is supplied in single-use vials (as lyophilized powder) of 1, 2, 5, or 8 mg, and following
reconstitution with normal saline, is administered intravenously over 2–3 minutes.
• When administered in doses sufficient to achieve supraphysiological concentrations, it is a
potent procoagulant that bypasses parts of the coagulation cascade.
• Current indications are for treatment or prevention of bleeding episodes in patients with
– Hemophilia A (factor VIII deficiency) with antibodies to factor VII
– Hemophilia B (factor IX deficiency) with antibodies to factor IX
– Acquired hemophilia (a rare condition that is associated with cancer, pregnancy, or
autoimmune disorders, and is characterized by development of antibodies against factors
VIII)
– Congenital factor VII deficiency
• The most common off-label use is for treatment of refractory bleeding in various settings,
including cardiovascular surgery, trauma, and obstetrics.
• Normal coagulation
– About 1% of circulating native factor VII is present in the activated form.
– Following tissue injury, tissue factor (TF) is released from the subendothelium of injured
vessels and forms a complex with circulating activated factor VII (TF–FVIIa).
– The TF–FVIIa complex then initiates the coagulation cascade by activating factors X and
IX on the injured cell surface.
Activated factor X generates small amounts of thrombin, which activates platelets, factor
VIII, and other cofactors.
Activated factor IX diffuses to the surface of the activated platelets at the site of injury,
and in combination with activated factor VIII, activates factor X. This leads to the
thrombin burst that is needed for fibrin clot formation.
• When administered in pharmacological doses (∼1,000 times greater than normal circulating
levels), rFVIIa improves the coagulation process at the site of injury by
– Directly (without forming a complex with TF) activating factor X on the activated platelets
at the site of injury, and thus bypassing the need for factors VIII and IX.
– Boosting the TF-dependent pathways
• The amount of thrombin generated by rFVIIa is directly proportional to the administered
dose.
• The circulating half-life of rFVIIa, which is independent of dose, is about 3 hours in adults
and 1 hour in children.
• Congenital or acquired hemophilia (approved indication). rFVIIa bypasses the need for
factors VIII and IX to form fibrin clot. High doses (90 μg/kg every 2 hours) are required to
achieve hemostasis.
• Congenital factor VII deficiency (approved indication). Lower doses (15–30 μg/kg every 4–6
hours) are required to achieve hemostasis.
• Functional platelet disorders (e.g., Glanzmann’s thrombasthenia, which is a congenital
defect in the platelet GPIIb/IIIa receptor; an approved indication in Europe) require high
doses similar to those used in patients with congenital hemophilia.
• Thrombocytopenia. Conflicting effectiveness data; not approved in any jurisdiction for this
indication.
• Prophylactic use (to prevent anticipated bleeding). A recent meta-analysis of randomized
studies in various settings, including cardiac surgery with cardiopulmonary bypass, hepatic
resection, liver transplantation, traumatic pelvic fracture, spinal surgery, and radical
prostatectomy, found modest benefits with rFVIIa in reducing blood loss and blood
transfusion, with no statistical increase in thromboembolic events. The studies excluded
patients at high risk for thromboembolic complications and the number of events was small.
• Therapeutic use (to treat established bleeding).
– Intracerebral hemorrhage: In a large phase III randomized study, rFVIIa at 80 μg/kg
reduced hemorrhage expansion, but showed no benefit in clinical outcomes and doubled
the incidence of arterial thrombotic events.
– Trauma: In a large phase III randomized study in patients who received 4–8 units of
packed red blood cells (pRBCs) and had ongoing blood loss, a total of 400 μg/kg of rFVIIa
had a modest beneficial effect in blood loss and blood transfusion without increasing
thromboembolic event rates. The trial was terminated early due to failure to show an
improvement in mortality rates, which was the desired outcome.
– Cardiac surgery with cardiopulmonary bypass: In a phase II randomized study in patients
with postoperative bleeding in the ICU, 40–80 μg/kg of rFVIIa reduced re-exploration
rates (by about 50%), transfusion rates, and blood loss. However, patients had a nearly
twofold increase in thromboembolic events, although this difference did not reach
statistical significance.
• Rescue use (to treat bleeding that is refractory to maximal standard therapy):
– No randomized trials have examined the use of rFVIIa as rescue therapy for refractory
hemorrhage.
– Observational studies in various settings (cardiac surgery, trauma, obstetrics), however,
suggest that it can be effective and safe in treating refractory hemorrhage.
– Risk may be prohibitive in patients at high risk for thromboembolic complications (e.g.,
previous stroke, carotid artery disease, and arterial insufficiency) or in patients with
established disseminated intravascular coagulation or sepsis (due to systemic TF
expression).
– Dose recommendations vary, but 35–70 μg/kg repeated once or twice seems to be
sufficient in most cases.
– The risk–benefit profile is more favorable if rFVIIa is administered early in the course of
refractory hemorrhage rather than as a last resort.
• A recent systematic review assessing the safety of the off-label use of rFVIIa found that it
increases the risk of arterial thromboembolic adverse events by nearly twofold.
• When patients with approved indications present for invasive procedures or surgery,
consultation with the hematologist is recommended to determine appropriate dosage and
frequency of rFVIIa administration.
• Off-label use considerations. Given its high cost and potential for thromboembolic
complications (twofold increase in arterial thromboembolic adverse events), its prophylactic
use should be avoided, particularly in patients with preexisting or acquired risk factors for
thromboembolic complications. If considering its use as rescue therapy for refractory
hemorrhage:
– Assess appropriateness on a case-by-case basis, based on an individualized risk–benefit
analysis that weighs the perceived risks of ongoing blood loss versus thromboembolic
complications.
– Use early in the course of hemorrhage, but correct the underlying coagulopathy and
anemia as best as possible. For example, transfuse pRBCs to maintain a Hct >25%,
platelets to maintain a count >80 × 109/L or to correct suspected platelet dysfunction
(e.g., postcardiopulmonary bypass), transfuse fibrinogen or cryoprecipitate to reach a
fibrinogen concentration of >1.5 g/L, transfuse plasma to reach an INR of <1.5.
– Correct acidosis and hypothermia
– Administer antifibrinolytic drugs if appropriate
• Monitoring: There are no routine laboratory tests for monitoring the effects of rFVIIa, but
the following tests may be relevant.
– PT: A plasma-based assay that measures the time to clot formation by a TF source. It is
shortened in all patients who receive rFVIIa irrespective of clinical response. However, if
it is not normalized after rFVIIa therapy, it predicts a lack of response.
– Activated PTT: A plasma-based assay that measures the time to clot formation by non-TF
sources (celite or kaolin). It is shortened by rFVIIa, likely due to the ability of rFVIIa to
directly activate factor X. It is not a reliable monitor of rFVIIa effect in patients who do
not have hemophilia.
– Thromboelastogram. A whole-blood assay that monitors the viscoelastic properties of the
forming clot. rFVIIa shortens the time to clot formation and improves clot formation
dynamics. It is not a reliable monitor of rFVIIa effect in patients who do not have
hemophilia.
REFERENCES
1. Gill R, Herbertson M, Vuylsteke A, et al. Safety and efficacy of recombinant activated
factor VII: A randomized placebo-controlled trial in the setting of bleeding after cardiac
surgery. Circulation. 2009;120:21–27.
2. Grottke O, Henzler D, Rossaint R. Activated recombinant factor VII (rFVIIa). Best Pract Res
Clin Anaestheiol. 2010;24(1):95–106.
3. Hauser C, Boffard K, Dutton R, et al. Results of the CONTROL trial: Efficacy and safety of
recombinant activated factor VII in the management of refractory traumatic hemorrhage. J
Trauma. 2010;69(3):489–500.
4. Hers I, Mumford A. Understanding the therapeutic action of recombinant factor VIIa in
platelet disorders. Platelets. 2008;19(8):571–581.
5. Karkouti K, Beattie W, Arellano R, et al. Comprehensive Canadian review of the off-label
use of recombinant activated factor VII in cardiac surgery. Circulation. 2008;118:331–338.
6. Levi M, Levy J, Andersen H, et al. Safety of recombinant activated factor VII in randomized
clinical trials. N Engl J Med. 2010;363(19):1791–1800.
7. Lin Y, Stanworth S, Birchall J, et al. Use of recombinant factor VIIa for the prevention and
treatment of bleeding in patients without hemophilia: A systematic review and meta-
analysis. CMAJ. 2001;183 (1):E9–E19.
8. Logan A, Goodnough L. Recombinant factor VIIa: An assessment of evidence regarding its
efficacy and safety in the off-label setting. Hematology Am Soc Hematol Educ Program.
2010:153–159.
9. Mayer S, Brun N, Begtrup K, et al. Recombinant activated factor VII for acute intracerebral
hemorrhage. N Engl J Med. 2008;358(20):2127–2137.
10. Roberts H, Monroe D, Hoffman M. Safety profile of recombinant factor VIIa. Semin
Hematol. 2004;41(Suppl 1):101–108.
11. Roberts H, Monroe D, White G. The use of recombinant factor VIIa in the treatment of
bleeding disorders. Blood. 2004;104(13):3858–3864.
• Prothrombin time (PT)
• Partial thromboplastin time (PTT)
CLINICAL PEARLS
• When patients with approved indications present for invasive procedures or surgery,
consultation with hematology is recommended to determine appropriate dosage and
frequency of rFVIIa administration.
• If considering the use of rFVIIa for an unapproved/off-label condition such as refractory
bleeding:
– Obtain informed consent from the patient or next of kin, if at all possible
– Assess appropriateness on a case-by-case basis, weighing the perceived risks of ongoing
blood loss versus thromboembolic complications (assume a twofold increase in risk)
– Use low doses (35–70 μg/kg, repeated once or twice if no response based on clinical
assessment)
– Use early in the course of hemorrhage, but correct the underlying coagulopathy as best as
possible.
– Avoid concomitant use of other activated clotting factors (risks unknown and may be
synergistic).
RECURRENT LARYNGEAL NERVE
Jane C. Ahn, MD
Sharon L. Lin, MD
BASICS
DESCRIPTION
• The recurrent laryngeal nerve (RLN) provides both sensory and motor innervation to the
larynx.
– Supplies motor function to all intrinsic muscles of the larynx except for the cricothyroid
muscle (innervated by the external branch of the superior laryngeal nerve).
– Supplies sensory innervation to the vocal cords and subglottis.
• The RLN innervates all of the intrinsic laryngeal muscles except for the cricothyroid
(innervated by the external branch of the superior laryngeal nerve). Specifically, all of the
muscles that are innervated by the RLN (e.g., lateral cricoarytenoid, interarytenoid, vocalis,
etc.), except for the posterior cricoarytenoid (only vocal cord abductor), adduct the vocal
cords.
• Coughing, gagging, and laryngospasm result from the efferent limb of the RLN
ANATOMY
• Originates as a branch of the vagus nerve (CN X).
• The right and left vagus nerves exit the skull base via the jugular foramens.
• In the neck, the right and left vagus nerves descend in the right and left carotid sheaths,
respectively, between the internal jugular vein and internal carotid artery, and into the
thoracic outlet.
• Within the thorax, the vagus nerve gives off the recurrent laryngeal nerve.
• The right RLN loops around the right subclavian artery at the level of the innominate artery
and ascends along the tracheoesophageal groove behind the common carotid artery.
• The left RLN follows the carotid artery into the mediastinum, loops around the aortic arch
lateral to the ligamentum arteriosum.
• Once the RLNs enter the larynx, they divide into motor and sensory branches.
• The left RLN has a longer course (∼12 cm from aorta to cricothyroid) compared to the right
RLN (∼5–6 cm from subclavian to cricothyroid), which may make it more prone to injury
(1).
• Blood supply to the RLN is provided by the inferior thyroid artery.
• Injury to the RLN can occur from:
• Inadvertent injury during surgical procedures
• Tumor
• Aortic aneurysms (hoarseness may be one of the first presenting signs)
• Trauma
• Neurotoxic drugs
• Viral or bacterial infections
• Vascular insult
• Surgical injury to the RLN can occur anywhere along the nerve’s course: Neck, chest, or
skull base.
• Most common surgical procedures citing RLN injury include
• Thyroid and parathyroid surgery (33% of all surgical cases) (2)
• Anterior cervical spine surgery (15%) (2)
• Carotid endarterectomy (11%) (2)
• Recurrent laryngeal nerve transmission may be transiently blocked when a supraclavicular,
interscalene, or stellate ganglion block is performed. It typically manifests as hoarseness.
• Recurrent laryngeal nerve paralysis
• May be difficult to assess because many patients can be asymptomatic, especially if caused
by slow growing tumor.
• Unliateral palsy
– Partial: Abductors are more vulnerable to injury. Therefore, partial nerve damage may
result in a selective abductor paralysis with a VC that lies in the midline (adducted
position)
– Complete: Affects both adductors and abductors and results in a vocal cord that lies
midway between adduction and abduction, just lateral to the midline.
• Bilateral palsy
– Partial: When the abductor is more severely affected than adductors, both vocal cords
meet in the midline and cause complete airway obstruction
– Complete: Vocal cords are positioned midway between abduction and adduction.
Breathing is still possible with a glottic opening smaller than normal.
• Intraoperative nerve monitoring (spontaneous electromyelography [EMG]) has gained
increasing popularity as a means of identifying the RLN during surgical procedures. The
EMG detects and records muscle electrical activity continually. Mechanical irritation of the
RLN triggers motor unit potential discharges and aids with detection of the nerve during
surgical dissection as well as inadvertent manipulation and injury (retraction, cautery,
scalpel). It requires the use of specialized equipment and precautions (3):
• Use of a specialized endotracheal tube with electrodes at the level of the glottis.
• Electrodes should make contact with the medial surface of the vocal cords (bilaterally) to
allow monitoring.
• An antisialagogue such as glycopyrrolate may help reduce saliva pooling at the vocal cords
that can impede monitoring.
• Frequent intraoperative suctioning may be required for saliva pooling.
• Use short-acting muscle relaxants for intubation as long-acting neuromuscular blockers will
prevent effective neuromonitoring.
• The endotracheal tube may migrate after positioning for surgery with neck extension and
should be considered if adequate EMG signal cannot be obtained.
• Regional anesthesia of the RLN and proper preparation can significantly aid successful
awake fiberoptic intubation (4):
• Thoroughly discuss procedure and reassure patient.
• Administer adequate sedation for a calm, cooperative patient.
• An antisialagogue such as glycopyrrolate can decrease secretions and improve visualization
during fiberoptic guidance.
• Topical local anesthetic can be applied through a variety of ways: Aerosol spray, atomizer,
nebulizer, and gargling.
• Translaryngeal nerve block delivers local anesthetic to areas supplied by the sensory
component of the RLN (subglottis, upper trachea).
• Identify structures by extending the patient’s neck and palpating the midline of the
cricothyroid membrane. Insert a 20G or 22G needle with an attached 5 cc syringe (filled
with 3–5 cc of local anesthetic) using the dominant hand and constantly aspirating. The
nondominant hand is usually “anchored” to the patient and helps stabilize the needle. The
presence of air bubbles in the syringe is an indicator of proper needle placement. Prior to
injection, ask the patient to forcefully inhale, which will help spread local anesthetic.
Potential complications of a translaryngeal block include bleeding, puncture of the
membranous portion of the trachea, and systemic local anesthetic toxicity. Use with caution
in patients where significant coughing is undesirable or those at high risk for aspiration as
their cough reflex will be greatly impaired.
GRAPHS/FIGURES
REFERENCE
1. Myssiorek D. Recurrent laryngeal nerve paralysis: Anatomy and etiology. Otolaryngol Clin
N Am. 2004;37:25–44.
2. Rosenthal LHS, Benninger MS, Deeb RH. Vocal cord immobility: A longitudinal analysis of
etiology over 20 years. Laryngoscope. 2007;117:1864–1870.
3. Randolph GW, Dralle H, Abdullah H, et al. Electrophysiologic recurrent laryngeal nerve
monitoring during thyroid and parathyroid surgery: International standards guideline
statement. Laryngoscope. 2011;121:S1–S16.
4. Simmons ST, Schleich AR. Airway regional anesthesia for awake fiberoptic intubation. Reg
Anes Pain Med. 2002;27(2):180–192.
• Laryngospasm
• Thyroidectomy
• Anterior cervical disc fusion (ACDF)
CLINICAL PEARLS
• RLN injury can occur with head and neck surgical procedures, most commonly thyroid,
anterior cervical spine, and carotid endarterectomy. Intraoperative nerve monitoring can
decrease the incidence of RLN injury.
• The RLN can be temporarily blocked with stellate ganglion blocks, interscalene blocks, or
supraclavicular brachial plexus blocks. It manifests as hoarseness that is self-limiting and
resolves when the local anesthetic wears off.
• Regional anesthesia of the RLN can significantly facilitate awake fiberoptic intubation in
difficult airway cases. The translaryngeal block should be performed with caution in
patients at high risk for aspiration or in patients where severe coughing is undesired.
• Unilateral RLN palsy may be asymptomatic or manifest as dysphagia and dysphonia. Partial
bilateral RLN injury can manifest as airway obstruction and require emergent intubation.
RENAL BLOOD FLOW
George J. Ranier, MD
BASICS
DESCRIPTION
• Renal blood flow (RBF) refers to the volume of blood that perfuses the kidneys per unit
time; renal plasma flow (RPF) refers to the volume of plasma that perfuses the kidneys per
unit time. When discussing glomerular filtration rate (GFR), RPF is more appropriate
(cellular components do not filter across glomerular capillaries).
• The kidneys receive enormous blood flow relative to their mass; not only do they have a
high metabolic requirement but they also function as a filtering and homeostatic organ. RBF
is ∼20% of the cardiac output or 1 L/min in a 70 kg adult.
• Blood that enters the kidney eventually reaches the nephrons, the functional filtering units
within the renal cortex. Each nephron consists of a system of small blood vessels (arterioles
and capillaries) and a system of tubules.
– Within the nephron, there are two sets of arterioles, afferent and efferent, that bring blood
to and from the glomerulus, respectively.
– The glomerulus is a capillary bed that is located within the renal cortex and is where the
initial step of urine formation occurs via plasma filtration. Blood that is not filtered from
the afferent arterioles, leaves the glomerulus via efferent arterioles and enters the
peritubular capillary network.
– The glomerulus is surrounded by the Bowman’s capsule, which collects the filtered plasma
and channels it into a system of renal tubules that eventually dumps urine into the renal
pelvis.
• Blood flow in the kidneys, as in any other organ, can be described mathematically by Ohm’s
law, where Pressure (P) = Flow (Q) multiplied by Resistance (R). Rearranging for flow, Q
= P R.
– RBF is dependent on mean arterial pressure (MAP) in the renal artery and vascular
resistance of the renal arterioles, primarily the afferent and efferent arterioles.
– Resistance to blood flow is determined by three factors: Vessel length, vessel radius, and
blood viscosity. Resistance is inversely proportional to the 4th power of the vessel’s radius
(Poiseuille’s law).
• Blood flow through the renal cortex is unique, in that there are two sets of vessels. The first
set is comprised of the afferent and efferent arterioles; the second set is comprised of
capillaries that form the glomerular tuft and peritubular capillaries.
– The resistance in these vessel sets makes up the majority of renal vascular resistance.
– Because they are in series, a change in vascular tone will produce the same effect on RBF
regardless of whether it is an afferent or efferent arteriole.
– Changes in resistance are additive
– Because the peritubular capillaries are downstream from the afferent arterioles,
glomerular capillaries, and efferent arterioles, they function as a lower pressure system.
This is important, because for plasma filtration to occur at the glomerulus, a higher
relative pressure is required, whereas, reabsorption within the peritubular capillaries
requires a lower relative pressure.
• A portion of the renal plasma flow (RPF) is filtered from the glomerular capillaries into the
Bowman’s capsule. The volume of this filtrate produced over time is called the glomerular
filtration rate (GFR).
– The filtration fraction is the ratio of glomerular filtration to RPF; normal values are 0.2.
– GFR for a healthy male adult is roughly 180 L/day. The high ratio of GFR to plasma
volume allows the kidneys to excrete waste products and maintain tight control over the
body’s internal milieu.
– The filtration rate across the capillary is governed by the membrane’s surface area and
permeability, as well as the filtration pressure.
– For GFR, this allows derivation of the following formula: Kf(PGC – PBC – πGC), where Kf is
the product of hydraulic permeability and surface area, PGC is the glomerular capillary
hydrostatic pressure, PBC is the hydrostatic pressure in the Bowman’s capsule, and πGC is
the oncotic pressure of glomerular capillary plasma. GFR equals the product of hydraulic
permeability and surface area (Kf) times the net filtration pressure (the mathematical sum
of hydrostatic and osmotic pressures acting across the glomerulus).
• Autoregulation of the RBF and GFR blunts the otherwise deleterious effects of variable BP.
Normal arterial BP can vary widely, and because the glomerular capillaries are thin-walled,
they can be easily damaged by excessive BP.
– Within a MAP of 80–180 mm Hg, RBF and GFR are relatively constant secondary to
autoregulation.
– Autoregulation occurs via two mechanisms: A myogenic response of vascular smooth
muscle and tubuloglomerular feedback. The myogenic response is a fast response to
stretch, while tubuloglomerular feedback acts via vasoconstrictive transmitters released by
salt-sensing cells within the macula densa.
– Within the nephron, alterations in afferent and efferent arteriolar tone regulate the
hydrostatic pressure within the glomerular capillaries (PGC). This layer of control over the
GFR is independent of overall RBF.
– It is important to remember that while autoregulation blunts changes in RBF and GFR that
would otherwise occur in direct response to changes in MAP, it does not totally negate
those changes.
ANATOMY
• The kidneys are bilateral retroperitoneal organs, each weighing about 150 g and supplied by
its own renal artery.
• Functionally and anatomically, the kidney can be divided into an outer portion, or cortex,
and an inner portion, or medulla.
• Blood enters each kidney via its associated renal artery. The renal artery progressively
divides into interlobar, arcuate, and then interlobular arteries. As these arteries branch, they
travel from the inner region of the kidney toward the cortex, where the interlobular arteries
eventually give rise to the afferent arterioles. The afferent arterioles lead to glomeruli and
form a “tuft” of capillaries. The glomerulus, with its surrounding Bowman’s capsule, forms
the renal corpuscles (found only in the renal cortex).
• Within the glomerulus, about 20% of the plasma is filtered into Bowman’s capsule, while the
remaining 80% (plus cellular components) flows into the efferent arterioles.
• Blood flowing from efferent arterioles may take several paths, depending on the location of
the glomerulus within the kidney. Efferent arterioles that arise from cortical glomeruli
subdivide into secondary capillaries, called peritubular capillaries, throughout the cortex.
These eventually form veins by which blood exits the kidney. But the efferent arterioles that
arise from juxtamedullary glomeruli take a different path. They course into the outer
medulla, subdivide, and eventually form the vasa recta. Both vasa recta and the glomeruli
contribute to the exchange of water and solutes that enable the kidney to regulate water
and electrolyte balance.
• All blood flowing into the kidney passes through the cortex, with a fraction of that blood
flow then entering the medulla (the medulla receives less blood flow than the cortex).
Because of this disparity of blood flow, in conditions of hypoperfusion the medulla is
particularly vulnerable to ischemic damage.
• The kidneys receive sympathetic innervation that controls RBF via afferent and efferent
arterioles, juxtaglomerular apparatus, and portions of the tubules. Parasympathetic
innervation has minimal influence.
• There are two main causative factors of perioperative renal insults that can lead to acute
kidney injury (AKI): Hypoperfusion/ischemia and nephrotoxic agents. AKI is diagnosed
when there is an absolute increase in serum creatinine by 0.3 mg/dL or a 50% increase from
baseline. Alternatively, it can be diagnosed as a reduction in urine output to <0.5
mg/kg/hr for ≥6 hours.
• AKI can be grouped into three anatomic categories: Prerenal, intrarenal, and postrenal.
• Prerenal AKI is the direct result of renal hypoperfusion, and is the most common cause of
AKI.
– Hypoperfusion may be caused by dehydration, acute blood loss, sepsis, congestive heart
failure, aortic cross-clamping, renal artery thrombosis or embolism, or any other process
that reduces extracellular fluid volume or circulating volume.
– Complete lack of blood flow to the kidneys for 30–60 minutes can result in irreversible
cell damage.
– Drugs such as ACE inhibitors and NSAIDs can also cause prerenal AKI by a reduction in
glomerular capillary perfusion.
– In the early phase of prerenal AKI, the renal parenchyma is still intact and functional.
During this period, autoregulatory mechanisms compensate to maintain the GFR by
controlling the tone of afferent and efferent arterioles.
– Prerenal AKI, if recognized, is often easily reversible but can progress to tubular cell injury
and intrarenal AKI if unrecognized.
– Prerenal AKI is also termed prerenal azotemia.
• Intrarenal AKI, or intrinsic AKI, is classified by the portion of the nephron that is involved.
This can include the tubules, interstitium, vasculature, and glomerulus.
– Acute tubular necrosis (ATN) involves specific injury to the renal tubules, and is most
commonly the result of ischemia secondary to reduced RBF. It progresses through four
distinct phases: Initiation, extension, maintenance, and recovery. Each phase is marked by
characteristic cellular events and rates of glomerular filtration.
In the first phase, or initiation phase, cellular ATP is depleted. Renal tubule epithelial
cells are injured, swell, and form bullae. Next, during the extension phase, inflammation
and microvascular congestion occur. As the insult progresses, cells become necrotic,
detach, and form casts in the distal tubules. This obstruction further reduces GFR.
During the third phase (or maintenance phase), GFR is at a nadir, but cells are
undergoing repair. In the final recovery phase, GFR improves as cellular function slowly
returns.
In addition to renal hypoperfusion, there are numerous toxins that can cause ATN
including IV contrast agents, aminoglycoside antibiotics, NSAIDs, the heme pigment
released during rhabdomyolysis, and cocaine.
– Diseases of the vasculature (micro or macro) can also cause intrinsic AKI via
hypoperfusion. In the instance of microvascular disease, this occurs as the consequence of
glomerular capillary thrombosis and microvascular occlusion. Examples include TTP,
HELLP syndrome, and hemolytic–uremic syndrome. Macrovascular disease is
characterized by atheroembolic events that occlude larger vessels.
• Postrenal AKI, as the name implies, results from obstruction of urinary outflow. This
obstruction can occur at any point from the tubules to the urethra. Examples include
prostatic hypertrophy, genitourinary tumors, renal calculi, thromboses, uric acid
precipitates from gout, and light chain proteins seen in patients with multiple myeloma.
• Anesthesia and surgery most often result in decreases in RBF, RPF, and GFR. Because the
majority of anesthetic agents have negative effects on BP and cardiac output, this is not
surprising. Additionally, the release of catecholamines that accompany surgical stimulation
has the added impact of increasing renal vascular resistance, which reduces RBF and RPF,
and may further decrease GFR.
• Short periods of relative hypotension are not uncommon in the perioperative setting, due to
either surgical or anesthetic manipulation.
– With decreased RBF, the kidneys are often able to preserve filtration via compensatory
mechanisms. Within the glomerular capillaries, filtration fraction is maintained by efferent
arteriolar vasoconstriction. This decreases RBF but increases glomerular capillary
pressure, and hence GFR.
– Longer periods of hypotension, as may accompany cross-clamping, hemorrhage, or sepsis,
result in afferent vasoconstriction and further decrease the RBF. The consequence is a
reduction in filtration fraction and GFR, with deleterious effects on oxygen delivery and
the potential for AKI.
– The presence of oliguria, defined as urine output <0.5 mg/kg/hr, while concerning, is of
limited predictive value for AKI, however.
• Infusions of commonly used vasopressor drugs, such as norepinephrine, have been shown to
decrease GFR in animals. This is likely true in humans; however, a survey of the literature
yields conflicting results.
• The effects of neuraxial blockade are variable, depending on the degree to which BP and
cardiac output drop. Because of the multitude of factors that influence RBF, including level
of block, underlying disease, endogenous catecholamines, angiotensin, ADH, and many
other circulating factors, it can be challenging to draw firm conclusions regarding the
ultimate impact of regional anesthesia on RBF and GFR. However, several meta-analyses
have found that epidural anesthesia reduces perioperative renal morbidity.
EQUATIONS
• Flow = MAP/Resistance; where Flow is renal blood flow, MAP is mean arterial pressure,
and Resistance is renal arteriolar resistance (comprised mainly by afferent and efferent
arterioles).
– Glomerular Filtration Rate: GFR = Kf (PGC – PBC – πGC)
• Filtration Fraction: FF = GFR/RPF
REFERENCES
1. Berne RM, Levy MN. Physiology. 2nd edn. St. Louis, MO: Mosby; 1988.
2. Eaton DC, Pooler JP. Vander’s Renal Physiology. 7th edn. New York, NY: McGraw Hill
Medical; 2009.
3. Goldman L, Ausiello D. Cecil Textbook of Medicine. 23rd edn. Philadelphia, PA: Saunders;
2008.
4. Legrand M, Payen D. Understanding urine output in critically ill patients. Ann Intensive
Care. 2011;1(1):13.
5. Mercatello A. Changes in renal function induced by anesthesia. Ann Fr Anesth Reanim.
1990;9(6):507–524.
6. Suleiman MY, Passannante AN, Onder RL, et al. Alterations of renal blood flow during
epidural anesthesia in normal subjects. Anesth Analg. 1997;84(5):1076–1080.
7. Waugh WH. Modest pressure natriuresis and autoregulation during water diuresis in dogs.
Blood Vessels. 1991;28(6):420–441.
• Epidural
CLINICAL PEARLS
• Even uneventful anesthetics and surgery often cause reductions in RBF and GFR.
• The kidneys possess the ability via autoregulatory mechanisms to maintain GFR even when
RBF is decreased and at times further reduce RBF by causing vasoconstriction.
RESCUE ECHOCARDIOGRAPHY
Timothy R. Ball, MD
William C. Culp, Jr., MD, FASE
BASICS
DESCRIPTION
Unexplained perioperative hemodynamic instability is a class I indication for perioperative
transesophageal echocardiography (TEE). Rescue echocardiography may be utilized to:
• Quickly identify potential causes of unexplained hypotension
• Assess the basic function of the left and right ventricles
• Guide fluid management and inotropic medication administration during perioperative
resuscitation
• A TEE uses high-frequency sound waves to depict the heart’s movement; esophageal
placement brings the transducer within close proximity to the heart, and removes
interference from the ribs or lungs.
• Ejection fraction is calculated or visually estimated as the percent of volume ejected at end
systole compared to the volume at end diastole.
– End-systolic and end-diastolic volumes can be estimated by measuring left ventricular
diameter or area.
ANATOMY
• For a rapid and simple TEE examination, the midesophageal and trans-gastric views are the
most helpful.
– Midesophageal views allow rapid visualization of ventricular function, as well as mitral,
aortic, and tricuspid valve functions. They include:
The 4-chamber view
The 5-chamber view
The aortic valve short-axis view
The aortic valve long-axis view
– Trans-gastric view allows quick estimation of volume status and ventricular function as
well as detecting pericardial effusions. This view of the left and right ventricles is attained
by delicate probe anti-flexion from the midesophageal, 4-chamber view.
• Contraindications for TEE
– Absolute contraindications include a history of:
Esophagectomy
Esophagogastrectomy
– Relative contraindications include a history of:
Esophageal trauma
Esophageal stricture
Esophageal fistula
Esophageal surgery
• Risks associated with TEE. The reported complication rates of TEE in the intraoperative
adult population and in the adult ICU population are 0.2 and 2.6–4.0%, respectively. They
include:
– Oropharyngeal trauma
– Esophageal perforation or other trauma
– Unintended tracheal extubation or compression/obstruction of the trachea
• Hypotension: While there are multiple etiologies for intraoperative hypotension, rescue TEE
can quickly differentiate many of these causes.
– Hypovolemia: Hemorrhage
– Vasodilation: Anaphylaxis, sepsis
– Systolic dysfunction: Ischemia, infarction
• Cardiac tamponade: A large pericardial effusion with collapsed cardiac chambers. Symptoms
can be non-specific with equivocal physical findings intraoperatively. TEE is the gold
standard for diagnosis.
• Pulmonary embolism: Can result from clot, air, fat, or other debris that enters the
pulmonary vasculature. It results in a mechanical obstruction (dead space) with a secondary
inflammatory response (shunting).
• Shunt: Intracardiac shunts such as atrial septal defects and ventricular septal defects
• Valvular pathology: Aortic stenosis, mitral stenosis, severe mitral regurgitation, and severe
aortic insufficiency
• Midline insertion of the TEE probe in an endotracheally intubated patient may be performed
with or without the aid of a laryngoscope. During insertion, the probe should be in a neutral
position to avoid resistance.
• Hypotension. Diagnosis may be made by imaging the left ventricle and measuring the
ejection fraction, end-diastolic area, and end-systolic area. Diastolic area measurements
function as reasonable, quick surrogates for true volume measurements in an emergency
and are easily planimetered.
– Hypovolemia: The appearance of normal left ventricular ejection fraction but low end-
diastolic area
– Vasodilation: Normal to high left ventricular ejection fraction with normal end-diastolic
area and markedly low end-systolic area
– Systolic dysfunction: Severely decreased ejection fraction of the left ventricle with very
large end-diastolic and end-systolic areas.
• Cardiac tamponade: Using midesophageal and trans-gastric views, a pericardial effusion may
be evident around the whole of the heart or isolated. Tamponade physiology may be seen
with collapse of the ventricles during diastole and atrial collapse during systole.
• Pulmonary embolism: Using a midesophageal 4-chamber view may reveal a dilated right
ventricle with a hypovolemic and even hyperdynamic appearing left ventricle; thrombus
may be visualized in the main pulmonary arteries (uncommonly seen). Large venous gas
embolisms may look similar with gas bubbles visualized on TEE as bright white “fireflies”
moving in the right ventricle. Extremely large gas embolisms may show the right ventricle
filled with an echogenic bright white substance. If a large gas or air embolism is suspected,
stop the surgical procedure including gas insufflation, and proceed as clinically indicated by
ACLS protocol. Persistent hemodynamic instability necessitates insertion of a TEE probe and
quick examination to rule out massive embolism or another potential cardiac cause such as
myocardial ischemia.
• Intracardiac shunts: May be seen in the midesophageal, 4-chamber view. Septal defects of
the atria and ventricles will require superimposing Doppler color over the septa which may
show flow across the septa. A bubble study with agitated saline may show a flow of bubbles
across the interatrial septum if the right atrial pressures are higher than the left atrial
pressures, but a lack of bubbles crossing the septum does not rule out a left to right shunt.
• Aortic valve pathology: Using the midesophageal, aortic valve short-axis view (change the
probe angle from 0 to 30% from a 4-chamber view) allows rapid visualization of the valve
to estimate valve opening. A highly echogenic (bright white) valve that appears to not open
well may be aortic stenosis. Superimposed color Doppler may show flow in the valve during
diastole in cases of aortic valve insufficiency.
• Mitral valve pathology: In the midesophageal, aortic valve long-axis view with
superimposed color Doppler (change the probe angle from 0% to 120% in the 4-chamber
view) the valve may have flow through it during systole indicative of regurgitation. A
calcified valve that is highly echogenic and a very large left atrium (greater than 4 cm in
diameter) may indicate mitral stenosis. The mitral valve may also be assessed in the
standard midesophageal, 4-chamber view with superimposed color Doppler.
REFERENCES
1. Savage RM, Aronson S, Shernan SK. Comprehensive Textbook of Perioperative
Transesophageal Echocardiography, 2nd ed. Lippincott Williams and Wilkins, 2011.
2. Practice Guidelines for Perioperative Transesophageal Echocardiography: An Updated
Report by the American Society of Anesthesiologists and the Society of Cardiovascular
Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology.
2010;112(1):1–13.
3. Helberath JN, et al. Safety of Transesophageal Echocardiography. J Am Soc Echocardiogr.
2010;23(11):1115–1127.
CLINICAL PEARLS
• During rescue TEE for a hemodynamically unstable patient, a quick limited examination is
warranted to rule out hypovolemia, vasodilation, and left ventricular dysfunction.
• In the presence of refractory hypoxemia, a rescue TEE may assist in the diagnosis of
pulmonary embolism or intracardiac shunt.
• Valvular pathology may also be seen and may require expert echocardiographer’s assistance.
RESIDUAL LUNG VOLUME
BASICS
DESCRIPTION
• Residual volume (RV) is the volume of air remaining in the lungs at the end of a maximal
forced expiration. Although, by definition, it does not function in volume exchange, it
continues to function in gas exchange.
• At RV, the low lung volume and external compressive forces collapse terminal bronchioles,
without causing atelectasis. The closure of these conducting zone bronchioles prevents
alveolar collapse and the complete collapse of lung (large inspiratory efforts are needed to
re-expand the alveoli).
• Residual volume
– Normal values for RV are about 20% of the total lung capacity (TLC). In a normal sized
adult male, the RV is about 1.2 L and in women about 1.0 L.
– Gas exchange. The RV provides a constant supply of oxygen during inspiration and
exhalation. Thus, it functions to provide stability and avoid rapid fluctuations in blood gas
uptake.
– Volume exchange. The RV cannot be expelled even with active, maximal exhalation.
Terminal bronchioles close at low lung volumes and with external forces. This prevents
complete alveolar and lung collapse that would require enormous inspiratory pressure to
re-expand the lungs.
• Volumes and capacities are a function of inward and outward forces.
– The lungs are an elastic structure made of collagen and elastic fibers. The natural
tendency of alveoli is to collapse inward due to the surface tension and contractile forces
of the lung parenchyma. Expansion is, thus, resisted and requires either negative pressure
across the lung and pleura (transpulmonary pressure) or positive pressure within the lung
(mechanical ventilation) to offset the contractile forces.
– The chest wall is also an elastic structure with properties similar to an expandable and
compressible spring. The natural tendency is to expand outward.
• Functional residual capacity (FRC). At the end of normal expiration, the outward expanding
forces are exactly balanced by the inward recoil of the lungs, known as the FRC. This is an
equilibrium point, and the volume at which the resting tidal volume begins and ends. It is
comprised of the RV and expiratory reserve volume (ERV); FRC = RV + ERV.
• Expiratory reserve volume (ERV). Defined as the volume from the end of normal exhalation
(or FRC) to RV. This volume may be expelled when exhalation is active and exceeds the
outward chest wall forces.
• Measurement. Isolated measurements of RV are rarely performed in clinical practice.
– Spirometry is a commonly used tool to measure inhaled and exhaled volumes. However,
because the RV does not participate in volume exchange, it cannot be measured in this
manner. Thus, indirect methods need to be utilized.
– Whole body plethysmograph is the “gold standard” in measuring lung volumes including
RV. It can be used in children and does not require patient cooperation with breathing.
However, it cannot be performed in a physician’s office and is available only in
specialized pulmonary function laboratory.
– Closed circuit breathing technique. The patient inhales a known concentration of an inert
indicator gas (e.g., nitrogen, hydrogen, helium) from a spirometer. The gas spreads
throughout the lungs and reaches an equilibrium. Exhaled gas is collected from the closed
system and the RV is determined by the dilution and eventual equilibrium of the indicator
gas.
– Open circuit technique. The patient breathes 100% oxygen at maximal expiration (down
to RV) and the concentration of nitrogen that is washed out in the expired gas is used to
calculate the RV.
– The closed and open circuit techniques may be limited by patient cooperation, the
presence of trapped air in alveoli (due to closed airways), or alveoli that take much longer
than the test period to equilibrate; these factors can result in inaccurate measurements.
• Factors that affect lung and RV include age, gender, height, and weight. Therefore, lung
volumes are usually expressed according to predicted volumes at a person’s body surface
area and is expressed at standard body temperature (37°C), atmospheric pressure, and
saturated with water vapor (BTPS).
– Age: RV increases due to the loss of lung recoil and decreased resistance to the collapse of
aged airways.
– Position: There is a small but insignificant decrease in the RV due to a change in position
from sitting to supine due to an increase in the amount of blood in the lung.
ANATOMY
• Alveoli are open and connect to the environment by conducting and transitional zones.
– Conducting zone. Describes terminal bronchioles not in contact with pulmonary blood
flow; does not take part in gas exchange. The closure of these bronchioles can occur
without atelectasis. The closure of conducting zone bronchioles is, thus, important in the
prevention of alveolar collapse and the complete collapse of lung.
– Transitional zone. Describes small alveolated tubes that cannot be easily separated from
the alveoli and take part in the gas exchange. They are susceptible to the surface tension
changes and alveolar collapse can occur.
• Increased RV and RV/TLC ratio (hyperinflation) results when emptying of the lungs is
impaired. Damage to the alveolar septa, peripheral airways, and lung parenchyma can be
seen with long-term smoking, alpha-1 antitrypsin, and emphysema. The decreased elastic
recoil of alveoli and hence radial traction of small airways leads to closure of peripheral
airways. With severe disease, bullae formation can occur (large air filled spaces that are not
in contact with the pulmonary capillaries) resulting in wasted ventilation.
– Oxygenation. This results in an increase in the alveolar to arterial oxygen gradient (A-a
gradient).
– Ventilation. Elimination of carbon dioxide is not generally affected as CO2 is 20 times
more diffusible than oxygen.
– FRC increases (FRC = RV + ERV)
– Clinically, this manifests as an increase in the A–P diameter of the lungs, muffled heart
sounds, and flattened diaphragm.
• Decreased RV results when external forces prevent adequate expansion; restrictive lung
disease. Oxygenation may be normal especially at rest. In advanced disease, hypoxia is
present due to V/Q mismatch and diffusion defect. CO2 elimination is not affected. FRC
decreases (FRC = RV + ERV)
– Parenchymal disease (interstitial pulmonary fibrosis). RV is decreased, FEV1 is preserved,
and the ratio of FEV1 to the FEV is often increased.
– Chest wall deformity includes scoliosis and pectus excavatum. Lung volumes are only
modestly decreased in these patients.
– Neuromuscular disorders include Duchenne’s muscular dystrophy, myasthenia gravis, and
amyotrophic lateral sclerosis. Respiratory muscle weakness results in low lung volumes.
• Anesthesia and medications.
– Increased RV and RV/TLC states are at risk of pneumothorax during IPPV and with the
administration of nitrous oxide. Inhalation induction may be delayed due to the increased
lung volumes (lower rate of rise in the alveolar concentration/fraction for a given
inspiratory fraction, hence decreased FA/Fi) or dead space (pulmonary blood does not
perfuse the alveoli and cannot deliver agent to the brain).
– Decreased RV states have a decreased FRC that predisposes to rapid hypoxemia as well as
faster uptake of inhaled anesthetic agents (brain tissue concentrations are achieved more
rapidly due to a faster rate of rise in the FA/Fi ratio).
• Abdominal surgery. Increases RV, but decreases ERV to a greater extent, with consequent
decreases in the FRC. Lower abdominal procedures can decrease the ERV by 25%, while
upper procedures can result in a 60% decrease.
• Lung resection. Preoperative clearance often involves an assessment of the RV and TLC to
determine suitability for surgery and predict postoperative pulmonary function. An RV/TLC
ratio >50% predicts high risk for pulmonary resection. A RV/TLC ratio >40% may be
associated with a 30% mortality versus 7% when the RV/TLC ratio is <40%.
• Severe COPD may be treated with lung volume reduction surgery (LVRS). The loss of
outward circumferential pull leads to collapse of the small airways. Reducing the overall
lung volume by multiple, peripheral wedge resections can restore the elastic pull on the
small airways and decrease obstruction; this can facilitate emptying of alveoli with resultant
decreases in the RV. Patients with severe, upper-lobe predominant emphysema, profound
breathlessness, identifiable distension, and hyperinflated lung tissue (FEV1 <40%, RV
>150%, TLC >120% of predicted values) are good candidates for LVRS.
EQUATIONS
TLC = VC + RV; where TLC is the total lung capacity, VC is the vital capacity, and RV is
residual volume
GRAPHS/FIGURES
ADDITIONAL READING
• Hedenstierna G. Alveolar collapse and closure of airways: Regular effects of anesthesia. Clin
Physiol Func Imaging. 2003;23(3):123–129.
• Levitzky MG. Alveolar Ventilation (Chapter 3). Levitzky MG: Pulmonary Physiology, 7e:
http://www.accessmedicine.com/content.aspx?aID =2773620.
• Naunheim KS, et al. Long-term follow-up of patients receiving lung-volume-reduction
surgery versus medical therapy for severe emphysema by the National Emphysema
Treatment Trial Research Group. Ann Thorac Surg. 2006;82(2):431–443.
• Rehder K, Marsh HM, Rodarte JR, et al. Airway closure. Anesthesiology. 1977;47(1):40–52.
• Stocks J, Quanjer PH. Reference values for residual volume, functional residual capacity and
total lung capacity. ATS Workshop on Lung Volume Measurements. Official Statement of the
European Respiratory Society. Eur Respir J. 1995;8(3):492–506.
• Wahba RM. Airway closure and intraoperative hypoxaemia: Twenty-five years later. Can J
Anaesth. 1996;43(11):1144–1149.
• Asthma
• Smoking
CLINICAL PEARLS
• Isolated measurement and interpretation of RV is uncommon.
• Increased RV may be seen with emphysema and alpha-1 antitrypsin deficiency. There is a
loss of circumferential outward pull of the small airways leading to small airway collapse
and trapping of air in the alveoli.
• Decreased RV may be seen with restrictive lung disease (parenchymal disease, chest wall
deformity, neuromuscular disorders).
RESPIRATORY ALKALOSIS
Mariya Svilik, MD
BASICS
DESCRIPTION
• Respiratory alkalosis is a physiologic state of high pH (>7.45) and low partial pressure of
carbon dioxide (paCO2) (<35 mm Hg).
• This clinical condition is caused by hyperventilation that results in excessive elimination of
CO2.
• Respiratory alkalosis is commonly classified as either:
– Acute respiratory alkalosis: Low paCO2, high pH, onset of 6–24 hours.
– Chronic respiratory alkalosis: Low PaCO2, near normal pH, onset of >6–24 hours. The
longer duration allows the body time to compensate by excreting sodium bicarbonate ions
renally.
• Since pH homeostasis is essential for proper protein function, and consequently organ
function, its derangement affects multiple organ systems including the cerebral,
cardiovascular, renal, pulmonary, and GI systems.
EPIDEMIOLOGY
Prevalence
In the general, in-patient population, the incidence can be as high as 26% (1).
Prevalence
Varies greatly with disease etiology
• Central nervous system (CNS). The medullary respiratory center is affected by disease
processes and input from peripheral and central receptors, as well as voluntary control from
the cerebral cortex:
– Infection
– Tumor
– Brain injury
– Drug poisoning such as salicylates
– Caffeine
– Liver failure
– Fever
– Pain
– Anxiety
• Pulmonary
– Hypoxia governs breathing to a greater extent than CO2, thereby triggering the respiratory
center to increase the respiratory rate and tidal volume (minute ventilation). It can result
from pulmonary emboli, pneumonia, pneumothorax, pulmonary edema, aspiration,
interstitial lung disease, asthma, emphysema or chronic bronchitis. Additionally, ascent to
high altitudes can decrease the fraction of inspired oxygen.
– Iatrogenic: Mechanical hyperventilation
• Cardiovascular: Congestive heart failure, right-to-left shunt, and anemia result in low-
oxygen states that stimulate peripheral receptors.
• Catecholamines increase ventilation via direct dilation of the smooth muscles of the bronchi.
• Nicotine and acetylcholine stimulate the carotid and aortic bodies.
• Hyperthyroidism increases the respiratory drive in response to hypoxemia and hypercapnia.
The specific mechanism is not known.
• Systemic sepsis results in tissue hypoxia as well as metabolic acidosis. In addition, the lungs
provide a large surface area for heat exchange thus helping to control body temperature via
neural input from the hypothalamus.
• Pregnancy: Respiratory alkalosis is a normal physiologic response. A sustained elevation of
progesterone causes a hypoxic ventilatory response as a result of its effect on carotid bodies,
while estrogen acts on the CNS thereby augmenting carotid sinus nerve activity on
ventilation.
• Carbon dioxide is a product of cellular metabolism and is excreted via the lungs. It is
transported in blood in three main ways:
– Bicarbonate ions in red blood cells (RBCs) and plasma (majority). After entering the RBC,
CO2 combines with water via carbonic anhydrase to form carbonic acid; it is then broken
down to H+ and HCO3−. The H+ binds to deoxyhemoglobin, while HCO3− is extruded
from the cell in exchange for a Cl- ion to maintain electroneutrality. This reaction also
occurs in the plasma, but at a slower rate due to the lack of carbonic anhydrase. This
mechanism for transport also serves to buffer the extracellular fluid compartment against
pH derangements.
– Bound to hemoglobin (Hgb) (carbaminohemoglobin) and protein
– Dissolved in blood; a small percentage exists in the gas form and exerts partial pressure
that can be measured on an arterial blood gas reading.
• Chemoreceptors exist in the central and peripheral system and serve to detect changes in
CO2 and pH; they send input to the medullary respiratory center.
– Central chemoreceptors are the primary regulators of respiratory rate and are located on
the ventrolateral surface of the medulla oblongata in the brain; they detect changes in pH
of CSF. Since CSF is separated from the blood, electrolytes do not diffuse freely into CSF.
However, volatile gases such as carbon dioxide can move easily through the barrier. Once
CO2 is in the CSF, it can react with water to eventually produce hydrogen ions and
bicarbonate and thereby alter the CSF pH. With time, the chemoreceptor will eventually
desensitize to the derangement.
– Peripheral chemoreceptors: aortic body and carotid body. Unlike the central
chemoreceptors, they do not desensitize to stimulus. The aortic body receptors detect
changes in the paO2 and paCO2 of the blood, whereas the carotid body receptors detect
changes in the paO2, paCO2, and pH of the blood. The chemoreceptors serve to increase or
decrease the respiratory rate and tidal volume, hence adjusting ventilation. Output from
the peripheral receptors reaches the central respiratory centers, which in turn affect the
ventilation.
• High altitude and hypoxia govern breathing to a greater extent than CO2. When the paO2
falls below 100 mm Hg, neural activity from peripheral receptors begins to increase.
However, the paO2 needs to reach 60–65 mm Hg for a substantial increase in minute
ventilation to occur and make the individual dependent on hypoxic ventilatory drive. This,
consequently can result in respiratory alkalosis.
• pH derangements result when the buffering mechanisms are overwhelmed.
– Henderson Hasselback equation:
– HCO3− + H+ ←→ H2CO3 ←→ CO2 + H2O
– Acute: pH = 0.008 × (40–paCO2) and the ΔHCO3− = 0.2 × ΔpaCO2
– Chronic: pH = 0.017 × (40–paCO2) and the ΔHCO3− = 0.5 × ΔpaCO2
• Electrolyte derangements
– Hypokalemia. To offset the pH imbalance, hydrogen ions shift from intracellular to the
extracellular space via the Na+-H+ ion exchanger (Na+ moves into the cell). The increase
in intracellular Na+ stimulates the Na+-K+-ATPase, which results in a secondary
intracellular shift of K+.
– Hypocalcemia. Alkalosis results in an increased negative charge on albumin that leads to
increased Ca++ binding and decreased unbound Ca++ ions. Additionally, calcium binds
to bone in exchange for hydrogen ions stored in bone material. Hypocalcemia can result in
tetany and paresthesias.
• Decreased cerebral blood flow (CBF). CBF is directly proportional to paCO2 values between
20 and 80 mm Hg. Normal brain blood flow is 50 mL/100 g/min. A paCO2 value of 20 mm
Hg will result in severely decreased CBF to 25 mL/100 g/min. Acute decreases below this
value can produce EEG signs of cerebral ischemia.
• Cardiovascular system. Hypocalcemia can result in dysrhythmias and vasodilation.
• Pulmonary system. Hypocarbia can result in decreased pulmonary vascular resistance as
well as increased bronchial smooth muscle tone from hypocalcemia.
• Medications. Respiratory alkalosis can potentiate the effects of nondepolarizing
neuromuscular blockade secondary to hypokalemia and alkalemia.
• Perioperatively, the end-tidal CO2 should be monitored with adjustments made to the
respiratory rate and tidal volume as appropriate. Arterial blood gas (ABG) measurements
can confirm paCO2 and pH values, particularly when there is an increase in dead space
ventilation.
• Increases in minute ventilation, particularly when spontaneously ventilating, may suggest
pain or awareness under anesthesia and administration of opioids or deepening of the
anesthetic should be considered.
• Respiratory alkalosis is a relatively common abnormality seen in in-patients. It may not
always be recognized preoperatively; however, a history of recent infection, liver or thyroid
disease, as well as psychological disturbances, may be clues to its presence.
• Diagnostic tests and interpretation
– ABG: Identify an elevated pH with a low paCO2. The pH value can aid with distinguishing
between acute and chronic states.
– Chemistry panel: To determine the effect on electrolytes such as K+, Cl−, HCO3−, and
Ca++. The bicarbonate value, which is decreased by the kidneys, can aid with
distinguishing between acute and chronic states.
– Liver function tests: To determine if liver failure may be the cause of respiratory alkalosis.
– Chest x-ray: Can help confirm pneumonia, pulmonary congestions, pneumothorax, lung
disease, pulmonary edema, cardiac enlargement, and congestion.
– Chest CT: If pulmonary embolism is suspected
– Head CT/MRI: Help to confirm an injury, tumor, or CVA
– CBC: If sepsis is suspected
– Cultures: If sepsis is suspected; if a CSF infection is suspected, perform cultures on CSF
fluid.
Respiratory alkalosis is a unique disorder that is always a sign of some other underlying
disease; thus, the etiology is, in itself, the differential diagnosis.
TREATMENT
• When detected preoperatively, the underlying cause should be sought and corrected. If
found intraoperatively, it is most commonly the result of mechanical hyperventilation;
however, other causes should also be at least considered.
• Medication: If alkalosis is >7.60, careful titration of HCl, ammonium chloride, and arginine
hydrochloride can be administered. All three medications must be administered carefully
under constant supervision. Although they have other uses, their main function here is as
systemic acidifiers. The HCl component of each of the drugs serves to buffer excess
bicarbonate.
• Additional treatment: If alkalemia is severe, consider patient intubation and mechanical
(hypo)ventilation as well as hemodialysis. In cases of chronic respiratory alkalosis,
correction to normocarbia needs to be gradual to avoid metabolic acidosis; the body
compensates via the kidneys by excreting extra HCO3− to normalize the pH.
• Complementary and alternative therapies: In cases of anxiety or panic attacks, the patient
can be instructed to breathe into a paper bag, thereby causing some of the CO2 to be
rebreathed. Patients can be taught to identify an episode of an acute anxiety attack and
practice this maneuver until the panic attack and resultant hyperventilation subsides. They
can also carry out relaxation and biofeedback exercises in order to manage the severity of
their anxiety and panic attacks.
• Surgical treatment of hyperthyroidism and liver disease can return the paCO2 to normal.
REFERENCES
1. alange P, Carlone S, Galassetti P, et al. Incidence of acid-base and electrolyte disturbances
in a general hospital: A study of 110 consecutive admissions. Recenti Prog Med.
1990;81(12):788–791.
2. Terzano C, Di Stefano F, Conti V. Mixed acid-base disorders, hydroelectrolyte imbalance
and lactate production in hypercapnic respiratory failure: the role of noninvasive
ventilation. PLoS One. 2012;7(4):e35245.
3. h YK. Acid-base disorders in ICU patients. Electrolyte Blood Press. 2010;8(2):66–71.
4. uintanilla AP. Acute acid-base disorders. 2. Specific disturbances. Postgrad Med.
1976;60(5):75–83
• Metabolic alkalosis
• Hypokalemia
• Hypocalcemia
• Minute ventilation
CODES
ICD9
276.3 Alkalosis
ICD10
E87.3 Alkalosis
CLINICAL PEARLS
Perioperatively, the anesthesia provider must keep in mind that respiratory alkalosis can
result in
• Cerebral ischemia. Rapid correction may alternatively result in vasodilation and intracranial
hypertension. Often during surgery, patients are intubated and are placed on mechanical
ventilation. Adjustments made to the ventilator tidal volume and respiratory rate can lead
to rapid correction of paCO2 to normal. However, such rapid corrections could result in
acute changes in CSF pH and consequently cerebral blood flow.
• Cardiac instability from hypotension or dysrhythmias.
• An increase in the affinity of O2 to Hgb will shift the O2–Hgb dissociation curve to the left.
This makes it more difficult for Hgb to offload oxygen to tissues and can potentially cause
tissue hypoxia.
• Prolonged respiratory depression from opioids (alkalemia).
• A potentiated effect of nondepolarizing neuromuscular blockade (hypokalemia and
alkalemia).
RESPIRATORY SYSTEM COMPLIANCE
Craig R. Cook, MD, PhD
BASICS
DESCRIPTION
• Respiratory compliance is defined as the change in respiratory system volume divided by the
change in distending airway pressure; C = ΔV/ΔP.
• Respiratory system (RS) compliance is the composite of chest wall (CW) compliance, and
lung (L) compliance. RS, CW, and L compliances are concepts of respiratory mechanics, the
branch of physiology studying the forces causing or opposing air movement in and out of
the lungs.
• Compliance is an index of the elastic properties of the respiratory system; it is also a
determinant of alveolar gas flow and work of breathing.
• The inverse, or reciprocal, of compliance is elastance: E = ΔP/ΔV.
• Measuring lung compliance provides useful data to quantify the severity of lung pathology
and to decide ventilatory strategies in the operating room and intensive care unit (ICU) (1)
[A].
• Respiratory system compliance is the change in milliliters per cmH2O pressure (mL/cmH2O).
It provides an objective measure and means to discuss an elastic structure’s ability (or
inability) to “stretch.”
• Compliance values vary with lung volume, and, thus, are not linear. CW, L, and RS
compliance are maximal at the functional residual capacity (FRC).
– FRC is defined as the balance point between the natural tendency of the CW toward
expansion and of the lung toward collapse. Such balance determines the lung volume at
rest.
– When lung values are above or below the FRC, compliance values decrease; there is a
reduced change in volume for a given pressure.
• Compliance is analogous to electrical capacitance, where chest wall and lung compliance are
in series. It is also calculated in the same manner: 1/total compliance = 1/lung compliance
+ 1/chest wall compliance. Typical values:
– Total compliance: ∼100 mL/cmH2O
– C(L): ∼150–200 mL/cmH2O
– C(CW): ∼200 mL/cmH2O
• Elastance is the reciprocal of compliance and is a measure of the RS’s tendency to recoil
toward its original dimensions following deformation and upon removal of a distending or
compressing force; it is analogous to the behavior of a stretched rubber band or spring.
– Chest wall recoil is due to anatomical structures such as the ribs and chest wall muscles,
whereas, lung recoil is due to elastin fibers and the surface tension forces in alveoli.
– Inspiration is caused by the active contraction of the diaphragm and other inspiratory
muscles. At rest, expiration is mainly passive and is due to relaxation of respiratory
muscles and the elastic recoil of lungs.
– Elastin protein is found in the lungs, as well as arteries, skin, and bladder. Following
inhalation, or stretch, it provides the force to return the lungs to their FRC. Pathologic
disease states include Marfan syndrome or α-1 antitrypsin disease.
• The surface tension of alveoli favors collapse of the lung following LaPlace’s law: P = 2T/R,
where P is pressure within the alveoli measured in pascals (Pa), T is the surface tension of
the alveoli measured in Newtons/meter, and R is the radius of the alveoli measured in
meters (m). Surfactant is a lipoprotein complex produced by type 2 alveolar cells. It
decreases alveolar surface tension (T), and hence increases compliance, decreases work of
breathing, and helps to prevent alveolar collapse.
ANATOMY
Determinants of respiratory system compliance include the lungs and chest wall (and any
associated disease or pathology). Of note, the abdominal contents are a major determinant of
respiratory compliance; increased intra-abdominal pressure (obesity, pneumoperitoneum,
pregancy) translates to decreased compliance.
• In a normal respiratory system, tidal volume ventilation should occur along the rectilinear
portion of the compliance curve. In disease states, however, it becomes more difficult to
adequately deliver tidal volume ventilation within the limits of the rectilinear portion of the
compliance curve.
• Restrictive pulmonary disorders decrease compliance of the lungs, chest wall, or both.
– Lung compliance: Pulmonary edema, fibrosis, pneumonia, acute respiratory distress
syndrome (ARDS), acute lung injury (ALI), pleural effusions, pneumothorax, mediastinal
masses, and vascular engorgement
– Chest wall: Kyphoscoliosis and muscular disease
– Both: Increased abdominal pressure from pregnancy, ascites, obesity, and laparoscopic
procedures.
• Obstructive lung disease. In emphysema or bullous lung disease, although static compliance
can be increased, dynamic compliance may be decreased.
• Age affects chest wall compliance. In the elderly, the thorax is stiff due to ossification and
increases outward forces. In infants, the CW has a very high compliance; as a result, during
passive expiration, the outward chest wall recoil does not oppose the lungs tendency toward
collapse. This may cause the FRC to decrease below the airway’s closing pressure. Positive
end-expiratory pressure (PEEP) may counteract this phenomenon and preserve FRC, and
hence, oxygenation and ventilation.
• In the operating room, the anesthesia provider can assess dynamic and static compliance.
– The anesthesia machine is capable of measuring pressures during “peak” and “plateau,” or
dynamic and static inspiratory breaths, respectively.
– These values and curves allow inferences and calculations of the compliance.
– Some machines are capable of generating pressure–volume curves; where the slope is
equal to compliance at a specific volume.
• Dynamic compliance (Cdyn) is specific to the peak inspiratory or distending compliance of
the lung and chest wall.
– C(dyn) = V(t)/(Ppeak – PEEP); volume change divided by peak airway pressure minus
end-expiratory pressure.
– Decreased dynamic compliance is seen with atelectasis, asthma, pulmonary edema, pleural
effusions, ascites, abdominal retractors or packing, pneumoperitoneum, and
endobronchial intubation.
– Artifactual increases in dynamic pressure measurements result from the breathing tube
and circuit apparatus: ETT diameter, secretions, kinking; ventilator settings. They do not
actually change compliance.
• Static compliance (Cstat) is specific to end- inspiration, when no gas flow is present. It is
mainly determined by the lung and chest wall compliance, but not by ventilator settings,
the breathing circuit, or ETT.
– C(stat) = V(t)/(Pplat – PEEP); volume change divided by plateau pressure minus end-
expiratory pressure
– Intrinsic PEEP (assessed by means of an end-expiratory pause) must be considered,
otherwise compliance could be miscalculated.
• Specific compliance: C/FRC. It mirrors the elasticity of the aerated lung tissues.
• Pressure–volume curves can be constructed to reflect changes in static and dynamic
compliance. Volume (y-axis) is plotted as a function of pressure (x-axis) and the slope
corresponds to compliance. Both inspiratory and expiratory compliance curves can be
constructed.
– The curves are nonlinear, but sigma shaped, when compliance is tested over a sufficient
range of vital capacity. In most patients, a lower and a superior inflection point can be
detected. These points correspond to volumes of the respiratory system at which its elastic
properties change rapidly. If present, the lower inflection point (LIP) identifies an abrupt
increase in the compliance that has been traditionally interpreted as a sign of lung tissue
recruitment. Alternatively, the upper inflection point (UIP) signifies an abrupt decrease in
compliance as a result of overdistention of alveoli. Hysteresis between the inspiratory and
expiratory compliance curves is also observed. Hysteresis reflects that, upon expiration, at
a given pressure, the lungs exhibit greater volume compared to inspiration. Thus, the
expiratory and inspiratory limbs of the compliance curve do not overlap.
• Compliance curves are utilized in the ICU to assess severity of lung diseases, guide
ventilatory management, and evaluate progression of the lung disease or efficacy of
undertaken treatments.
• General anesthesia affects chest wall compliance. Volatile IV anesthetics as well as paralysis
result in diaphragm relaxation with consequent cranial displacement of the abdominal
contents. This results in increased intra-abdominal pressure with decreased CW and L
compliance (2)]A].
• Intraoperative clinical changes in compliance can be anticipated based on patient-related
and procedure-related risk factors. Ventilator settings (PEEP, TV, RR) should be adjusted
accordingly. Decreased compliance can be seen with:
– Patient-related risk factors: Age, high BMI, smoking, respiratory infections, pregnancy,
abdominal distension, chest deformations.
– Procedure-related risk factors: Thoracic and abdominal procedures, Trendelenburg,
surgical retractors, cardiopulmonary bypass, one lung ventilation, and
pneumoperitoneum.
– Atelectasis from pulmonary edema, low tidal volumes, pulmonary disease, foreign body
aspiration, and endobronchial intubation can decrease compliance.
– An abrupt increase in peak pressures, in the absence of any of the previously mentioned
changes, may suggest a tube kinking or occlusion by secretions, as well as an asthma
attack.
– Increases in compliance may also be seen with alveolar recruitment, resolution of lung
parenchyma pathological processes, and changes in ventilator setting or in CW
compliance.
• ARDS and ALI are disorders that profoundly affect pulmonary compliance.
– During lung expansion with positive pressure inhalation, new alveoli are recruited and
start to open (reflected by the LIP on pressure-volume curves).
– On exhalation, some alveoli collapse or are derecruited (reflected by a steep slope change
in the expiratory pressure-volume curve).
– The exact physiologic meaning of the LIP is still debated. Traditionally, its presence has
been interpreted as the airway pressure value at which many alveolar units are recruited
simultaneously, but studies in ICU patients have shown that it may be more influenced by
the CW than the L component. Additionally, CT studies have shown that recruitment
occurs along the entire compliance curve, independent of the LIP.
– Maintaining airway pressures between the LIP and UIP may prevent cyclic alveolar
derecruitment and overdistention. Ventilation outside the inflection points can cause shear
stress with resultant release of inflammatory mediators that can have both a local and
systemic effect and contribute to multiorgan failure. Traditionally, in ICU patients, the
PEEP level is set above the LIP (2,3,4)[A].
• Respiratory compliance is also a determinant of the respiratory work of breathing, and
influences the patient’s ability to sustain unsupported ventilation. Monitoring compliance
can provide additional useful information in a ventilator weaning process.
• 1/total compliance = 1/lung compliance + 1/chest wall compliance
• Total elastance = lung elastance + chest wall elastance
• C(dyn) = V(t)/(Ppeak – PEEP)
• C(stat) = V(t)/(Pplat – PEEP)
• LaPlace’s law: P = 2T/R; P is pressure within the alveoli measured in pascals (Pa), T is
surface tension of the alveoli measured in newtons/meter, R is radius of the alveoli
measured in meters (m).
GRAPHS/FIGURES
FIGURE 1. Pressure-volume curve reflecting volume as function of pressure; the slope corresponds to compliance. The
upper inflection point (UIP) represents an abrupt decrease in compliance from overdistention of alveoli. The lower
inflection point (LIP) reflects an abrupt increase in compliance from lung tissue recruitment. Hysteresis is also
demonstrated.
REFERENCES
1. Perchiazzi G, Giuliani R, Ruggiero L, et al. Estimating respiratory system compliance
during mechanical ventilation using artificial neural networks. Anesth Analg.
2003;97:1143–1148.
2. Pelosi P, Luecke T, Rocco PR. Chest wall mechanics and abdominal pressure during general
anaesthesia in normal and obese individuals and in acute lung injury. Curr Opin Crit Care.
2011;17(1):72–79. (A)
3. arris RS. Pressure-volume curves of the respiratory system. Respir Care. 2005;50(1):78–98.
(A)
4. lbaiceta GM, Blanch L, Lucangelo U. Static pressure-volume curves of the respiratory
system: Were they just a passing fad? Curr Opin Crit Care. 2008;14(1):80–86. (A)
ADDITIONAL READING
• Stahl CA, Moller K, Schumann S, et al. Dynamic versus static respiratory mechanics in acute
lung injury and acute respiratory distress syndrome. Crit Care Med. 2006;34(8):2090–2098.
• Acute respiratory distress system
• Atelectasis
CLINICAL PEARLS
• Compliance can be assessed and monitored intraoperatively and in the ICU. Pressure–
volume loops are graphically displayed by several anesthesia machines and ICU ventilators.
These graphs inform us of dynamic compliance values and changes, as well as about
modifications of inspiratory and expiratory resistances. If compliance decreases, the P–V
loop moves down toward the pressure axis. Over distention can be detected by a
pronounced increase in airway pressure at end-inspiration with a very modest change in
volume. Increased respiratory resistances determine an enlargement of the area of
hysteresis.
• Rapid changes in compliance in intraoperative patients must be investigated to rule out
possible complications, like asthma, and obstruction or kinking of the ETT.
• If the change in compliance is caused by pneumoperitoneum insufflation, alarms based on
airway pressures should be reset accordingly to the new baseline.
RETAINED PLACENTA REMOVAL
BASICS
DESCRIPTION
General
• The third stage of labor denotes the interval between vaginal delivery of the neonate and
placental separation. Normally, placental separation and delivery occurs in <10 minutes. If
the placenta is not detached within 30 minutes, the third stage of labor is considered
prolonged.
• Normal placental adherence is likely to be caused by the persistence of one of the placental
inhibitory factors (nitric oxide or progesterone). Prior to the onset of labor, levels reduce;
allowing placental detachment. Normal shearing, detachment, and expulsion are dependent
on the contraction of the retroplacental myometrium.
• Retained or adherent placental tissue prevents adequate contraction of the uterus and results
in postpartum hemorrhage.
– The succenturiate lobe of the placenta is usually the portion that is left behind. It is a
small accessory lobe that is connected to the main part of the placenta by a blood vessel.
– Trapping of detached placenta behind a closed cervix can also occur; but is less common
– Variants of accreta where placental tissue is attached deep into the uterine wall can result
in severe forms of retained placenta and blood loss.
• Manual removal of the placenta is achieved by inserting a hand inside the uterus and
separating the placenta from the uterine wall.
– Uterotonics (oxytocin, methylergonovine) are administered before and/or after removal to
stimulate contraction and prevent bleeding; uterine massage can also aid with contraction.
– In the event that the placenta is trapped behind a closed cervix, uterolytics
(nitroglycerine, volatile anesthetics) may be warranted, followed by administration of
uterotonics after removal.
– If retained placenta is difficult to remove and comes out in fragments, a curettage may be
indicated to scrape the inside of the uterus to remove the fragments.
– In placenta accreta, the removal of fragments may be difficult or impossible and require
emergent hysterectomy and or ligation of bilateral iliac vessels.
• Risk Factors
– Previous retained placenta
– Previous injury/scar to the uterus
– Preterm delivery
– Induced or augmented labor
– Multiple gestation
– Prior dilatation and curettage
Position
Lithotomy position with legs resting on stirrups.
Approximate Time
Ranges from 20 minutes to 1 hour for manual placental removal and D&C.
EBL Expected
Ranges from mild (100 mL) to profound (2,000 mL or more)
Hospital Stay
Depends on the severity of blood loss, concomitant organ dysfunction, and extraction
procedure (e.g., hysterectomy versus uncomplicated manual extraction).
• D&C instruments
• Capability to proceed with hysterectomy
• Set-up for invasive monitoring
• Blood warmer
• Rapid Infuser
EPIDEMIOLOGY
Prevalence
At 30 minutes, the median rate of retained placenta was shown to be 2.67% in developed
countries versus 1.46% in developing countries (1).
Prevalence
5–10% of major obstetric hemorrhage cases. More frequent among gestations <26 weeks
compared to those >37 weeks.
Morbidity
Related to the direct consequences of blood loss as well as the potential complications of
hemostatic and resuscitative interventions.
Mortality
Postpartum hemorrhage is potentially life-threatening. Data from retained placenta is not
available. However, mortality is rare in developed countries due to early intervention and
resuscitation.
• Assess the severity of blood loss and optimize volume status, including the potential need
for emergent blood transfusion.
• The anesthetic plan should provide good analgesia with or without uterine relaxation.
• Emergent hysterectomy or bilateral iliac vessel ligation are rare, but possible interventions.
SYMPTOMS
• Dizziness
History
• Placenta not expelled or partially expelled after delivery of the fetus
• Estimated blood loss
• Amount of crystalloids or blood transfused
• Existing labor epidural
Signs/Physical Exam
• Pallor
• Cold clammy skin
• Dry mucus membranes and decreased skin turgor
• Tachypnea
• Tachycardia
• Narrow pulse pressure
• Poor capillary refill
• Decreases urine output
• Altered sensorium
MEDICATIONS
• Oxytocin
• Methergine
• Prostaglandins
• Magnesium
Labs/Studies
• CBC, platelets; results may not be immediately available.
• PT, PTT, fibrinogen; results may not be immediately available
• Type and crossmatch
• Ultrasound of the abdomen may be performed by the obstetric team to help evaluate the
location of retained placental products.
• Coagulopathy may be due to severe blood loss and depleted clotting factors, or secondary to
severe preexisting preeclampsia.
• Oliguria and acute renal failure if severe blood loss.
• Sheehan syndrome (hypopituitarism); during pregnancy, the pituitary gland is enlarged
without a corresponding increase in blood supply. Second, the anterior pituitary is supplied
by a low-pressure portal venous system. Major hemorrhage or hypotension during the
peripartum period can result in ischemia of the affected pituitary regions leading to
necrosis. The first sign is loss of lactation. Therapy requires hormone replacement. The
posterior pituitary is usually not affected due to its direct arterial supply.
TREATMENT
Premedications
• Aspiration prophylaxis may be considered, but should not delay induction in truly emergent
procedures. Antacids may not be feasible in altered patients.
• Fluid resuscitation
• Blood transfusion if necessary
• Blood consent for potential transfusion
• Potential to proceed with hysterectomy
INTRAOPERATIVE CARE
• Regional techniques allow the avoidance of airway instrumentation and may be considered
in volume repleted and hemodynamically stable patients.
– Spinal anesthetic may be appropriate in patients without an epidural catheter. It has the
benefit of a fast onset, dense blockade, and definitive end-point (CSF)
– Epidural catheter bolus may be appropriate if the patient has an existing, well-functioning
epidural in place.
• Minimal sedation and analgesia may be appropriate if the placenta is already separated and
trapped by the closed cervix.
• General anesthesia (GA) is recommended if bleeding is excessive, the patient is
hypovolemic, there is no well-functioning epidural in situ, uterine instrumentation is
needed, placenta accreta has been diagnosed, or a hysterectomy is strongly possible.
Monitors
• Standard anesthesia monitoring
• Foley catheter to measure urine output and aid in the assessment of urine output
• Consider invasive monitoring with an arterial line or CVP line if significant bleeding and
unstable vitals.
• Spinal anesthetic should be dosed to achieve a T10 sensory level.
• Epidural “topping off” is performed with a local anesthetic. Consider one with a quick onset
such as chloroprocaine, mepivacaine, and lidocaine (with bicarbonate). Goal of a T10
sensory level.
• Sedation and analgesia should be titrated to effect. This can result in transient hypotension.
• GA should be induced with a rapid sequence induction
– Cricoid pressure should be applied and suction readily available.
– Ketamine as an induction agent may be considered if the patient is hemodynamically
unstable.
– Pregnant women have an increased risk of difficult airways; be prepared with special
intubating devices as appropriate.
Maintenance
• Uterolytic administration. Be aware of potential side-effects
– Oxytocin: hypotension (increased when administered as a rapid IV bolus), water
intoxication, uterine rupture
– Ergometrine: nausea, vomiting, abdominal pain, hypertension, cardiac arrhythmias
– Prostaglandins: bronchospasm, increased pulmonary vascular resistance
• Uterolytics are utilized when the placenta is trapped behind a closed cervix.
– Nitroglycerin is commonly used.
IV dosing is rapid in onset (within 60 seconds) and short in duration (60 seconds); there
are minimal hemodynamic effects at doses of 50 μg.
SL dosing is also rapid in onset (35–65 seconds); 2 sprays of 0.4 mg for a total of 0.8 mg.
May cause hypotension, especially in hypovolemic patients.
– Inhalational agents provide good uterine relaxation at concentrations >1 MAC, but may
result in hypotension.
• Extubation should occur after the patient is awake, fully reversed, has good respiratory
effort, and regained protective airway reflexes.
• Consider leaving the patient intubated when hemodynamically unstable or in DIC.
FOLLOW-UP
BED ACUITY
• Vigilance for bleeding
• Consider supplemental oxygen with nasal cannula or face mask as appropriate
ANALGESIA
• Pain is typically mild and PO opioids are often sufficient.
• If the patient had a hysterectomy, analgesia may be provided with neuraxial opioids or PCA.
• Epidural catheters should be removed only after documenting normal coagulation status
when bleeding was significant.
COMPLICATIONS
• Perforation of the uterus may result from manual exploration of the uterus or curettage.
• Laparotomy and possible hysterectomy may be necessary if other techniques are
unsuccessful or a placenta accreta is present.
• Hemorrhage can result in hypotension and the need for blood transfusion; may be necessary
to administer type O uncrossmatched blood.
• Complications due to blood transfusion (TRALI) and excess fluid resuscitation (pulmonary
edema)
• Infection
REFERENCES
1. heung WM, Hawkes A, Ibish S. The retained placenta: Historical and geographical rate
variation. J Obstet Gynaec. 2011;31(1):37–42.
2. Leduc D, Senikas V, Lalonde AB, et al. Active management of third stage of labor:
Prevention and treatment of postpartum hemorrhage. J Obstet Gynaecol Can.
2009;31(10):980–993.
3. Mercier FJ, Van de Velde M. Major obstetric hemorrhage. Anesthesiology Clin.
2008;26(1):53–66.
4. Ahonan J, Stefanovic V, Lassila R. Management of post-partum haemorrhage. Acta
Anesthesiol Scand. 2010;54(10):1164–1178.
• Postpartum hemorrhage
• Hysterectomy
CODES
ICD9
• 666.02 Third-stage postpartum hemorrhage, delivered, with mention of postpartum
complication
• 666.04
ICD10
• O72.0 Third-stage hemorrhage
• O73.0 Retained placenta without hemorrhage
CLINICAL PEARLS
• Management of a retained placenta should be active.
• Uterotonics are the first line of treatment; however, uterolytics may be required when the
placenta is retained behind a closed cervix.
• Check volume status and estimated blood loss. May require aggressive resuscitation with
fluids and blood.
• Avoid spinal anesthetic in the presence of profound hypotension and inadequate fluid
resuscitation.
RETINAL DETACHMENT
Allen Hu, MD
BASICS
DESCRIPTION
General
• Retinal detachment (RD) is a condition in which the retina is separated from the underlying
retinal pigment epithelium (RPE) accompanied by the collection of subretinal fluid. The
cells of the nerve tissue are isolated from their supplies of nourishment and can die, leading
to a loss of vision. There are four types of RD:
– Rhegmatogenous (“rhegma” = tear) detachments occur when fluid from the vitreous
cavity flows through a retinal tear and dissect underneath the retina, causing detachment
from the wall of the eye (most common). Tears are either triangular or circular.
– Tractional detachments occur when scar tissue from inside the eye contracts and pulls the
retina away from its attachment to the wall of the eye (more common in diabetics).
– Exudative or serous detachments occur when fluid collects in the normally closed space
from uveitis or choroid tumor. Unlike rhegmatogenous detachments, the fluid does not
come through a tear in the retinal tissue.
– Combined tractional/rhegmatogenous detachments
• RD is a common ophthalmic emergency that may require urgent surgery to prevent
blindness. Principles of surgical repair involve identification and treatment of causes and
the recreation of a firm adhesion (pneumatic retinopexy and/or scleral buckle) between the
retina and the wall of the eye.
– Tears are treated by promoting adhesion between the outer retinal layers and RPE with
diathermy, cryotherapy, laser endophotocoagulator, or indirect laser photo coagulator.
Note: Tears may occur without detachment and may be treated in the office setting when
discovered to prophylact detachment.
– A scleral buckle is a silicone band or sponge that is sutured and tightened to the sclera to
indent it toward the detached retina and establish contact between the retina and retinal
pigment layer. This promotes closure of breaks and decreases the effects of traction and
other factors responsible for RD.
– Vitrectomy involves operating on the retina from within the eye. Three small incisions are
made to allow for infusion of fluid into the eye, insertion of a fiberoptic light source, and
insertion of an instrument (microscissors, forceps, knife, or vitrector). The instrument is
used to remove the vitreous gel under the eye, followed by a pneumatic retinopexy
(injection of gas or air intravitreally to flatten the retina from inside). The tamponading
agent is typically a gas such as sulfur hexafluoride (SF6) or perfluoropropane (C3F8) that
may remain in the eye for as long as 6 weeks. If a more permanent endotamponade is
necessary, silicone oil may be used. Patients may require another surgery in the future to
remove the silicone oil.
• After RD surgery, patients may need to maintain the head in a certain position to ensure the
endotamponade agent is positioned against the retinal break.
Position
• Supine with the head typically immobilized (tape over the forehead), nonoperative eye
covered with a shield, and whole face and body draped
• Access to the airway is limited.
Incision
Access to the eyeball through an incision in the lower or lateral conjunctiva.
Approximate Time
Variable; 1–3 depending on position and extent of RD and the combination of procedures
required (scleral buckle, vitrectomy, injection of gas bubble, laser, cryopexy or cautery).
EBL Expected
Minimal and typically insignificant
Hospital Stay
Most patients are discharged home the same day from the recovery room. Inpatient stay is
rarely required.
Specialized pars plana vitrectomy machine with wide angle viewing systems, laser, cryopexy,
and diathermy
EPIDEMIOLOGY
Prevalence
• It is relatively uncommon with an annual incidence of ∼36,000 in the US. Estimated
incidence of 12 in 100,000 in the general population with an annual risk of 0.01%, and
lifetime risk of 0.6%.
• RD is more common with aging as the vitreous gel begins to develop pockets of liquefaction.
As these pockets become more numerous, they combine to form larger pockets and can
break away from the retina. Once the seal is compromised, the structures “peel” away from
each other.
Morbidity
• Worsened prognosis when affects the macula.
• Considerable morbidity due to loss of vision or decreased visual acuity.
Mortality
Rare
• Emergency surgery is rarely indicated. Most surgeries are performed within 24 hours if the
macula is “on” (macula spared) or within 7 days if the macula is “off” (macula involved).
• A retrobulbar block (or general anesthesia) can provide a still patient with immobility of the
eye and analgesia or anesthesia.
• If general anesthesia is used, smooth induction and emergence are critical to avoiding
increases in intraocular pressure.
• Long-acting gas such as SF6 and C3F8 may be injected for treatment of RD. Use of nitrous
oxide in these patients is contraindicated both intraoperatively and postoperatively for up to
6 weeks. Animal experiments show that the intraocular pressure can double in about 25
minutes with the use of 75% nitrous oxide; this may result in retinal artery occlusion,
retinal ischemia, and eventual vision loss. Although intracavitary dwell time of these gases
is about 28 days, permanent vision loss has occurred with the use of nitrous oxide as late as
6 weeks following surgery.
SYMPTOMS
• Floaters and light flashes are not due to RD but can occur.
• Visual acuity may be normal if the macula is not involved. Central visual field and visual
acuity is affected in the presence of macular involvement.
History
• Patients with high myopia, cataract surgery, severe ocular trauma, ocular infections, lattice
degeneration, and glaucoma are at higher risk for development of rhegmatogenous retinal
detachment (RRD).
• Lattice degeneration is the most common cause of vitreoretinal degeneration. The risk of RD
with lattice degeneration increases in association with the degree of myopia.
• Patients present with painless loss of vision
• Traumatic RD involves a history of direct trauma to the eye.
Signs/Physical Exam
• Direct or indirect ophthalmoscopic examination, aided by scleral depression, shows an
opaque, elevated, corrugated retina that freely undulates with eye movement.
• Retinal tears are often multiple.
Labs/Studies
Significant media opacities, such as hyphema (blood in anterior chamber) or vitreous
hemorrhage as a result of trauma, can preclude direct examination of the retina. A B-scan
ultrasound examination may be needed to rule out RD.
Usually none
TREATMENT
Premedications
• Patients are generally anxious secondary to the anticipated operation on the eye,
postoperative pain, and visual outcomes.
• Detailed explanations, assurance of analgesia, and midazolam IV may help alleviate the
anxiety.
Difficulty reading the written informed consent forms.
Systemic antibiotics are not usually required. Antibiotics are injected into the conjunctiva at
the end of surgery.
INTRAOPERATIVE CARE
• Most procedures are performed under regional anesthesia via either a retrobulbar or
peribulbar block.
– A retrobulbar block provides adequate analgesia and akinesia of the ocular muscles.
Complications (rare) include risk of globe perforation especially in patients with high
myopia; retrobulbar hemorrhage; or injection into the CSF via the dural sheath around the
optic nerve, resulting in apnea, hypotension, and bradycardia. Treatment involves
hemodynamic support and ventilation until the effects of local anesthesia are terminated,
usually in a few hours.
– Peribulbar blocks have fewer complications, but may provide inadequate anesthesia.
Supplemental topical anesthesia is frequently required, especially toward the end of a
prolonged surgery.
• General anesthesia may be chosen due to patient preference, extent of planned surgery, or
surgeon’s preference.
Monitors
• Standard ASA monitors and neuromuscular twitch monitor during general anesthesia.
• Invasive monitors are rarely required given minimal hemodynamic perturbations but are
dictated by the patient’s underlying medical status.
• Retrobulbar block is usually performed by inserting a needle above the inferior orbital rim.
After passing the equator of the globe, the needle is redirected cephaladly toward the apex
of the orbit. Length and gauge of the needle, choice of local anesthetic drug, and volume
vary. The use of additional supplemental drugs also varies.
• Retrobulbar or peribulbar block is performed under monitored anesthesia care (MAC). A
variety of anesthesia drugs, such as propofol, alfentanil, remifentanil, or fentanyl, may be
used alone or in combination to provide sedation during the block. The goal is to provide
adequate sedation, amnesia, and analgesia for injection without significant
cardiorespiratory depression.
• Consider full stomach or other associated injuries if the RD is due to eye trauma. Most
patients can be scheduled to avoid full stomach precautions.
• If general anesthesia is indicated, plan for a smooth induction to avoid coughing and
bucking. Endotracheal intubation is safest for airway management.
Maintenance
• MAC can be provided with a number of intravenous agents. Avoid oversedation with
resultant hypoxia, hypercarbia, and inability to follow commands
• General anesthesia is maintained with a choice of inhalational agent in oxygen and air;
avoid the use of nitrous oxide. However, if used, nitrous oxide needs to be turned off for
20–30 minutes prior to the injection of intraocular gas.
• Supplemental analgesia may be provided by titrating small doses of fentanyl or longer
acting opioids (also provides postoperative analgesia).
• Complete neuromuscular paralysis, with monitoring of neuromuscular function, helps avoid
unintentional movement of the patient during surgery under general anesthesia.
• Antiemetics should be given prophylactically to prevent nausea and vomiting as they can
increase intraocular pressure.
• A local anesthetic, usually bupivacaine, may be injected or instilled into the retrobulbar
space at the end of surgery under general anesthesia to provide postoperative analgesia.
• Coughing and bucking on the endotracheal tube should be avoided during extubation. Deep
extubation may be achieved by a combination of techniques using inhalational or IV
anesthesia, or instillation of lidocaine via the endotracheal tube.
FOLLOW-UP
BED ACUITY
No special monitoring is required. However, patients may be instructed to maintain their
head in a certain position (e.g., head down) as soon as possible, which may interfere with
airway protection and oxygenation. They are usually discharged home from the recovery
room after all criteria for discharge are met.
ANALGESIA
Postoperative analgesia is usually adequate with combined oral codeine/acetaminophen
medications for 24 hours. Severe pain may require evaluation by the ophthalmologist.
COMPLICATIONS
• Scleral buckle: Choroidal or retinal incarceration, suprachoroidal or subretinal hemorrhage,
strabismus and diplopia, worsening of myopia, late extrusion, and infection of buckle.
• Vitrectomy and pneumatic retinopexy: Induced cataract, glaucoma, retinal trauma, optic
nerve trauma, intraocular bleeding.
• Rare cases of venous air embolism have been reported during air/fluid exchange.
PROGNOSIS
With appropriate surgical intervention, anatomic success rates of 90–95% can be achieved;
nonetheless up to 40% of treated patients have visual acuity of 20/50 or worse. Postoperative
visual acuity is adversely affected by preoperative involvement of the macula and longer
duration of RD. It is also adversely affected by macular edema and formation of macular
pucker.
REFERENCES
1. Brucker AJ, Hopkins TB. Retinal detachment surgery: The latest in current management.
Retina. 2006;26(6 Suppl):S28–S33.
2. D’Amico DJ. Primary retinal detachment. N Engl J Med. 2008;359:2346–2354.
• Oculocardiac reflex
• Total spinal
CODES
ICD9
• 361.00 Retinal detachment with retinal defect, unspecified
• 361.81 Traction detachment of retina
• 361.9 Unspecified retinal detachment
ICD10
• H33.009 Unsp retinal detachment with retinal break, unspecified eye
• H33.20 Serous retinal detachment, unspecified eye
• H33.40 Traction detachment of retina, unspecified eye
CLINICAL PEARLS
• Most cases of RD require surgery. However, urgent surgery is rarely required and most cases
can be delayed for adequate preoperative evaluation and preparation.
• Long-acting gases such as sulfur hexafluoride or perfluoropropane, may be injected into the
intravitreous cavity for tamponade. Use of nitrous oxide in these patients is contraindicated
both intraoperatively and postoperatively for up to 6 weeks.
• Further, the above gases may be injected in an office setting (pneumopexy) for retinal tears
under local anesthesia. Elicitation of such a history is important if these patients present for
surgery unrelated to the eye.
RETINOPATHY OF PREMATURITY (ROP)
Amitabh Goswami, DO, MPH
BASICS
DESCRIPTION
• Retinopathy of prematurity (ROP) describes the abnormal development of retinal
vasculature in preterm infants that can result from oxygen therapy; formerly known as
retrolental fibroplasia.
• It remains the most common cause of childhood blindness in the US.
• Anesthesia providers are often involved in providing care to patients presenting for
ophthalmic procedures. In addition, in premature patients who present for unrelated
surgery, a clear understanding of the pathogenesis along with appropriate preventive
measures may reduce the incidence of this unfortunate disease.
EPIDEMIOLOGY
Prevalence
In patients diagnosed with ROP, the severe form comprises 36% of cases.
Prevalence
• 8% in infants >32 weeks
• 19% in infants 27–31 weeks
• 43% in infants <27 weeks
• Prematurity: <1,000 g, <29 weeks gestation
• Infant comorbidities and treatment
– Hypoxia/hyperoxia
– Apnea/bradycardia
– Hypercapnia/hypocapnia
– Asphyxia/acidosis/shock
– Anemia requiring blood transfusions
– Sepsis
– Intraventricular hemorrhage and seizures
– Nutritional deficiency
– Bilirubinemia requiring phototherapy
– Ventilator support
– Surfactant therapy
• Pregnancy complications that predispose to prematurity include:
– Hypertension
– Diabetes
– Bleeding
– Smoking
• ROP develops in two main stages: Hyperoxia followed by hypoxia of the retinal vasculature.
• The hyperoxic stage. Normal vascularization is affected and vessel growth ceases. Because of
the high rate of blood flow to the choroidal circulation, the retina is particularly affected.
• The hypoxic phase follows. Normal photoreceptor development requires high levels of
oxygen. However, the abnormal, underdeveloped retinal vasculature (secondary to
hyperoxia) cannot meet oxygen demands. Consequently, hypoxia-inducible factor and
vascular endothelial growth factor are released and stimulate “neovascularaization" with
abnormal proliferation from the retina to the vitreous. Neovascularization can cause fluid
leak, hemorrhage, and retinal scar formation with traction of the retina. In severe cases,
traction can lead to detachment and blindness.
• Progression. Spontaneous recovery is seen in up to 85% of cases, with mild ROP having the
most favorable prognosis (usually regresses in 2–3 months). Moderate ROP may resolve in 6
months; however, severe ROP can result in blindness or limited vision.
• Fetal prematurity is also associated with hyaline membrane disease (60–80%).
• Exposure to high FiO2 while in utero does not result in ROP due to hemoglobin F.
• Classification strategies based upon opthalmoscopic findings at the junction of the vascular
and avascular retina:
– STAGE 1: Demarcation line
– STAGE 2: Ridge formation
– STAGE 3: Ridge with extraretinal fibrovascular proliferation
– STAGE 4: Sub-total retinal detachment
– STAGE 5: Retinal detachment
– Rush disease: Rapid progression (days) to severe ROP and retinal detachment
– Plus disease: Dilation and tortuosity of arterioles and venules in the posterior pole.
• Elective or outpatient procedures should be deferred until the preterm infant reaches at least
50 weeks postconceptual age.
• Noninvasive spectrophotometric retinal oximeters have improved the ability to regulate
oxygen tensions. Previously, the lack of noninvasive techniques to measure retinal oxygen
tension or saturation of retinal blood vessels obligated clinical decisions to be based on
arterial measurements alone.
• Perioperatively, however, preventive measures include minimizing oxygen administration
while avoiding arterial hypoxemia:
– Maintain PaO2 between 60 and 80 mm Hg
– Maintain the SaO2 between 92% and 96%
• All premature infants with birth weights <1,200–1,700 g should be screened at 4–6 weeks.
• Larger premature infants should be screened if oxygen therapy exceeds 50 days.
• Early pediatric ophthalmologist consultation.
• History. An ophthalmic history with attention to birth history, birth weight, birth trauma,
asphyxia, maternal drug history, cardiovascular and respiratory status.
– Signs and exam may reveal a shallow anterior chamber, corneal edema, iris atrophy, poor
papillary dilation, leukocoria (white pupils), vitreous hemorrhage, nystagmus, strabismus,
retrolental fibroplasias, and retinal detachment.
TREATMENT
Peripheral retinal ablation can be accomplished with

• Laser therapy (treatment of choice) allows for deep tissue penetration, is minimally invasive,
and can be less painful than other modalities.
• Cryotherapy freezes abnormal retinal tissue. However, it requires general anesthesia, is more
painful, and expensive.
• Scleral buckle and vitrectomy may be needed for retinal detachment.
• Other treatment modalities include
– Exogenous rHuEPO (erythropoietin)
– Intravitreal injection of bevacizumab has been reported as a supportive measure in
aggressive ROP.
– Serum IGF-1 from breast milk or exogenous IGF-1.
– Maintaining serum glucose <120 mg/dL.
– Treatment of anemia with a liberal transfusion policy.
– Photopic adaptation by adjusting illumination and retinal oxygen consumption can be
reduced.
– Vitamin E supplements
– Omega-3 supplements
FOLLOW-UP
• Initial exam between 31 and 32 weeks postconceptual age.

• Follow-up exam every 1–2 weeks until the periphery is vascularized, then monthly exams.
• Parents must be taught to care for their blind or visually impaired child.
• Referrals to PT, OT, and agencies for the blind to help families avoid developmental delays.
REFERENCES
1. Good WV. Retinopathy of prematurity and the peripheral retina. J Pediatr.
2008;153(5):591–592.
2. Jussain N, Clive J, Bhandari V. Current incidence of retinopathy of prematurity, 1989–
1997. Pediatrics. 1999;104:e26.
3. Quinn GE. International classification of retinopathy of prematurity. The Committee for the
Classification of Retinopathy of Prematurity revisited. Arch Ophthalmol. 2005;123:991–
999.
4. Phelps DL. ETROP Cooperative Group. The early treatment for retinopathy of prematurity
study: Better outcomes, changing strategy. Pediatrics. 2004;114(2):490–491.
5. journalofpediatricophthalmology.com An Epidemiological Analysis of Retinopathy of
Prematurity Over Ten Years.
• Anemia of prematurity
• Retinal detachment surgery
• Oxygen toxicity
CODES
ICD9
362.20
ICD10
• H35.101 Retinopathy of prematurity, unspecified, right eye
• H35.102 Retinopathy of prematurity, unspecified, left eye
• H35.109 Retinopathy of prematurity, unspecified, unspecified eye
CLINICAL PEARLS
• The incidence and severity of ROP increases with decreasing gestational age and birth
weight.
• Fetal hemoglobin (HbF) may protect against ROP.
• Prevention of ROP ultimately depends on the prevention of premature birth.
• Anesthesia providers should avoid the administration of “hyperoxic" gases to patients at risk
for ROP. Furthermore, these patients also pose a challenge, as their associated comorbidities
may have competing interests (increased need for oxygen delivery).
RETROPHARYNGEAL AND PERITONSILLAR ABSCESS
Dam-Thuy Truong, MD
Angela Truong, MD
BASICS
DESCRIPTION
General
Deep neck space infections encompass a wide range of clinical severity.
• In the early period, diffuse cellulitis can usually be treated with antibiotics.
• In the late period, if the retropharyngeal and peritonsillar abscesses are left untreated the
suppurative collections may rapidly expand to the mediastinum, carotid sheath, and base of
the skull or cause lethal airway obstruction.
Position
• Supine; head elevated 20°
• OR table straight or turned 90–180°
Incision
Intraoral
Approximate Time
60–120 minutes
EBL Expected
50–150 mL
Hospital Stay
3–5 days
Cricothyrotomy set and tracheostomy sets opened and ready for use in the OR
EPIDEMIOLOGY
Prevalence
• Peritonsillar abscess in adolescents and adults: 30 per 100,000
• Retropharyngeal abscess is most common in pediatric patients age 6 months to 6 years
(mean age 3–5)
Prevalence
Increased in low socioeconomic status and/or those with chronic oral, dental, and respiratory
infections due to poor oral hygiene or inadequate health care
Morbidity
Related to hospitalization, surgical procedures, general anesthesia, and potential
complications
Mortality
Overall mortality 1–2.6%. Results from:
• Airway obstruction with progression of edema and airway manipulation during attempts to
secure the airway
• Invasion or rupture into neighboring structures (Carotid sheath). Septic mediastinitis has a
50% mortality.
• Meticulous planning and cooperation between the anesthesia provider and otolaryngologist
must be maintained throughout the case.
• All necessary equipment for airway management should be ready in the operating room,
including a variety of laryngoscopes, different sized endotracheal tubes (ETTs), laryngeal
mask airways (LMA), fiberoptic bronchoscopes, jet ventilation equipment, and tracheostomy
sets.
• Despite the severity of the situation, airway control should be done meticulously, gently,
and patiently.
– Maintain spontaneous ventilation until after successful intubation: Avoid sedatives,
hypnotics, and muscle relaxants.
– Maintain airway patency: Avoid airway trauma causing complete airway obstruction.
– If unsuccessful, discontinue fiberoptic intubation (FOI) attempts and proceed to
tracheostomy before complete airway obstruction or respiratory arrest occurs.
SYMPTOMS
Fever, malaise, irritability, lethargy, sore throat, dysphagia, odynophagia, difficulty breathing
History
Recent URI, trauma to neck or oral cavity (head and neck surgery, dental procedure),
immunosuppressed state
Signs/Physical Exam
• Toxic appearance, febrile, trismus, neck swelling, torticollis, decreased neck range of
motion, nuchal rigidity, retropharyngeal bulge
• Tachypnea and stridor indicate impending airway obstruction.
• Hemorrhage from ear, nose, or mouth signals carotid artery rupture.
MEDICATIONS
• Antibiotics
• Dexamethasone
Labs/Studies
• CBC: Elevated WBC (range 3,100–45,000/microliter with a mean of 17,000/microliter). A
normal count does not rule out retropharyngeal abscess since 18% of patients have a WBC
<8,000/microliter.
• Throat culture; aspirated pus for Gram stain, culture, and sensitivity; blood culture
• CT scan of neck: Hypodense lesion in the retropharyngeal space with peripheral ring
enhancement, soft tissue swelling, and mass effect
• Lateral neck x-rays: Swelling of the posterior pharyngeal wall is diagnostic for
retropharyngeal abscess.
• Nasopharyngoscopy is performed with topical anesthesia to the nasopharynx and can help
assess airway edema upon initial presentation and can be done periodically for ongoing
airway evaluation.
Septic shock and multiorgan system failure (acute renal failure and adult respiratory distress
syndrome)
TREATMENT
Premedications
• Avoid sedatives in potential airway compromise
• Anticholinergics to help decrease secretions
• Steroids to help decrease edema
• Fluid resuscitation for dehydration
• Initiate antibiotics treatment
• Pediatric cases require consent from parents
• Potential for a surgical airway
• Aerobes, anaerobes, Gram-negative organisms, and/or mixed flora.
• IV broad-spectrum antibiotics: Clindamycin and metronidazole
– Adult: Clindamycin 600–900 mg IV q8h with metronidazole 1 g IV load followed by 500
mg q6h
– Child: Clindamycin 25–40 mg/kg/d IV divided q6–8h with metronidazole 30 mg/kg/d
divided q8h
INTRAOPERATIVE CARE
• Local anesthesia for needle aspiration
• General anesthesia for incision and drainage
Monitors
• Arterial line in cases with
– Anticipated large blood loss
– High risk of perioperative airway compromise
– Severe comorbidities
• The choice of techniques to secure the airway must be carefully individualized, depending
on anticipated difficulties and the expertise and skills of the anaesthetist and
otolaryngologist in charge.
• A routine induction, laryngoscopy, and intubation may be considered in the following
circumstances:
– Early diagnosis
– Minimal neck edema
– No trismus
– Normal airway with no special risk for difficult ventilation and intubation
• Inhalation induction with oxygen and sevoflurane may be carefully and deliberately
performed in young children who cannot cooperate for awake fiberoptic bronchoscopy or
tracheostomy.
– Maintain spontaneous respirations with gentle manual CPAP to prevent airway collapse
and inflation of the stomach
– Intubate only after an adequate depth of anesthesia is achieved to prevent laryngospasm
– Use a smaller ETT than usual because of the potential for edema of the airway
• Awake FOI should be performed in cooperative patients with the potential for airway
compromise. It requires judicious topicalization of the airway with local anesthetic.
– All the steps of the procedures should be clearly explained to the patient to gain complete
cooperation.
– Because of copious secretions, pretreatment with anticholinergics may be needed and it
may take longer to achieve optimal conditions for intubation.
– Localization of the glottic opening may be facilitated by delivering high flows of oxygen
through the fiberoptic bronchoscope to disperse secretions, or compression of the chest
wall to create air bubbles coming from the larynx.
– A small and well-lubricated LMA may be inserted gently to help focus on the larynx and
help in the guidance of the fiberoptic bronchoscope armed with an Aintree catheter to
successfully intubate the trachea.
• Awake tracheostomy should be performed by an experienced otolaryngologist when extreme
anatomical airway distortion is present.
– Generally considered the gold standard in securing these difficult airways
– Severe neck swelling and inability of the patient to lie supine requires a very experienced
otolaryngologist to achieve success under these difficult conditions.
Maintenance
Standard maintenance for general anesthesia with the use of short-acting, easily reversible
agents
• Extubate when fully awake
• Keep intubated postoperatively if airway edema persists
FOLLOW-UP
BED ACUITY
• Postanesthesia care unit
• Intensive care unit if the patient is to remain intubated
ANALGESIA
Careful titration of opioid analgesic drugs or NSAIDs as appropriate
COMPLICATIONS
• Intraoperative loss of airway control; accidental extubation
• Massive hemorrhage
• Severe supraglottic and glottic edema
PROGNOSIS
Excellent in patients without serious comorbidities
REFERENCES
1. Ho AM, Chung DC, To EW, et al. Total airway obstruction during local anesthesia in a non-
sedated patient with a compromised airway. Can J Anesth. 2004;51(8):838–841.
2. McGuire G, El-Beheiry H, Brown D. Loss of the airway during tracheostomy: Rescue
oxygenation and re-establishment of the airway. Can J Anaesth. 2001;48(7):697–700.
3. Ovassapian A, Tuncbilek M, Weitzel E, et al. Airway management in adult patients with
deep neck infections: A case series and review of the literature. Anesth Analg.
2005;100(2):585–589.
4. Parhiscar A, Har-El G. Deep neck abscess: A retrospective review of 210 cases. Ann Otol
Rhinol Laryngol. 2001;110(11):1051–1054.
5. Potter JK, Herford AS, Ellis E III. Tracheostomy versus endotracheal intubation for airway
management in deep neck space infections. J Oral Maxillofac Surg. 2002;60(4):349–354.
• Trismus
• Laryngospasm
CODES
ICD9
• 475 Peritonsillar abscess
• 478.24 Retropharyngeal abscess
ICD10
• J36 Peritonsillar abscess
• J39.0 Retropharyngeal and parapharyngeal abscess
CLINICAL PEARLS
• Avoid blind nasotracheal intubation, rigid direct laryngoscopy, and rigid fiberoptic stylets
due to their low success rates and high risk of serious complications.
• FOIs
– Do not attempt FOI in cases of impending complete airway obstruction; proceed directly
to awake tracheostomy.
– Secretions and tissue edema can present barriers to effective topicalization. To that extent,
supplement by spraying the airway with local anesthetic through the fiberoptic
bronchoscope.
– Limit the number of FOI attempts; if unsuccessful, proceed to tracheostomy before airway
obstruction or respiratory arrest occurs.
• Back up plans/safety precautions
– Before starting the FOI, it is prudent to have the surgeon examine the neck and mark the
site for tracheostomy in the event that an emergent surgical airway needs to be
performed. Consider prepping the site.
– Prior to beginning airway manipulation, a cricothyroid puncture with a 14 g angiocatheter
may be inserted to facilitate jet ventilation in the case of a dire emergency.
– Have available a rescue emergency ventilatory support plan in case both FOI and
tracheostomy attempts are unsuccessful: LMA, cricothyrotomy, jet ventilation.
RH FACTOR
BASICS
DESCRIPTION
• Rh (“Rhesus factor”) is a glycoprotein with antigenic properties that can be present on red
blood cell (RBC) membranes. Individuals
– With Rh antigen are denoted Rh positive (or their blood type followed by a positive; for
example, A+, B+, AB+, O+)
– Without Rh antigen are denoted Rh negative (or their blood type followed by a negative;
for example, A−, B−, AB−, O−)
• In 1940, Drs. Karl Landsteiner and Alexander S. Wiener described an antiserum that was
produced by immunizing rabbits with RBCs from Rhesus macaque; it agglutinated about
85% of human RBCs. The antigen that induced this immunization was named Rh factor to
indicate that Rhesus blood was the donor for the production of the serum
• The Rh blood group is the second most immunogenic and clinically significant blood group
system after ABO.
• The Rh blood group system consists of more than 45 antigens, among which the D, C, c, E,
and e are most important.
• Agglutinins (antibodies) develop spontaneously in the plasma to the ABO blood group
system, whereas antibodies to the Rh system are produced either through blood transfusion
or placental transfer from the fetus during pregnancy.
• Rh antigen is determined as follows
– Homozygous Rh positive, antigen DD (Rh+)
– Heterozygous Rh positive, antigen Dd (Rh+)
– Homozygous Rh negative, antigen dd (Rh–)
• D antigen is wildly prevalent and more antigenic in the population than E or C. However,
even in Rh negative individuals, E and C antigens may present and can cause a mild
transfusion reaction.
ANATOMY
The genes encoding the Rh proteins (RHD) are present on the short arm of chromosome 1.
• Rh incompatibility
– Low incidence in the general population.
– When an Rh negative person receives Rh positive blood, anti-Rh agglutinins develops
slowly over a period of 6 weeks to 4 months.
– The slow development of Rh antibody will not produce any immediate transfusion
reactions on first exposure. However, should the same person be exposed to Rh positive
blood a second time, there will be an enhanced transfusion reaction against the transfused
RBCs (hemolysis occurs at a slower rate compared to acute hemolytic reactions from ABO
incompatibility).
• Hemolytic disease of the newborn (HDN)
– A serious and potentially fatal disease produced by hemolysis of Rh positive fetal RBCs.
When an Rh negative mother becomes pregnant with an Rh positive baby, the fetal Rh
positive RBCs enter the maternal circulation during delivery and initiate an immune
response in the mother. In subsequent pregnancies, the Rh antibodies enter the fetal
circulation through the placenta. If the second baby is also Rh positive, then these
antibodies lyse the fetal blood cells.
– Severity: Can range from mild (fetus is minimally anemic) to moderate and severe
(profoundly anemic and an excessive amount of bilirubin will be produced). In extremely
severe conditions, the fetus develops erythroblastosis fetalis that is characterized by
ascites, edema, pleural and pericardial effusions, high output cardiac failure, and
extramedullary hematopoiesis.
– Fetal bilirubin: Transported to the mother through the placental circulation and
metabolized by the maternal liver. Immediately after the birth, the excess bilirubin cannot
be metabolized by the immature fetal liver and the baby becomes extremely jaundiced.
The excess bilirubin crosses the blood–brain barrier and reaches the CNS and produces a
condition called kernicterus. Kernicterus is characterized by the loss of reflexes, posturing,
inactivity, poor feeding, bulging fontanelles, and seizures. Later, the infant may develop
hearing loss, and mental retardation.
• RBCs. ABO and Rh compatibility should be performed and confirmed prior to any blood
transfusion. In an emergency situation, patients should receive O Rh Negative blood (O−).
Men and postmenopausal women may receive O+ blood.
• Fresh-frozen plasma (FFP). ABO compatibility is preferred, but may not be necessary in an
emergency. Because FFP may contain only a small amount of RBCs, sensitization to Rh is
unlikely; thus, donor FFP may be administered regardless of the recipient’s Rh status. No
prophylaxis is typically required; however, if administered to a woman of childbearing
potential, there is some evidence to support prophylaxis.
• Platelets. Platelets possess ABO antigens, but not Rh. ABO and Rh typing are not necessary,
but incompatibility can decrease post-transfusion counts (mainly from ABO
incompatibility). Because platelets contain only a small amount of RBCs, sensitization to Rh
antigen is unlikely; thus, donor platelets may be administered regardless of the recipient’s
Rh status. No prophylaxis is typically needed; however, if administered to a woman of
childbearing potential, there is some evidence to support prophylaxis.
• Cryoprecipitate. ABO compatible units are preferred when large volumes are needed;
however, Rh compatibility does not appear to be necessary.
• Rh incompatibility following blood transfusion in the general population creates difficulties
in finding future compatible donors.
• Risk factors for Rh isoimmunization during pregnancy.
– Spontaneous abortion
– Placenta previa
– Placental abruption
– Ectopic pregnancy
– Abdominal/pelvic trauma
– Intra uterine fetal death
– Amniocentesis
– Cordocentesis
– Chorionic villous biopsy
– Routine pregnancy
• Rh typing is performed in every pregnant patient via a serum blood draw. If the mother is
Rh negative, Rh typing is performed on the father.
• Fetal Rh typing can be done from amniocentesis or chorionic villus sampling (CVS).
• In Rh negative mothers with a second Rh positive fetus, serial measurements of maternal
antibody titers are performed during pregnancy. Additionally, frequent ultrasonography is
performed to monitor the fetal well-being and to detect anemia and signs of hydrops, like
the diameter of the umbilical vein, placental thickness, and pericardial effusion.
• Color-flow Doppler: Measuring the peak systolic middle cerebral artery (MCA) velocity by
ultrasound has proved to be a reliable method to detect fetal anemia. Peak systolic velocity
is measured by using the pulsed Doppler. Measurements can be started as early as 18 weeks
of gestation and are to be repeated at 1- to 2-week intervals until 35 weeks.
• Anti-D IgG prophylaxis coats and destroys Rh positive fetal cells when they enter the
maternal circulation, thereby preventing maternal sensitization. It is administered in the
following situations
– Rh incompatible transfusion in women with childbearing potential
– Rh negative mothers with an Rh positive fetus (regardless of antibody levels). It is given as
either a single injection of 300 μg IM (1,500 UI) at the 28th week of gestation or two
injections of 100–125 μg (500–625 UI), at the 28th week and 34th week of pregnancy.
Additionally, because the half-life of IgG is 17–21 days, an additional 300 μg is
administered within 72 hours of delivery. Prophylaxis does not appear to have any side
effects on the fetus and can decrease the risk of alloimmunization of an Rh negative
gravid women to 0.2% during that pregnancy, as well as the probability of immunization
in subsequent pregnancies.
– As a “booster” dose in Rh negative mothers with an Rh positive fetus
Threatened abortion
Hydatidiform mole
Ectopic pregnancy
Fetal death
Blunt trauma to the abdomen
Placenta previa
Placental abruption
Amniocentesis
External cephalic version.
• Fetal intraperitoneal blood transfusions are considered to correct fetal anemia and prevent
hydrops fetus. It involves delivering blood (fresh, packed, Type O, Rh negative, cross-
matched with maternal serum, gamma irradiated to prevent graft-versus-host reaction) in
10 mL aliquots to raise hematocrit levels to 40%. If blood has been stored, the additive can
be removed by washing. If antigen-compatible allogenic blood is unavailable, then maternal
RBCs may be utilized (it does not have to be ABO matched). A Tuohy needle is introduced
into the peritoneal cavity of the fetus under ultrasound guidance and an epidural catheter is
threaded. Specific indications include
– A mother who has a history of previous perinatal loss.
– Previous need for neonatal exchange transfusion.
– High antibody titer.
– MCA Doppler suggests anemia.
– Ultrasound evidence of fetal hydrops
• Fetal intrauterine intravenous transfusion (IVT) is used to treat hydrops fetalis and may
require repeat procedures. Anesthesia for the mother is required (sedation or neuraxial). For
the fetus, a needle is inserted under ultrasonographic guidance into an umbilical vein and
neuromuscular blockade is administered (vecuronium 0.1 mg/kg). Subsequently, blood that
is packed, fresh, Type O, Rh negative, cross-matched with maternal serum, and gamma
irradiated to prevent graft-versus-host reaction is injected. Maternal blood may be used if
antigen-compatible allogenic blood is unavailable (does not require ABO matching). The
amount needed is calculated as follows: fetal weight (g) × 0.14. The mother is subsequently
admitted to the hospital for 24 hours of observation with continuous monitoring of the
fetus. The procedure can be repeated every 10 days for 3 weeks, depending on the severity
of the fetal anemia. Complications include transient fetal bradycardia, cord hematoma,
umbilical vein compression, and fetal death.
• Management of the sensitized newborn
– Mild hemolytic disease (mildly anemic with Hg >14 g/dL and bilirubin <4 mg/dL):
Treated with early phototherapy.
– Moderate hemolytic disease: Although the newborn has some degree of anemia and is not
jaundiced at birth, he or she can rapidly develop hyperbilirubinemia in the first 24 hours.
This can lead to kernicterus and permanent neural damage. The neonate can receive an
exchange transfusion with type-O Rh-negative blood along with intense phototherapy.
– Severe hemolytic disease: These newborns are either stillborn or hydrops fetus at birth
– Use of IVIG in doses of 0.5–1 g/kg in single or multiple dose regimens have been able to
effectively reduce the need for exchange transfusion in the baby.
• Emerging treatment methods: Serial plasmaphereses followed by weekly IV immune
globulin to the mother is a recent advance.
REFERENCES
1. Elalfy MS, Elbarbary NS, Abaza HW. Early intravenous immunoglobin (two-dose regimen)
in the management of severe Rh hemolytic disease of newborn-a prospective randomized
controlled trial. Eur J Pediatr. 2011;170(4):461–467.
2. Liumbruno GM, D’Alessandro A, Rea F, et al. The role of antenatal immunoprophylaxis in
the prevention of maternal-foetal anti-Rh (D) alloimmunisation. Blood Transfus.
2010;8(1):8–16.
3. Mari G, Russell L. Noninvasive diagnosis by Doppler ultrasonography of fetal anemia due
to maternal red-cell alloimmunization. N Engl J Med. 2000;342:9–14.
4. Moise KJ. Management of rhesus alloimmunization in pregnancy. Obstet Gynecol.
2008;112(1):164–176.
5. Ruma MS, Moise KF, Kim E, et al. Combined plasmapheresis and intravenous immune
globulin for the treatment of maternal red cell alloimmunization. Am J Obstet Gynecol.
2007;196(2):138.e1–6.
• Transcranial Doppler
• Platelets
CODES
ICD9
• 773.0 Hemolytic disease of fetus or newborn due to Rh isoimmunization
• 999.70 Rh incompatibility reaction, unspecified
ICD10
• P55.0 Rh isoimmunization of newborn
• T80.40XA Rh incompat react due to tranfs of bld/bld prod, unsp, init
CLINICAL PEARLS
• Approximately 1% of all pregnant women develop Rh alloimmunization.
• Since the introduction of exchange and intrauterine transfusions, perinatal mortality has
reduced from 50% to 2–3% or less.
• About 10% of the infants who received in utero therapy for hemolytic disease of the
newborn later develop neurological developmental impairment and hearing loss because of
prolonged exposure to high levels of bilirubin and its toxic effect on the developing eighth
cranial nerve.
• Interestingly, a fetus that is ABO incompatible is less likely to have HDN, because of the
rapid removal of the ABO-incompatible RBCs by the naturally occurring anti-A/B
antibodies.
RHEUMATOID ARTHRITIS
Tayab R. Andrabi
BASICS
DESCRIPTION
Rheumatoid arthritis (RA) is a chronic, systemic autoinflammatory disorder characterized by
• Deforming symmetrical polyarthritis of varying distribution and severity
• Association with synovitis of joint and tendon sheaths
• Articular cartilage loss
• Erosion of juxta-articular bone (2).
EPIDEMIOLOGY
Prevalence
In the US, ∼70 per 100,000 people are diagnosed yearly.
Prevalence
• 2–3 times greater in women than men (4).
• Increases with age, approaching 5% in women over age 55
• Patients are most commonly first affected in their third to sixth decade of life (4).
• Approximately 1–2% worldwide distribution
Morbidity
Relative to the general population, patients with RA are at a
• 1.3–1.7 fold higher risk of heart failure (5,6)
• 1.5–2 fold higher risk of myocardial infarction (MI)
• 1.4–2.7 fold higher risk of stroke
Mortality
The life span is thought to be shortened by ∼10 years (1–7), and standardized mortality
ratios for RA range from 1.28 to 3.0 (5).
• The initiating cause of RA remains unknown, but several factors may contribute.
• Approximately 70% of cases are associated with the HLA-DR4 subtype, and 80% of patients
are seropositive for rheumatoid factor.
• Environmental factors also seem to play a role, including as yet unidentified viral or
bacterial agents.
• Other risk factors associated with the development of RA include female gender, a family
history of RA, food allergies and intolerances, altered gut flora, psychological stress,
exposure to heavy metals, and smoking (4).
There are two popular theories regarding the pathogenesis of RA. The first holds that the T
cell, through interaction with an as yet unidentified antigen, is primarily responsible for
initiating the disease and driving the chronic inflammatory process. The second theory holds
that while T cells may be important in initiating the disease, chronic inflammation is self-
perpetuated by macrophages and fibroblasts in a T-cell independent manner.
• Careful assessment for atlantoaxial subluxation (present in up to 25% of patients) and
concomitant organ dysfunction. The anesthetic plan should be tailored to specific
manifestations (e.g., renal, cardiac, pulmonary disease, etc).
• Stress dose steroids should be considered for patients on chronic therapy.
SYMPTOMS
Morning stiffness, pain, fatigue, malaise, and depression
History
Insidious onset
Signs/Physical Exam
• Symmetric joint swelling
• Careful palpation of affected joints can help to distinguish between swelling from
inflammation versus bony enlargement from osteoarthritis.
• Ulnar deviation of the fingers at the MCP joints, hyperextension or hyperflexion of the MCP
and PIP joints, flexion contractures of the elbows, and subluxation of the carpal bones and
toes (“cocked-up”).
TREATMENT HISTORY
Total joint arthroplasties can reduce pain and improve function. Other operations include the
release of nerve entrapments (e.g., carpal tunnel syndrome), arthroscopic procedures, and
occasional removal of a symptomatic rheumatoid nodule.
MEDICATIONS
• NSAIDs
• Corticosteroids
• Disease modifying anti-rheumatic drugs (DMARDs): Methotrexate, sulfasalazine, leflunomide
(Arava®), etanercept (Enbrel®), infliximab (Remicade®), adalimumab (Humira®), abatacept
(Orencia®), rituximab (Rituxan®), anakinra (Kineret®), antimalarials, gold salts, D-
penicillamine, cyclosporin A, cyclophosphamide, and azathioprine (Imuran) (2).
Labs/Studies
• Cervical spine x-ray: Some authorities recommend that all RA patients should undergo
preoperative screening or recent assessment of the cervical spine.
• Cervical MRI scan is indicated when neurological signs are present, there is severe pain, or
significant abnormality is noted on the plain x-ray film.
• ENT consult: A fiberoptic nasopharyngoscopy is indicated for patients with hoarseness
because of the likelihood of cricoarytenoid involvement.
• Neurological. Peripheral neuropathy in the lower extremities is often present with mild,
primarily sensory, dysfunction. Entrapment neuropathy, such as carpal tunnel or tarsal
tunnel syndromes, may also be seen. Acute subluxation of the cervical spine is a particularly
worrisome complication that can cause permanent quadriparesis or death from spinal cord
or vertebral artery compression. There are four subtypes:
– Anterior comprises 80% of atlantoaxial subluxation. The C1 vertebra moves forward on C2
because of destruction of the transverse ligament and there is a risk of spinal cord
compression by the odontoid peg. Subluxation exists when the distance between the atlas
and the odontoid peg exceeds 4 mm in patients older than 44 years and 3 mm in younger
patients. Anterior atlantoaxial subluxation is worsened by neck flexion.
– Posterior comprises 5% of atlantoaxial subluxation. Destruction of the odontoid peg may
cause backward movement of C1 on C2, which may be evident on lateral extension views
of the neck. Posterior atlantoaxial subluxation is worsened by neck extension.
– Vertical comprises 10–20% of atlantoaxial subluxation. Destruction of the lateral mass of
C1 can lead to subluxation of the odontoid peg through the foramen magnum and
compression of the cervicomedullary junction.
– Lateral or rotatory subluxation (rare) results from degenerative changes in the C1/C2 facet
joints. It can lead to spinal nerve compression and vertebral artery compression.
• Ocular: Keratoconjunctivitis of Sjögren syndrome (most common), episcleritis (mild pain
and intense redness), scleritis and corneal ulcerations (rare, but serious)
• Sjögren syndrome is a chronic inflammatory disorder characterized by lymphocytic
infiltration of lacrimal and salivary glands; seen in 10–15% of patients with RA. This leads
to impaired secretion of saliva and tears and results in the sicca complex: Dry mouth
(xerostomia) and dry eyes (keratoconjunctivitis sicca).
• Cardiac: Pericardial effusions, pericarditis, cardiac tamponade, myocarditis, amyloidosis,
granulomatous disease, endocarditis, left ventricular failure, coronary artery disease (5).
• Pulmonary: Restrictive defects from interstitial lung disease (fibrosing alveolitis),
rheumatoid nodules, reduced chest wall compliance (costochondral disease)
• Vascular: Rheumatoid vasculitis (small digital infarcts along the nailbeds). The abrupt onset
of an ischemic mononeuropathy (mononeuritis multiplex) or progressive scleritis is typical
Raynaud’s phenomenon.
• Renal: Chronic renal failure from drug treatment is seen in ∼25% of patients.
• Subcutaneous nodules are the most characteristic extraarticular lesion of the disease; occurs
in 20–30% of cases. They are located most commonly on the extensor surfaces of the arms
and elbows, but are also prone to develop at pressure points on the feet and knees. Rarely,
nodules may arise in visceral organs, such as the lungs, the heart, or the sclera of the eye.
• Airway
– Involvement of the cricoarytenoid joints may result in dyspnea, stridor, hoarseness, and
occasionally severe upper airway obstruction (3). Patients may also present with a mass in
the larynx, which can cause significant disfiguration of the surrounding structures (4).
– Laryngeal amyloidosis and rheumatoid nodules may also cause obstruction of the larynx.
– The temporomandibular joint (TMJ) may be involved causing limitation of mouth opening
and render direct laryngoscopy impossible.
– Acute subluxation may cause spinal cord and/or vertebral artery compression leading to
quadriparesis or sudden death
• Felty syndrome is a rare complication and is characterized by splenomegaly and leukopenia
(predominantly granulocytopenia). Recurrent bacterial infections and chronic refractory leg
ulcers are the major complication.
Unstable atlantoaxial subluxation may require stabilization prior to elective surgery.
TREATMENT
Premedications
Patients may have held their NSAIDs for surgery and have pain or discomfort. Preoperative
opioids may be considered.
If an awake fiberoptic intubation (FOI) is planned, indications as well as sedation goals
should be discussed with the patient and family.
INTRAOPERATIVE CARE
Regional anesthesia in conjunction with, or in lieu of, general anesthesia should be
considered whenever acceptable. Regional and local anesthesia have the advantage of
avoiding neck and airway manipulation as well as the systemic effects of drugs used for
general anesthesia. However, nerve blocks may be technically challenging because of the loss
of anatomic landmarks from contractures and flexion abnormalities.
Monitors
• IV access may be difficult due to vasculitis or thin and fragile skin
• Invasive monitors may be considered depending on concomitant disease and surgical
procedure
– Radial arterial lines may be difficult or inaccessible because of flexion deformities of the
wrist joint
– Central venous catheters in the internal jugular vein may be difficult to insert secondary to
limited neck mobility.
• Laryngeal mask airway (LMA). If the angle between the oral and pharyngeal axes at the
back of the tongue is <90°, it may be difficult to insert; a reinforced LMA may be
preferable. Intubating LMAs (ILMA) may be used to achieve blind endotracheal intubation
with minimal cervical spine movement. However, the great amount of force that may be
exerted on the posterior wall of the pharynx at C2–C3 make the ILMA less attractive as a
primary method of intubation.
• Endotracheal tube. If the patient does not have signs or symptoms of atlantoaxial
subluxation, TMJ disease, or a reduction in neck movement, direct laryngoscopy may be
acceptable. However, if suspected, consider alternate strategies
– Indirect video laryngoscopy
– FOI: If the patient appears easy to ventilate, an asleep FOI may be considered. However, if
there are concerns, an awake FOI should be performed.
– Surgical tracheostomy can be performed under local anesthesia in patients with
cricoarytenoid involvement (2).
Maintenance
• Maintenance with volatile, IV, or a balanced technique are appropriate.
• Positioning: Meticulous attention should be paid to padding pressure points and maintaining
neutral joint positions.
• Methylcellulose eye drops may be appropriate since up to 15% of patients with RA suffer
from keratoconjunctivitis.
• Stress dose steroids should be administered in patients who are taking on a dose >10 mg
daily
• Ventilator settings may need to be adjusted in patients with restrictive lung disease.
Involvement of the cricoarytenoid joints may result in dyspnea, stridor, hoarseness, and
occasionally severe upper airway obstruction.
FOLLOW-UP
BED ACUITY
Depends on the surgical procedure, concomitant organ disease, or intraoperative events
• Restart anti-inflammatory medications as soon as possible
• Continue steroid dosing
REFERENCES
1. Fombon FN, Thompson JB. Anaesthesia for the adult patient with rheumatoid arthritis.
BJA. 2006;6(6):235–239.
2. Furst DE, Breedveld FC, Kalden JR. Updated consensus statement on biological agents for
the treatment of rheumatoid arthritis and other immune mediated inflammatory diseases.
Ann Rheum Dis. 2003;62:ii2–9.
3. Wolfe F, Freundlich B, Straus WL. Increase in cardiovascular and cerebrovascular disease
prevalence in rheumatoid arthritis. J Rheumatol. 2003;30(1):36–40.
ADDITIONAL READING
• Raynaud’s disease
CODES
ICD9
714.0 Rheumatoid arthritis
ICD10
• M06.9 Rheumatoid arthritis, unspecified
• M06.30 Rheumatoid nodule, unspecified site
CLINICAL PEARLS
• Airway and neck assessment is crucial; atlantoaxial subluxation may be present and there is
a potential risk of spinal cord damage.
• Regional anaesthesia should be considered as an alternative to general anesthesia.
RIGHT BUNDLE BRANCH BLOCK (RBBB)
Tyken C. Hsieh, MD
BASICS
DESCRIPTION
Impairment of conduction in the right bundle branch, which comprises one-half of the
conduction system within the ventricles.
EPIDEMIOLOGY
Prevalence
• Increases with age: <1% at age 50 years; 17% by age 80 years.
• Most common in elderly men
Morbidity
Generally asymptomatic
Mortality
Unlike isolated left bundle branch block (LBBB), isolated right bundle branch block (RBBB)
has an excellent prognosis. However, in the presence of known or suspected coronary artery
disease (CAD), particularly acute myocardial infarction, RBBB is an independent predictor of
increased cardiovascular complications and mortality.
• Etiology
– Structural heart disease (chronic pulmonary hypertension causing right ventricular
hypertrophy; acute pulmonary hypertension as in pulmonary embolism; myocardial
ischemia/infarction; idiopathic)
– Functional: A transient “rate-related bundle-branch block” may occur with tachycardia
where subsequent electrical impulses arrive before full repolarization, producing a
functional delay in conduction.
– Iatrogenic: Secondary to right heart instrumentation, such as central venous or pulmonary
artery catheter placement. It is also a common (50%) complication of alcohol septal
ablation for hypertrophic obstructive cardiomyopathy.
– Pseudo-RBBB pattern: Brugada syndrome.
– Normal variant
• Risk factors
– Advanced age. RBBB is usually a marker of a progressive degenerative disease that also
affects the myocardium.
• The right bundle branch is one of the two subdivisions of the cardiac conduction system
below the bundle of His. It is a long, filamentous structure of rapidly conducting Purkinje
cells that courses within the interventricular septum. At approximately the level of the right
anterior papillary muscle, it branches into fascicles that spread out to supply the right
ventricle (RV).
• Normal impulse conduction along the left and right bundle branches results in rapid,
coordinated, and synchronized depolarization of the left ventricle (LV) and RV. Impairment
of conduction through the right bundle is termed RBBB.
• In RBBB, impulses travel normally down the left bundle branch to depolarize the septum
and LV, so the initial portion of the QRS complex is normal (septal Q wave followed by an
initial R-wave). However, RV depolarization through conduction tissue is blocked and
depends on propagation between LV myocytes, and is therefore both slowed and delayed.
This delayed LV-to-RV depolarization results in a secondary positive deflection (a secondary
R-wave, denoted R’ or r’) in the right precordial leads V1 and V2, and a negative deflection
(deep, broad, “slurred” terminal S-wave) in the lateral leads I and V6. The QRS complex is
always widened at >120 ms (normal <100 ms).
Isolated RBBB does not require changes to anesthetic management. However, an attempt
should be made to rule out possible causes or comorbidities that would change management,
including CAD, pulmonary hypertension, or arrhythmias.
SYMPTOMS
Inquire about history of palpitations, arrhythmias, syncope, angina, shortness of breath, and
exercise intolerance.
History
• Associated with advanced age.
• May also be associated with CAD or acute or chronic pulmonary hypertension.
Signs/Physical Exam
While there may be physical exam findings with comorbidities, RBBB is a strictly
electrocardiographic diagnosis.
TREATMENT HISTORY
There is no specific treatment for RBBB
MEDICATIONS
Class I or III antiarrhythmic medications may slow conduction through the bundle branches.
Labs/Studies
ECG criteria for RBBB
• Complete RBBB
– QRS duration greater than or equal to 120 ms in adults; AND,
– An rsr′, rsR′, or rSR′ pattern (colloquially referred to as “rabbit ears” or “M”-shaped
morphology) in leads V1 or V2. The R′ or r′ deflection is usually wider than the initial R-
wave. In a minority of patients, a wide and often notched R-wave pattern may be seen in
lead V1 and/or V2. When a pure dominant R-wave with or without a notch is present in
V1, the R duration is >50 ms; AND,
– S-wave of greater duration than R-wave or >40 ms in leads I and V6 in adults
• Incomplete RBBB
– Same criteria as for complete RBBB, except QRS duration is between 110 and 120 ms in
adults
• Baseline ECG in patients with RBBB should be performed to rule out high-grade conduction
blocks, arrhythmias, myocardial ischemia/infarction, or evidence of RV hypertrophy.
If RBBB occurs in the context of pulmonary hypertension, there may be associated RV
hypertrophy, dilation, or dysfunction. LV or RV function may be impaired in the setting of
myocardial ischemia.
Acute myocardial ischemia, recent myocardial infarction, or a new high-grade
atrioventricular conduction block.
CLASSIFICATIONS
Ischemia in the setting of RBBB. The activation of the LV is unaffected, allowing for ischemia
patterns (ST elevation and depression) to be recognized. Whereas in LBBB, abnormal
repolarization of the LV affects interpretation of the ST segments (and thus diagnosis of
ischemia).
TREATMENT
In patients with preexisting LBBB, passage of a pulmonary artery catheter may precipitate
temporary RBBB as the catheter contacts the interventricular septum, leading to complete
(third-degree) heart block and asystole. Thus, an alternative mechanism to pace the heart
must be immediately available. This could include an internal temporary endocardial pacing
wire, transcutaneous pacing pads, or epicardial pacing wires.
Premedications
Isolated RBBB does not require specific premedication.
INTRAOPERATIVE CARE
Isolated RBBB does not affect the choice of anesthetic technique, monitors, induction/airway
management, maintenance, or extubation and emergence.
Monitors
• Additional hemodynamic monitors (e.g., arterial line), as dictated by comorbidities.
RBBB does not affect induction or airway management in the absence of significant cardiac
comorbidities.
Maintenance
Volatile or IV anesthetics are all acceptable.
RBBB does not affect plans for extubation or emergence.
FOLLOW-UP
BED ACUITY
Postoperative monitoring according to comorbidities and surgical acuity.
A postoperative 12-lead ECG may be indicated if there is concern for development of new
arrhythmia or conduction disturbance.
COMPLICATIONS
A RBBB may be induced during central venous catheter placement, pulmonary artery catheter
placement, or alcohol septal ablation procedure.
REFERENCES
1. Dorman T, Breslow MJ, Pronovost PJ, et al. Bundle-branch block as a risk factor in
noncardiac surgery. Arch Intern Med. 2000;160:1149–1152.
2. Ginsburg G, Neelakantan S, Harrell PG. Acute right bundle branch block as a presenting
sign of acute pulmonary embolism. Anesth Analg. 2006;103(3):789–791.
3. Horton CL, Brady WJ. Right bundle-branch block in acute coronary syndrome: Diagnostic
and therapeutic implications for the emergency physician. Am J Emer Med. 2009;27:1130–
1141. http://emedicine.medscape.com/article/894927-overview Surawicz B, Childers R,
Deal BJ, et al. AHA/ACCF/HRS recommendations for the standardization and
interpretation of the electrocardiogram. Part III: Intraventricular conduction disturbances.
JACC. 2009;53(11):976–981.
• Left bundle branch block
FIGURE 1. Right Bundle Branch Block. Lead V1 demonstrates a secondary positive deflection, or secondary R wave (R’ or
r’). Lateral leads such as V6 demonstrate a negative S-wave that is deep and broad, and described as “slurred.” The QRS
complex is widened >120 ms and reflects delayed LV-to-RV depolarization.
CODES
ICD9
426.4
ICD10
I45.10 Unspecified right bundle-branch block
CLINICAL PEARLS
• RBBB is common in advanced age.
• Isolated RBBB is generally asymptomatic, and does not in itself require changes to anesthetic
management.
• In patients with RBBB, one should rule out associated CAD, pulmonary hypertension, or
high-grade atrioventricular conduction block.
• RBBB can be precipitated by pulmonary artery catheter placement in the setting of
preexisting LBBB, and alternative pacing capability should be immediately available during
this procedure.
ROTATOR CUFF SURGERY
Jane C. Ahn, MD
Sharon L. Lin, MD
BASICS
DESCRIPTION
General
• The rotator cuff comprises a group of 4 muscles and their tendons that attach to the humeral
head.
– Functions to stabilize the glenohumeral joint as well as arm rotation and elevation.
– “SITS” muscles: Supraspinatus, Infraspinatus, Teres minor, Subscapularis.
• Rotator cuff disease can range from impingement syndrome to full-thickness tears. Tears
commonly result from degeneration with resultant chronic tendonitis. Patients presenting
for surgery are usually refractory to conservative therapy (leads to improvement in 40–80%
of patients (1)) or have an acute, massive injury.
• Procedures involve debridement, repair of partial and full-thickness tears, use of muscle
flaps and tendon transfers for massive cuff tears, and prosthetics. They can be approached
via open, mini-open, or arthroscopic repair.
• Open repair
– Used primarily for massive tears
– More postoperative pain compared to arthroscopic repair
– Longer recovery time
• Mini-open repair
– Most of surgery is performed arthroscopically
– Minimizes deltoid injury
• Arthroscopic repair
– Lower risk of infection and deltoid injury
– Mild postoperative pain and stiffness
– Risk of respiratory compromise from extravasation of irrigation fluid with prolonged
procedures.
Position
• Rotator cuff surgery is usually performed in the lateral decubitus or beach chair position
depending on surgeon preference. Both have advantages and disadvantages (2).
• Lateral decubitus position benefits:
– Arm placed in traction allowing better visualization
– Decreased risk of hypotension and bradycardia
– Cerebral perfusion pressure is well maintained
• Lateral decubitus position disadvantages
– Traction on operative extremity increases the risk for brachial plexus injury
– Must reposition and redrape to convert to open procedure
– Regional blocks as a sole technique are not well tolerated in prolonged procedures and
obese patients
• Beach chair position benefits
– Upright, anatomic position
– Ease of exam and mobility of the arm under anesthesia
– No need to reposition or redrape if arthroscopic case is converted to open
– Regional anesthesia as the sole technique is well tolerated
• Beach chair position disadvantages
– Increased risk of profound hypotensive and bradycardic events
– Increased risk of cerebral and spinal cord ischemia and transient vision loss related to
hypotensive events
– Increased risk of air embolus
Incision
Incision size depends on surgical technique: (3)
• Arthroscopic: 4–7 mm
• Mini Open: 3–4 cm
• Open: 4–6 cm
Approximate Time
Depends on procedure and approach
EBL Expected
Depends on extent of procedure and approach. Arthroscopic debridement can be minimal,
whereas open procedures, muscle flaps, and prosthetics can be more extensive.
Hospital Stay
• Arthroscopic procedures can be performed as an outpatient.
• More extensive or complicated repairs may require an inpatient stay for post-operative pain
control.
• Arthroscopic equipment if mini-open or arthroscopic techniques planned.
• Appropriate tables for positioning (beach chair versus lateral decubitus).
EPIDEMIOLOGY
Prevalence
Approximately 150,000 rotator cuff repairs are performed in the US annually (4).
Prevalence
• Increases with age, suggesting that rotator cuff tears develop over time.
• Affects 7–30% of adults at any given time (5).
Morbidity
• Positioning complications
• Air embolism may also occur from irrigation fluid bags that are under pressure
Mortality
Air embolism, rare
• Deliberate or controlled hypotension may reduce blood loss, which can also improve
surgical visualization and prosthetic binding. However, it must be weighed against the
potential for end-organ ischemia, particularly in the beach chair position (cerebral
perfusion).
• Hypotension in the beach chair position should be aggressively treated to avoid cerebral and
spinal cord ischemia.
• Brachial plexus blocks as a sole anesthetic may be considered; sedation should be titrated
appropriately to avoid airway compromise.
• Positioning considerations should be made
SYMPTOMS
Symptoms depend on degree of rotator cuff injury and can vary. Some patients are
asymptomatic.
• Pain
• Weakness
• Range of motion limitation
• Limitation of ADLs (activities of daily living)
• Atrophy of shoulder musculature
History
• Baseline neurological deficits should be assessed for and clearly documented when
performing a brachial plexus block.
• Patients may report progressive worsening of pain, weakness, and range of motion in the
affected shoulder.
• Acute rotator cuff tears may have a history of recent trauma.
Signs/Physical Exam
Functional deficits depend on location of tear
MEDICATIONS
Pain medications: NSAIDS, opioids, and muscle relaxants
Labs/Studies
Imaging related to the surgery includes MRIs and ultrasounds.
Degenerative joint disease
TREATMENT
Premedications
Anxiolytics and opioids as needed for brachial plexus block, or prior to general anesthetic
induction.
If a brachial plexus block or catheter is planned as the primary anesthetic or for postoperative
pain control, review risks and benefits of regional anesthesia and sedation goals.
Prophylaxis with a third-generation cephalosporin against Staphylococcal skin flora.
INTRAOPERATIVE CARE
• The anesthetic approach must consider the patient’s and surgeon’s preference as well as the
anesthesia provider’s comfort with the procedure.
• Brachial plexus block as the sole technique (interscalene or supraclavicular block).
– Potential benefit of reduced hemodynamic instability, postoperative delirium, recovery
room stay, and systemic opioid administration; as well as avoidance of airway
instrumentation and mechanical ventilation.
– Potential drawbacks include failed blocks, local anesthetic systemic toxicity, or injury
from placement (hemorrhage, nerve damage).
– Appropriate for the beach chair position. Poorly tolerated in the lateral decubitus position,
particularly in obese patients where airway management and access are concerns.
– Placement should allow enough time for onset.
– Equipment to convert to a general anesthesia (GA) should be available in the event of a
failed or partial block, oversedation, agitation, or anxiety.
• General
– Can be used in both beach chair and lateral decubitus positions.
• Combination of regional and GA
– Can be used in both the beach chair and lateral decubitus positions.
– Peripheral nerve block/catheter reduces postoperative pain while GA with ETT guarantees
secured airway.
Monitors
• End-tidal carbon dioxide monitoring can help detect oversedation with brachial plexus
blocks.
Airway management may be with a nasal cannula, LMA, or ETT.
Maintenance
• GA: Balanced anesthetic with volatile or IV drugs. Opioid titration when no brachial plexus
block.
• Brachial plexus block: Light sedation with propofol, dexmedetomidine, or midazolam.
• Venous air embolism. Arthroscopic pumps deliver pressures >30 mm Hg that allow air
bubbles to enter the joint. This, combined with venous sinusoid exposure in the beach chair
position can result in venous air entrainment. Case reports have also cited unintentional air
insufflation as well as unrecognized air reservoirs in the 3 L arthroscopic fluid bags as
causes.
• Arrhythmias from local anesthetics containing epinephrine have been reported (7).
• GA: Standard extubation criteria
• Brachial plexus block: Reorient patient
FOLLOW-UP
BED ACUITY
• Routine arthroscopic procedures are typically done as an outpatient.
• Extensive, open procedures may require a regular hospital bed for inpatient stay.
ANALGESIA
• IV and oral medications
• Single-shot interscalene block with long-acting local anesthetic (bupivacaine or
ropivacaine). Insertion of a catheter allows for continuous infusion of local anesthetic.
COMPLICATIONS
• Profound hypotension and bradycardia can occur in 20% of patients undergoing shoulder
arthroscopy in the beach chair position (2). This can result in cerebral ischemia, spinal cord
ischemia, and visual loss (2).
• Air embolism in the beach chair position; also from pressurized irrigating fluid bags.
• Airway compromise from extravasated irrigation fluid with prolonged arthroscopic
procedures (6,8).
• Deltoid dysfunction and postoperative pain (especially with open procedures).
• Neurapraxia from brachial plexus traction in the lateral decubitus position.
• Brachial plexus block complications; local anesthetic systemic toxicity or needle injury
(bleeding, nerve injury).
REFERENCES
1. eruto CM, Ciccotti MG, Cohen SB. Shoulder arthroscopy positioning: Lateral decubitus
versus beach chair. Arthroscopy. 2009;25(8):891–896.
2. Ghodadra NS, Provencher MT, Verma NN, et al. Open, mini-open, and all-arthroscopic
rotator cuff repair surgery: Indications and implications for rehabilitation. J Orthop Sports
Phys Ther. 2009;39(2):81–89.
3. Freely BT, Gallo RA, Craig EV. Cuff tear arthropathy: Current trends in diagnosis and
surgical management. J Shoulder Elbow Surg. 2009;18:484–494.
4. Bedl A, Dines J, Warren RF, et al. Massive tears of the rotator cuff. J Bone Joint Surg Am.
2010;92:1894–1908.
5. Antonucci S, Orlandi P, Mattei PA, et al. Airway obstruction during arthroscopic shoulder
surgery: Anesthesia for the patient or for the surgeon? Minerva Anestesiol. 2006;72:995–
1000.
6. Venkat G, Moon YL, Na WC, et al. Upper airway compromise by extravasated fluid: A rare
complication after arthroscopic repair of atrophic cuff tear. Orthopedics. 2009;32(10). doi:
10.3928/01477447-20090818-32.
7. Zmistowski B, Austin L, Ciccotti M, et al. Fatal venous air embolism during shoulder
arthroscopy. J Bone Joint Surg Am. 2010;92:2125–2127.
8. Cho SH, Yi JW, Kwack YH, et al. Ventricular tachycardia during arthroscopic shoulder
surgery: A report of two cases. Arch Orthop Trauma Surg. 2010;130(3):353–356.
CODES
ICD9
• 726.2 Other affections of shoulder region, not elsewhere classified
• 726.13 Partial tear of rotator cuff
• 727.61 Complete rupture of rotator cuff
ICD10
• M75.100 Unsp rotatr-cuff tear/ruptr of unsp shoulder, not trauma
• M75.110 Incmpl rotatr-cuff tear/ruptr of unsp shoulder, not trauma
• M75.120 Complete rotatr-cuff tear/ruptr of unsp shoulder, not trauma
CLINICAL PEARLS
• Place the noninvasive BP cuff on the nonoperative arm rather than the calf to obtain more
accurate BP measurements for patients in the beach chair position.
• Obese patients are at greater risk of hypotension in the beach chair position because
compression of the vena cava decreases venous return.
• Hyperextension and rotation of the head can decrease vertebral artery blood flow causing
infarcts of the posterior cerebral circulation.
• Monitor for fluid extravasation and airway edema with excessive irrigation in prolonged
arthroscopy procedures.
• Consider regional, general, or combined regional and general techniques on a case by case
basis.
• A brachial plexus block will block the diaphragm (C3, C4, C5) and may cause respiratory
embarrassment in patients with underlying pulmonary disease. Conversely, the
administration of opioids for analgesia has drawbacks.
SACROILIAC (SI) JOINT INJECTIONS
BASICS
DESCRIPTION
• Pain from the sacroiliac (SI) joint accounts for 10–30% of cases of low back pain.
• SI pain is more common in women. During pregnancy, the incidence may be as high as 80%.
• The symptoms of SI joint pain can be difficult to distinguish from other pain syndromes such
as lumbar facet arthropathy, lumbar radiculopathy, hip arthropathy, and myofascial pain.
• Functions of the SI joint include shock absorption during weight bearing and storage of
elastic energy via force transfer into the sacrum.
• The mobility of the joint is limited, but it is capable of small amounts of rotation and
translation.
ANATOMY
• The SI joint is the largest axial joint in the body. It is a diarthrodial joint, meaning that it
has a joint capsule, synovial fluid and lining, and cartilaginous surfaces that allow
movement.
• Anterior capsule: Only portion that is truly synovial. It is innervated by the ventral rami of
L4 through S2 with possible contributions from L2 and L3.
• Posterior capsule: Poorly developed posterior ligamentous structure that serves to limit
motion. It is innervated by the dorsal rami of L5 through S3 with possible contributions
from L3, L4, and S4.
• Causes of SI joint pain:
– Axial loading; forces are transmitted along the axis of the spine
– Extraneous compression or transference of shearing forces, for example, from the lower
extremities or pelvis
– Abrupt rotation
– Abnormal mechanics, such as hypomobility or hypermobility of the joint complex
– Disruption or tension of the joint capsule, synovium, or ligaments
– Fracture
– Chondromalacia
– Inflammation from infection, malignancy, or spondyloarthropathy
– Malignancy
• Predisposing factors
– Leg length discrepancy
– Gait abnormality
– Strenuous exercise
– Scoliosis
– Lumbosacral spinal fusion or other lumbar spine surgery
– Infection
– Trauma
– Spondyloarthropathy
– Pregnancy
• Findings on history
– Pain in the superomedial and possibly superolateral buttock inferior to the posterior
superior iliac spine (PSIS)
– Absence of pain above L5
– Referred pain to the lateral thigh and groin, or less commonly to the posterior thigh or leg
– Aggravation with bending, sitting, or rising
– Relief with standing or walking
• Physical exam findings. Each of the tests described below are considered positive if they
produce pain localized to the SI joint and/or reproduce the patient’s pain.
– Tenderness to palpation at the posterior aspect of the joint
– Provocative tests such as the
Patrick test: With a supine patient, flex the ipsilateral knee and place the foot on the
contralateral patella or thigh. Stabilize the contralateral hip and lower the knee toward
the examining table.
Gaenslen test: Place the patient supine, while allowing one leg to hang over the table.
Have the patient pull the knee on the table up to the chest. Apply pressure to the leg
hanging off the table.
Yeoman test: Place the patient prone and extend the leg at the hip while rotating the
ilium.
Thigh thrust: With the patient supine, the hip is flexed to 90° with the knee flexed. The
examiner places a hand on the sacrum for stabilization and applies a posterior shearing
stress to the SI joint through the femur.
Posterior shear: With the patient in the prone position, the palm of the examiner’s hand
is placed over the posterior iliac wing. An inferiorly directed thrust produces a shearing
force across the SI joint.
Distraction: With the patient supine, a posterolateral force is applied to both the anterior
and superior iliac spines to stretch the anterior SI ligaments and synovium.
Compression: With the patient in a lateral position, downward pressure is applied to the
uppermost iliac crest, directed toward the opposite iliac crest. This is intended to stretch
the posterior SI ligaments and compress the anterior SI joint.
Gillet test: With the patient upright (standing), the examiner’s left thumb is placed over
the posterior-most portion of the left PSIS and the right thumb overlies the midline of
the sacrum at the same level. The patient maximally flexes the left hip and knee with a
minimum of 90° of hip flexion. The thumb placements are reversed to test the right side.
A negative test finds the thumb on the PSIS moving caudally in relation to the thumb on
the sacrum. A positive finding occurs when the thumb on the PSIS does not move at all
or moves cranially in relation to the thumb placed on the sacrum. This test assesses
movement of the innominate bone posteriorly on the sacrum, thus if it does not move
caudally, the joint is not moving correctly in posterior tilt.
• Diagnosis
– Pain relief from an intraarticular injection is the gold standard.
– Individual factors in the history and physical exam have low sensitivity, low specificity, or
both.
– Radiologic imaging has a low sensitivity and is not useful as a screening test.
• Management
– Conservative therapies
Bracing
Manual manipulation
Physical therapy
NSAIDs and amitriptyline may be used for pain control
– Disease-modifying antirheumatic drugs (DMARDs), steroids, or biologic agents may be
used to treat spondyloarthropathies and improve pain.
– Invasive therapies include intraarticular and periarticular joint injections, radiofrequency
ablation (RFA), and some alternative therapies
– Intraarticular injections with local anesthetic and steroid can be both diagnostic and
therapeutic. Most studies have shown benefit from intraarticular steroid injections from 1
to 12 months.
The most common method of performing an intraarticular SI injection is with
fluoroscopic guidance. Sterile technique must be maintained.
An AP view of the joint is obtained with the patient prone. The C-arm is rotated
obliquely until a clear view of the joint is obtained in which the anterior and posterior
portions of the joint overlap.
Using a 22- to 25-gauge needle, the posterior joint is entered close to the most inferior
aspect. After negative aspiration, contrast is injected to confirm intraarticular spread,
and a mixture of local anesthetic and steroid is injected into the joint.
– Periarticular steroid injections have also been shown to provide good short-term relief.
These are performed in a manner similar to intraarticular injections, with the exception
that the steroid is deposited around the joint as opposed to inside it.
– RFA of the dorsal rami supplying the posterior joint may provide longer-lasting relief in
patients who respond well to intraarticular blocks. The joint itself can also be targeted for
RFA, but RFA of the nerves is more effective. There is debate as to how many
intraarticular injections should be done before proceeding to RFA.
– Other treatments that have been used but are less well studied include surgical
stabilization, hyaluronic acid injections, botox injections, prolotherapy, and
neuroaugmentation.
GRAPHS/FIGURES
FIGURE 1. Anterior view of the anatomy of the sacroiliac joint.
FIGURE 2. Intraarticular sacroiliac injection. The sacroiliac joint is approached posteriorly.
REFERENCE
1. Benzon HT, Rathmell JP, Wu CL, et al. (eds). Raj’s Practical Management of Pain, 4th ed.
Philadelphia: Mosby/Elsevier, 2008.
2. Cohen SP. Sacroiliac joint pain: A comprehensive review of anatomy, diagnosis, and
treatment. Anesth Analg. 2005;101:1440–1453.
3. Dreyfuss P, Henning T, Malladi N, et al. The ability of multi-site, multi-depth sacral lateral
branch blocks to anesthetize the sacroiliac joint complex. Pain Medicine. 2009;10:679–
688.
4. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical
examination in diagnosing sacroiliac joint pain. Spine. 1996;21:2594–2602.
5. Ostgaard HC, Andersson GJ, Karlsson K. Prevalence of back pain in pregnancy. Spine.
1991;16:549–552.
6. Raj PP, Lou L, Erdine S, et al. (eds). Interventional Pain Management: Image-Guided
Procedures, 2nd ed. Philadelphia: Saunders Elsevier, 2008.
7. Rathmell JP. Atlas of Image-Guided Intervention in Regional Anesthesia and Pain Medicine
and Complications in Regional Anesthesia and Pain Medicine. Philadelphia: Lippincott
• Radiation exposure
• Facet joint injections
CLINICAL PEARLS
• The SI joints are a common source of low back pain.
• Intraarticular blocks are useful for both diagnosis and treatment of SI joint pain.
• Both conservative and invasive therapies are available.
• Spillover of local anesthetic onto the sciatic nerve may produce short-term lower extremity
weakness after both intraarticular and periarticular injections.
SARCOIDOSIS
Linh Trang Nguyen, MD
BASICS
DESCRIPTION
• Sarcoidosis is a multisystem inflammatory disease characterized by noncaseating epithelioid
granulomas.
• Virtually every organ may be involved with the lung being most frequently affected (>90%
of patients). Other common areas include the skin (30%), eyes (25%), and lymph nodes (1).
5% of patients have diagnosed cardiac involvement, although autopsies reveal up to 30%
subclinical involvement (2).
• It is a diagnosis of exclusion. Granulomas must be present in at least 2 organs. Lymphoma as
well as mycobacterial and fungal infections need to be considered in the differential
diagnosis of sarcoidosis when the CXR shows bilateral hilar adenopathy. A tissue diagnosis
is usually required, and other causes of multisystem granulomatous diseases must be
excluded (3).
EPIDEMIOLOGY
Prevalence
• In the US: 10.9 cases per 100,000 among the white population (1)
• 35.5 cases per 100,000 among the black population (1)
Prevalence
• Most patients are between 20 and 40 years old, although it can be seen in children and the
elderly (a second peak occurs in women over 50 years of age) (4,5).
• In Europe, the majority of sarcoidosis patients are white or Nordic (4).
• More prevalent among nonsmokers
Morbidity
• May be asymptomatic
• Chronic in one-third of patients (1)
• Two-thirds of patients experience spontaneous remission within 10 years of diagnosis.
However, 10–30% of patients have a more chronic or progressive course (1).
• In blacks, the disease presentation is usually more severe and chronic. Additionally, more
extensive and chronic pulmonary disease is seen (1,6).
Mortality
Ranges from 1% to 5% (6). Often due to severe involvement of lung parenchyma, leading to
pulmonary fibrosis and respiratory failure; myocardial involvement, leading to lethal
arrhythmias (VT) and congestive heart failure; and neurological involvement (2)
Unknown etiology (3). The hypothesis is that sarcoidosis is due to environmental exposure to
an infectious (herpes virus, mycobacterium, propionibacterium) or noninfectious agent
(beryllium, mold, mildew, pesticides) which triggers an inflammatory response in a
genetically predisposed host (HLA-A1, B8, DR-3) (1,2,3,7)
• Noncaseating granulomas, which consist of macrophages, CD4 type I helper T cells, CD8 T-
lymphocytes, and B-lymphocytes, form in many organs and disrupt the normal architecture
of the organ (1,3)
• If there is spontaneous resolution of the granulomas, then there are no clinical sequelae.
However, at least 20% of patients appear to develop a chronic form of the disease;
associated with the secretion of high levels of interleukin 2, interferon gamma and tumor
necrosis factor (TNF) (1). These cytokines play an important role in the granulomatous
inflammatory process, and are the targets of immunosuppressive drugs used to treat
sarcoidosis.
• Severe organ impairment occurs if there is scarring or fibrosis from the granuloma
resolution.
• Assess the severity of disease and identify the organ systems involved
• Medications. History and side effects, especially for immunosuppressive and antimalarial
drugs, should be elicited. Patients on corticosteroids may require a stress dose.
SYMPTOMS
• Can be vague, and mimic those of cancer symptoms, including fatigue, weight loss, body
aches, lack of energy, fever
• Dry eyes, blurry vision, light sensitivity, eye pain with ophthalmic involvement
• Dyspnea, dysphagia with laryngeal involvement (8)
• Syncope, heart failure with cardiac involvement
• Shortness of breath, dry, nonproductive cough with pulmonary involvement
• Arthritis with joint involvement
History
• Disease onset, length of time since diagnosis
• Cardiopulmonary functional status
Signs/Physical Exam
• Eye redness from uveitis
• Dysphonia, stridor with laryngeal involvement (8)
• Arrhythmia, jugular venous distension, hepatomegaly, lower extremity edema from
congestive heart failure
• Hypoxemia from pulmonary sarcoidosis, fine crackles, expiratory wheeze may be present on
lung exam
• Tender, red skin nodules from erythema nodosum. Subcutaneous tissue surrounding the
sarcoid osseous lesions may be inflamed, erythematous, and swollen
• Hepatomegaly, jaundice
• Joint swelling and erythema
MEDICATIONS
• Not all patients require therapy; spontaneous remission occurs in a large number of patients.
• Glucocorticoids are considered first-line therapy (1). The treatment duration ranges from 6
to 9 months (topical, inhaled, oral depending on organ involved); optimal dosing and
duration are unknown (7). For pulmonary sarcoidosis, 3–4 weeks are usually needed before
major improvements are seen. Side effects include weight gain, osteoporosis, glucose
intolerance, delayed wound healing, and infections (6).
• Other immunosuppressive drugs, including chloroquine, methotrexate, azathioprine, TNF-
alpha inhibitors (infliximab, adalimumab) are considered second-line therapy. Side effects
include myelosuppression and leucopenia, elevated LFTs, infections, lymphoma, and
cardiomyopathy (6).
• Cyclophosphamide and thalidomide are used only in unremitting, refractory disease that is
unresponsive to first- or second-line therapy. Cyclophosphamide may cause hemorrhagic
cystitis, and thalidomide may cause deep vein thromboses (6).
Labs/Studies
• BUN, Cr: Assess renal function
• Serum calcium: May be elevated from increased intestinal absorption due to overproduction
of calcitriol by pulmonary macrophages
• CBC: May demonstrate the presence of anemia, thrombocytopenia, eosinophilia
• LFTs: May be elevated with liver involvement. If so, may consider testing synthetic function
with coagulation tests.
• Hemoglobin A1C: May be elevated due to chronic corticosteroid use
• Serum ACE levels: Angiotensin converting enzyme is secreted by the epithelioid cells of
granulomas, and may reflect the granuloma load. However, ACE levels has not been found
to be useful in monitoring disease activity and treatment response (3).
• PFT: May reveal reduced lung volumes (decreased FEV1 and FVC), and decrease in the
diffusing capacity for carbon monoxide (3)
• CXR: May show hilar lymphadenopathy and interstitial infiltrates 95% cases have bilateral
lymphadenopathy, 5% cases have unilateral lymphadenopathy (1)
• EKG: May demonstrate abnormalities such as atrioventricular (AV) block and ventricular
arrhythmias (2)
• Echocardiogram study to assess left ventricular function and to look for the presence of
pulmonary hypertension
• High-resolution CT to look for hilar and mediastinal lymphadenopathy
• Ophthalmologic examination looking for signs of uveitis
• Muscle enzymes may be elevated with sarcoid myositis (7)
Sarcoidal granulomas in the different tissues and organs lead to the following presentations:
• Nervous system: Peripheral neuropathies, meningitis, encephalitis, seizures, diabetes
insipidus due to pituitary involvement, cranial nerve palsies, especially CN2 and CN7
paraplegia or quadriplegia with spinal cord involvement (1)
• Eyes: Uveitis, blindness in severe cases (8)
• Larynx (0.5–8.3%): Vocal cord edema, supraglottic obstruction from granulomas of
epiglottis, aryepiglottic folds, and arytenoids (8)
• Cardiac: Restrictive cardiomyopathy, conduction abnormalities, and arrhythmias (2)
• Lungs: Most commonly affected and includes parenchymal disease, hilar and mediastinal
involvement, pulmonary fibrosis, and pulmonary hypertension
• Liver: Hepatomegaly
• Spleen: Splenomegaly
• Kidneys: Glomerulonephritis, interstitial nephritis, nephrocalcinosis, and nephrolithiasis
• Skin: Erythema nodosum
• Osseous involvement in 13% of patients (7)
• Joints: Arthritis
• Sarcoid myopathy in 75% of patients. May be asymptomatic (the majority) or may cause
myositis leading to muscle contracture and hypertrophy (7).
• Lung involvement is common; there is no need to postpone an elective surgery unless there
is an active infection, severe wheezing, or recent pulmonary embolism.
• Right heart failure and cor pulmonale
• High-grade AV block requiring pacemaker implantation
• Ventricular arrhythmia requiring implantable cardioverter-defibrillator (ICD) placement
• Left ventricular dysfunction requiring optimization with heart failure medications (ACE
inhibitors, ARBs, beta-blockers, diuretics) and cardiac resynchronization therapy
CLASSIFICATIONS
• Onset: Acute, subacute, or insidious
• Pulmonary sarcoidosis is classified as stage 0–4 depending on the presence of intrathoracic
adenopathy, pulmonary infiltrates, and pulmonary fibrosis (3).
• Lofgren syndrome is a type of acute sarcoidosis characterized by the triad of erythema
nodosum, bilateral hilar adenopathy, and arthritis (1).
• Heerfordt’s syndrome is a rare type of sarcoidosis consisting of uveitis, parotid swelling,
fever, and facial nerves palsy (3).
TREATMENT
Premedications
• Stress-dose steroids should be considered for patients on chronic steroids.
• Prophylactic dexamethasone may be considered for patients with laryngeal involvement
requiring airway instrumentation.
• Pacemaker and ICDs, if present, should be appropriately interrogated and managed.
Regional anesthesia, if planned
INTRAOPERATIVE CARE
Depends on surgical procedure and patient preference. Regional anesthesia should be
considered when there is severe lung involvement and cor pulmonale. Thrombocytopenia
may be present, and may limit the choice of regional technique such as epidurals
Monitors
• Consider arterial line placement in patients with severe lung or cardiac involvement to
monitor arterial blood gases and for beat-to-beat blood pressure monitoring
• Laryngeal involvement may require fiberoptic intubation or the use of a smaller
endotracheal tube.
• Airway compression may present due to enlarged paratracheal lymph nodes.
Maintenance
• Ventilation: In patients with pulmonary hypertension, hypoxia and hypercarbia increase
pulmonary pressures and should be avoided. In patients with pulmonary fibrosis, avoid
excessive airway pressures to reduce the incidence of barotrauma.
• Medications. Altered drug metabolism and excretion may be present with concomitant
kidney and liver disease.
• Fluids. Meticulous management in patients with cardiomyopathy.
• Attention to pressure points, and adequate padding in patients on chronic steroids and
fragile skin
Full reversal of neuromuscular blockade is warranted before extubation of a patient with
limited pulmonary reserve.
FOLLOW-UP
BED ACUITY
Depends on the surgical procedure, severity of disease, and perioperative events
• Judicious use of opioids in patients with poor pulmonary function; consider regional
anesthesia
• Supplemental oxygen should be administered, as appropriate
• Monitor for life-threatening airway obstruction and respiratory arrest in patients with
laryngeal involvement
• Cardiac monitoring should be considered for patients with conduction abnormalities and
arrhythmias.
COMPLICATIONS
• Fluid overload, cardiac arrhythmias, congestive heart failure, and pulmonary edema may
occur in patients with cardiac sarcoidosis and cardiomyopathy.
• Hypotension from adrenal cortical suppression from chronic corticosteroid use may occur.
REFERENCES
1. Iannuzzi MC, Fontana JR. Sarcoidosis: Clinical presentation, immunopathogenesis, and
therapeutics. JAMA. 2011;305(4):391–399.
2. Soejima K, Yada H. The work-up and management of patients with apparent or subclinical
cardiac sarcoidosis: With emphasis on the associated heart rhythm abnormalities. J
Cardiovasc Electrophysiol. 2009;20(5):578–583.
3. Baughman RP, Culver DA, Judson MA. A concise review of pulmonary sarcoidosis. Am J
Respir Crit Care Med. 2011;183(5):573–581.
4. American Thoracic Society. What is Sarcoidosis? American Journal of Respiratory and
Critical Care Medicine. 2006;173:P3–P4.
5. Baughman RP, Teirstein AS, Judson MA, et al. Clinical Characteristics of Patients in a Case-
Control Study of Sarcoidosis. American Journal of Respiratory and Critical Care Medicine.
2001;164:1885–1889.
6. Lazar CA, Culver DA. Treatment of sarcoidosis. Semin Respir Crit Care
Med.2010;31(4):501–518.
7. Sweiss NJ, Patterson K, Sawaqed R, et al. Rheumatologic manifestations of sarcoidosis.
Semin Respir Crit Care Med. 2010;31(4):463–473.
8. Mayerhoff RM, Pitman MJ. Atypical and disparate presentations of laryngeal sarcoidosis.
Ann Otol Rhinol Laryngol. 2010;119(10):667–671.
CODES
ICD9
• 135 Sarcoidosis
• 517.8 Lung involvement in other diseases classified elsewhere
ICD10
• D86.0 Sarcoidosis of lung
• D86.3 Sarcoidosis of skin
• D86.9 Sarcoidosis, unspecified
CLINICAL PEARLS
• Sarcoidosis is a systemic disease, with an uncontrolled cellular immune response affecting
multiple organs therefore, a complete preoperative assessment is necessary, with particular
emphasis on pulmonary and cardiac involvement. Due to the lack of a pathognomonic test
for sarcoidosis, and the nonspecific symptomatologies, patients may present to the
preoperative clinic without an established diagnosis of sarcoidosis. Instead, they may have
been given a diagnosis of asthma or bronchitis.
• Immunosuppressive drugs used to treat sarcoidosis may cause significant toxicities and
should be carefully reviewed.
SCIATIC NERVE BLOCK
Jane C. Ahn, MD
Sharon L. Lin, MD
BASICS
DESCRIPTION
• The sciatic nerve is the largest peripheral nerve in the human body; it provides motor and
sensory innervation.
• The sciatic nerve block can be used in combination with a lumbar plexus, femoral, or
saphenous block in order to provide anesthesia and analgesia to the entire lower extremity.
Additionally,
– It may provide site-specific anesthesia and minimize the need for general anesthesia
during outpatient surgery, thus minimizing the length of stay and cost (1).
– It provides postoperative analgesia, decreasing opioid consumption and side effects (1).
– A catheter can be placed to provide continuous infusion of local anesthetic and prolonged
analgesia.
• Sciatic nerve blocks can be performed utilizing a variety of technologies including
peripheral nerve stimulation (PNS) and/or ultrasound guidance (US).
• The sciatic nerve provides sensory innervation to the posterior thigh, knee, part of the knee
joint, and the entire leg below the knee except for the medial aspect (this is supplied by the
saphenous nerve, a branch of the femoral nerve).
• It supplies motor function to hamstrings and flexor and extensor muscles of the ankles and
feet.
• A distal sciatic nerve block (popliteal block) will spare sensation to the posterior thigh and
knee as well as motor function to the hamstrings.
ANATOMY
• The sciatic nerve originates from the lumbosacral plexus, L4-S3 nerve roots.
• It exits the greater sciatic foramen and travels caudally along the piriformis muscle posterior
to the femur.
• It bifurcates into 2 terminal branches ∼7–8 cm proximal to the popliteal crease in the
popliteal fossa: Tibial nerve (located medially) and common peroneal nerve (located
laterally).
• The tibial and common peroneal nerves are enclosed in a common nerve sheath.
• Major complications from lower extremity nerve blocks are rare compared to other
peripheral nerve blocks (e.g., brachial plexus and eye blocks)
• Nerve injury may be due to the following (2):
– Trauma from the needle
– Local anesthetic neurotoxicity
– Local anesthetic systemic toxicity
– Ischemic injury secondary to pressure and volume of the local anesthetic
– Addition of vasoconstrictors
– Hematoma or vascular injury
– Surgical trauma and positioning
– Tourniquet injury
– Postoperative swelling and positioning
– Preexisting pathology
• Sciatic nerve injury accounts for 3% of nerve injuries associated with peripheral nerve
blocks from ASA Closed Claims Database (3).
• A sciatic nerve block is an alternative to epidural or spinal anesthesia for lower extremity
surgery if used in conjunction with a lumbar plexus, femoral, or saphenous nerve block. It
can also serve as an alternative to patient refusal or when coagulopathies preclude neuraxial
blocks.
• The sciatic nerve can be blocked anywhere along its course from the parasacral space to the
popliteal fossa:
– A proximal sciatic block is recommended in combination with lumbar plexus or femoral
block for procedures involving the thigh, knee, or thigh tourniquet.
– A distal sciatic block (popliteal block) is recommended in combination with a saphenous
block for procedures of the lower leg, ankle, or foot. It has the benefit of allowing the
patient to ambulate with crutches because hamstring function is preserved.
• Peripheral nerve stimulation versus ultrasound. Data indicates that US guidance for sciatic
nerve blocks can improve the onset and success of sensory blockade as well as decrease the
local anesthetic requirements and time to perform the block (level IB evidence for Grade A
recommendation (4). However, clinical relevance in differences between PNS versus US
techniques is ultimately dependent on experience and comfort of the clinician.
• The parasacral approach (of Mansour) blocks the entire sacral plexus before it forms the
sciatic nerve when it exits the greater sciatic foramen. It is the most proximal approach (5)
(Figure 1).
– Position: Lateral (Sim’s) position
– Landmarks: Posterior superior iliac spine (PSIS) and ischial tuberosity with a line
connecting the two points
– Needle insertion point: 6 cm inferior to the PSIS along the line
– Depth: ∼5–8 cm
– Redirection: If bone is contacted, the needle should be redirected 1 cm inferior and
advanced no further than an additional 2.5 cm
– Other: Performed in close proximity to pelvic vessels and viscera
FIGURE 1. Parasacral approach (of Mansour). a = posterior superior iliac spine, b = ischial tuberosity. The needle
insertion point is ∼6 cm inferior to Point a.
• The classic approach (Labat–Winnie) blocks the sciatic nerve after it exits the greater sciatic
foramen distal to the piriformis muscle (6).
– Position: Lateral (Sim’s) position
– Landmarks: Greater trochanter (GT), PSIS, sacral hiatus. One line is drawn connecting the
GT and PSIS and a second line is drawn connecting the GT and sacral hiatus. A
perpendicular line bisecting the first line and intersecting the second line is drawn
– Needle insertion point: The intersection of the perpendicular line with the 2nd line (GT to
sacral hiatus).
– Other: The needle traverses multiple muscle layers and may cause greater discomfort.
• The anterior approach blocks the sciatic nerve as it passes posteriorly behind the femur at
the level above the lesser trochanter (7) (Figure 2).
– Position: Supine
– Landmarks: Inguinal ligament (line connecting anterior superior iliac spine and pubic
tubercle). A perpendicular line is drawn bisecting the inguinal ligament and extending 8
cm caudad.
– Needle insertion point: Needle is inserted perpendicular to the skin, 8 cm distally along
the line perpendicular to the midpoint of the line connecting the anterior superior iliac
spine and pubic tubercle.
FIGURE 2. Anterior approach to the sacral nerve. The inguinal ligament is identified by drawing a line from the anterior
superior iliac spine to the pubic tubercle. At the midpoint, a perpendicular line is drawn caudally. Needle insertion is 8 cm
from this point.
– Depth: ∼10–11 cm
– Other: May require multiple needle passes to “walk off” the lesser trochanter. By also
blocking the posterior femoral cutaneous nerve, tourniquet pain can be prevented. The
femoral nerve may be inadvertently encountered when performing the block; therefore
monitor for patellar stimulation.
• Subgluteal approach (di Benedetto) blocks the sciatic nerve more distally, caudal to the
gluteus muscles (6). It is located in a palpable sulcus between the biceps femoris and
semitendinosus muscles (aka “Sciatic Line”) (Figure 3).
– Position: Lateral (Sim’s)
– Landmarks: GT, ischial tuberosity with a line connecting the two points. A second line is
drawn from the midpoint of the first line, perpendicular and extending 4 cm caudally.
– Needle insertion point: Needle is inserted perpendicular to the skin, 4 cm caudally in the
line perpendicular to the midpoint of the line connecting the GT and ischial tuberosity. A
depression should be palpated at this level and represents the groove between the biceps
femoris and semitendinosus muscles.
– Other: There is no difference in block failure rate between the classic and subgluteal
approach (5).
FIGURE 3. Subgluteal Approach.
• Posterior popliteal approach blocks the sciatic nerve above the popliteal crease before
dividing into the tibial and common peroneal branches (8).
– Position: Prone
– Landmarks: At the level of popliteal crease, palpate the biceps femoris tendon (laterally)
and semimembranosus and semitendinosus tendons (medially). Ask the patient to tense
hamstrings to accentuate the tendons. Follow the biceps femoris cephalad until the border
of the popliteal apex is reached (the intersection of biceps femoris and semimembranosus
and semitendinosus muscles).
– Needle insertion point: 0.5 cm below the apex of the fossa
– Other: A higher rate of success is noted if inversion is elicited with nerve stimulation
compared to eversion (8). Tibial nerve stimulation results in plantar flexion of the foot or
toes. The common peroneal nerve stimulation results in dorsiflexion of the foot or
extension of the toes (Figure 4).
FIGURE 4. Popliteal approach to the sciatic nerve on ultrasound. BFlh is biceps femoris long head. BFsh is biceps femoris
short head.
• The lateral popliteal approach also blocks the sciatic nerve above the popliteal crease before
bifurcating, but allows the patient to remain supine that may be helpful in patients who are
obese or unable to tolerate prone position due to pain or orthopedic apparatus (9) (Figure
5).
– Position: Supine
– Landmarks: Groove between the biceps femoris and vastus lateralis muscle on the lateral
aspect of the leg.
– Needle insertion site: Is in a horizontal plane 11 cm cephalad to the most prominent point
of the lateral femoral epicondyle.
– Depth: Insert needle until the femur is contacted, then redirect 30° posteriorly until
plantar flexion is elicited with nerve stimulation.
– Other: See posterior popliteal block approach
FIGURE 5. Lateral Popliteal Approach.
REFERENCE
1. lein SM, Evans H, Neilson KC, et al. Peripheral nerve block techniques for ambulatory
surgery. Anesth Analg. 2005;101(6):1663–1676.
2. Liguori GA. Complications of regional anesthesia: Nerve injury and peripheral blockade. J
Neurosurg Anesthesiol. 2004;16(1):84–86.
3. Lee LA, Domino KB. Complications associated with peripheral nerve blocks: Lessons from
the ASA Closed Claims Project. Int Anesth Clin. 2005;43(3):111–118.
4. Salinas FV. Ultrasound and review of evidence for lower extremity peripheral nerve blocks.
Reg Anesh Pain Med. 2010;35:S16–S25.
5. Ripart J, Cuvillon P, Nouvellon E, et al. Parasacral approach to block the sciatic nerve: A
400 case study. Reg Anesth Pain Med. 2005;30:193–197.
6. Di Benedetto P, Bertini L, Casati A, et al. A new posterior approach to the sciatic nerve
block: A prospective randomized comparison with the classic posterior approach. Anesth
Analg. 2001;93:1040–1044.
7. Chelly JE, Delaunay L. A new anterior approach to the sciatic nerve bock. Anesthesiology.
1999;91(6):1655–1660.
8. Borgeat A, Blumenthal S, Karovic D, et al. Clinical evaluation of a modified posterior
anatomical approach to performing the popliteal block. Reg Anesth Pain Med.
2004;29:290–296.
9. Taboada M, Alvarez J, Cortes J. The effects of three different approaches on the onset time
of sciatic nerve blocks with 0.75% ropivacaine. Anesth Analg. 2004;98:242–247.
• Femoral nerve block
• Epidural
CLINICAL PEARLS
• There are multiple approaches to blocking the sciatic nerve along its course as it originates
from the lumbosacral plexus and travels distally.
• Avoid epinephrine for proximal sciatic nerve blocks due to the risk of sciatic nerve ischemia
resulting from a combination of vasoconstrictive effects, nerve stretching, and compression
from a tourniquet.
• Give patients clear instructions regarding fall precautions as they may have hamstring
weakness (proximal sciatic nerve block) or foot drop (popliteal block).
• The lateral approach to the popliteal block may be well suited for patients who are obese or
unable to tolerate the prone position.
SCLERODERMA
Andrea Parsons, MD
BASICS
DESCRIPTION
• Scleroderma is an inflammatory, connective tissue disease characterized by vascular
sclerosis, and fibrosis of the skin and viscera.
• Patients with the disease may present for surgical management of pericardial effusions,
upper gastrointestinal procedures, dysrhythmias, and renal dysfunction, or for nonrelated
problems.
EPIDEMIOLOGY
Prevalence
• Difficult to determine due to its variable protein manifestations
• Diffuse scleroderma: 20 in 1,000,000 people
Prevalence
• Four times more likely to develop in women
• Onset most commonly between 30 and 50 years of age
• African Americans have an increased prevalence compared to Caucasians as well as greater
diffuse skin involvement, incidence of pulmonary fibrosis, and overall worsened prognosis.
Morbidity
• Prognosis depends on the extent of visceral involvement rather than cutaneous involvement.
• Cardiac, renal, and GI tract involvement can result in a significant decline in quality of life.
Mortality
• Limited disease: May have a normal life expectancy.
• Severe diffuse disease is seen in up to 10% of patients and has a 50% survival rate at 5
years.
• Leading causes of death: Pulmonary hypertension, pulmonary fibrosis.
• Highest mortality among connective tissue diseases; no cure.
The exact inciting cause of scleroderma is unknown, but genetic, environmental, and
infectious causes have been postulated.
• Scleroderma is a multisystem connective tissue disease with variable clinical presentation. It
is characterized by inflammatory processes that result in functional and structural
abnormalities of small blood vessels:
– Tissue fibrosis results from fibroblast activation and excessive production of extracellular
matrix (collagen deposition); this is the hallmark of the disease
– Smooth muscle proliferation with impaired relaxation
– Vessel damage
– Platelet aggregation with luminal obliteration
– These changes affect the myocardial, renal, and GI vascular beds
• Management should focus on the severity of organ system involvement.
• The airway should be carefully examined; patients may have a limited mouth opening as
well as oral and nasal telangiectasias that can cause profuse bleeding if traumatized.
• Pulmonary function should be assessed as pulmonary fibrosis can lead to restrictive lung
disease.
• Cardiac status should be assessed for fibrosis of the conduction system and pulmonary
hypertension.
SYMPTOMS
Swelling of hands and feet, joint contractures, tight facial skin, heartburn, fatigue, shortness
of breath
History
• Organ system involvement and severity of disease: Skin, heart, lung, kidney, GI tract,
thyroid
• History of anti-inflammatory use (corticosteroids, immunomodulators)
• GERD symptoms and medications
Signs/Physical Exam
Edema of hands and feet, sclerodactyly, calcinosis, Raynaud’s phenomenon, telangiectasias,
dyspnea, dysphagia, weakness, weight loss
MEDICATIONS
• Dihydropyridine calcium channel blockers (amlodipine), nitrates, and alpha-adrenergic
blockers are given to improve vascular flow.
• Cyclophosphamide can be given to slow the progression of pulmonary fibrosis.
• Prostaglandins are often given for severe pulmonary hypertension.
• Immunomodulators and corticosteroids can be given to help treat myositis and alveolitis in
certain patients.
• Antiplatelet therapy and anticoagulation have been used for patient with severe Raynaud’s
phenomenon.
Labs/Studies
• CBC to assess for anemia
• Complete metabolic panel to assess for renal impairment
• Coagulation studies if the patient has malabsorption (decreased vitamin K-dependent
clotting factors) or liver disease
• ECG to assess for conduction abnormalities
• CXR, ABG if significant pulmonary impairment
• Type and screen or type and cross if anemia is present.
• Pulmonary function test if lung disease is severe (typical results for restrictive lung disease
include low FVC, low FEV1, and elevated FEV1/FVC)
• Stress test, echocardiogram, etc. if cardiac involvement is significant.
• Thyroid function tests if thyroid disease is present.
Scleroderma can affect multiple systems:
• Nervous system: Neuropathies due to thickened nerve sheath connective tissue (carpal
tunnel syndrome, trigeminal neuralgia)
• Cardiac: Conduction abnormalities; cardiac dysfunction related to systemic and pulmonary
hypertension (e.g., congestive heart failure); pericarditis, pericardial effusions; coronary
vasospasm
• Respiratory: Diffuse interstitial pulmonary fibrosis leading to decreased lung compliance;
aspiration pneumonitis; chest wall restriction; weakness
• Renal: Renal dysfunction due to accelerated hypertension
• GI: Hypomotility of the esophagus and small intestines, which can be accompanied by
bacterial overgrowth with resultant malabsorption; xerostomia (dry mouth) or Sjögren’s,
esophagitis; GERD and Barrett’s esophagitis; primary biliary sclerosis; esophageal strictures;
esophageal adenocarcinoma
• Musculoskeletal: Arthritis; myopathy, myositis
• Endocrine: Hypothyroidism
• Hematologic: Anemia occurs due to malabsorption of iron, vitamin B12, and folate.
• Vascular: Raynaud’s phenomenon, digital ischemia, and ulcers
• Cutaneous: Sclerodactyly; edema of the hands and feet; skin tightening; calcinosis;
telangiectasias; contractures
Significant cardiac arrhythmias, active congestive heart failure, pericardial effusion; acute
renal failure; high aspiration risk in patients with full stomach
CLASSIFICATIONS
• Localized scleroderma: Involvement is confined to the skin
• Limited systemic sclerosis/scleroderma: Cutaneous manifestations mainly affect the hands,
arms and face; CREST syndrome—Calcinosis, Raynaud’s phenomenon, Esophageal
dysfunction, Sclerodactyly, and Telangiectasias
• Diffuse systemic sclerosis/scleroderma: Rapidly progressing, affects widespread areas of skin
and at least one internal organ
TREATMENT
Premedications
• Aspiration prophylaxis with antacid, H2-receptor antagonist, and/or metoclopramide
• Antisialagogue if fiberoptic intubation planned
• Anxiolysis
• Stress dose steroids should be considered if the patient has been treated for more than 2
weeks within the past 6–12 months to avoid manifestations of adrenal insufficiency.
Steroids with glucocorticoid and mineralocorticoid activity should be administered.
INTRAOPERATIVE CARE
• Regional anesthesia can be technically difficult due to skin and joint changes. Additionally,
use caution with regional techniques if patients are on antiplatelet/anticoagulation therapy
or if coagulation studies are abnormal.
• Avoid drugs that are cleared by the kidneys or use reduced doses if renal impairment is
present
Monitors
• Avoid orogastric and nasogastric tubes, esophageal stethoscope with esophageal strictures
• Avoid nasal or oral manipulation in patients with telangiectasias
• Foley catheter for assessment of urine output, especially in patients with renal impairment
• Use caution with invasive peripheral arterial monitoring as patients have vasomotor
instability (Raynaud’s phenomenon)
• Placement of IVs, central venous catheters, etc. can be challenging due to skin changes.
INDUCTION/AIRWAY MANAGEMENT
• Induction agents can result in profound hypotension due to vasomotor instability and
contracted intravascular volumes.
• Contracted skin around the mouth can result in limited mandibular range of motion and
mouth opening; an awake fiberoptic intubation should be considered.
• Normal airway exam: Consider a rapid sequence intubation as patients are at high risk for
aspiration due to relaxed lower esophageal sphincters, dysmotility, etc. Perform gentle
laryngoscopy to avoid disrupting telangiectasias.
Maintenance
• Caution with positioning and tape for IV sites, ETT, and eyes due to skin sensitivity.
• Avoid disturbances that can increase pulmonary vascular resistance (hypoxemia,
hypercarbia, acidosis, etc.).
• Positive pressure ventilation is often necessary due to restrictive lung disease.
• Increased FiO2 and PEEP is often needed due to impaired diffusion capacity.
• Avoid hypothermia. Use convective blanket warmers, fluid warmers, and maintain a warm
room temperature to avoid peripheral vasoconstriction.
• Intractable intraoperative hypotension may be due to adrenal insufficiency, treat with stress
dose steroids.
EXTUBATION/EMERGENCE
• Postoperative ventilation may be required if lung disease is severe.
• Consider reversing nondepolarizing muscle relaxants to avoid postoperative weakness.
• Careful observation for respiratory depression associated with opioids and other sedatives.
FOLLOW-UP
BED ACUITY
• Telemetry if cardiac involvement is significant
• Intensive care unit if the patient requires postoperative ventilatory support
• Consider postoperative ECG
• CXR if signs of CHF are present
• CBC
COMPLICATIONS
Aspiration pneumonitis, postoperative ventilation, weakness, cardiac arrhythmias
REFERENCES
1. Gabrielli A, Avvedimento EV, Krieg T. Scleroderma. N Engl J Med. 2009;360(19):1989–
2003.
2. Abraham DJ, Krieg T, Distler J. Overview of pathogenesis of systemic sclerosis.
Rheumatology. 2009;48 (Suppl 3):iii3–7.
3. Roberts JG, Sabar R, Gianoli JA. Progressive systemic sclerosis: Clinical manifestations and
anesthetic considerations. J Clin Anesth. 2002;14(6):474–477.
• Raynaud’s syndrome
CODES
ICD9
710.1 Systemic sclerosis
ICD10
M34.9 Systemic sclerosis, unspecified
CLINICAL PEARLS
• May present with challenging airways; prepare for an awake fiberoptic intubation.
• Determine the extent of organ system involvement, obtain appropriate labs and studies to
further assess severity of disease, and treat appropriately.
• IV access can be difficult to obtain due to swelling and contractures.
• Postoperative ventilation is often necessary if the patient has significant lung disease.
SCOLIOSIS REPAIR
Chris A. Steel, MD
BASICS
DESCRIPTION
General
• Scoliosis is a lateral and rotational deformity of the spine with a Cobb angle >10°. The
angle is measured by drawing a parallel line from the superior border of the most displaced
caudal vertebral body and then a second line is drawn parallel to the inferior border of the
most displaced cephalad vertebral body. Perpendicular lines to both are drawn and the
intersecting angle is measured.
• Types of scoliosis include idiopathic or acquired, congenital, neuromuscular (DMD is the
most common disorder), myopathic, traumatic, and tumor-related disorders. Idiopathic or
acquired scoliosis is the most common cause of scoliosis as well as the most common
indication for surgery because it often involves lateral curvature and rotation of the thoracic
and lumbar spine along with vertebra and rib cage deformity. Additionally, it is commonly
performed as a staged anterior and posterior procedure.
• Conservative treatment involves a brace and observation. Surgery can prevent curve
progression and correct the deformity; and is indicated when there is rapid progression or
the curvature is >40° in the lumbar spine or >50° in the thoracic spine. With increased
curvature, rotation progresses and the chest cavity narrows; this can result in restrictive
lung diseases, respiratory insufficiency, pulmonary hypertension, and in severe cases, cor
pulmonale.
• Posterior approach involves a midline incision followed by dissection of subcutaneous tissue
and muscle in order to provide adequate exposure of the spine. Instrumentation with
pedicle screws or laminar hooks is inserted to stabilize the spine; rods are then used to
reduce the curvatures and realign the spine. For severe deformities, additional, complicated
deformity correction maneuvers are performed such as vertebral column resections (VCRs)
or pedicle subtraction osteotomy (PSO). Bone graft is placed over the posterior elements to
create fusion.
• Anterior approach is utilized when the deformity is primarily at the thoracolumbar junction
(T12-L1). One lung ventilation (OLV) or left side rib removal may aid with thoracic
exposure. A vascular surgeon is usually present to aid with surgical exposure due to the
concern of great vessel lacerations. Additionally, a chest tube is typically placed if a
thoracotomy is performed.
• Anterior spinal fusion may be performed in conjunction with either the posterior or lateral
approach to improve reduction in the curve and enhance fusion. This technique is utilized
in patients with severe deformities or who are still growing (anterior column will continue
to grow and reduction would be affected). After the disc is removed, bone graft is inserted
into the disc space to facilitate fusion and maintain proper distance between vertebrae.
Stabilizing screws and rods can be placed into the lateral vertebral body to improve
alignment and assist fusion.
POSITION
• Prone for posterior approach. Shoulders should be abducted <90° and elbows flexed <90°,
padded, and ulnar nerves free. Eyes and nose should be protected and free of pressure;
consider using Prone-View, Gardner-Wells tongs, or Mayfield head holder. Breasts and
genitalia should be appropriately padded. Use of a spinal frame allows the abdomen to hang
free and without IVC compression. The neck should be kept midline and neutral in a slight
reverse Trendelenburg position (∼30°).
• Supine for anterior approach with arms tucked, padded, and ulnar nerves free.
• Lateral decubitus position for a transthoracic or thoracoabdominal approach. Adequate
padding and an axillary roll should be placed.
Incision
Length depending on the number of levels involved.
APPROXIMATE TIME
Approximately 1.5–2.5 hours for a single level; add 1 hour for each additional level.
EBL EXPECTED
300–5,000 mL; variable and based on the number of levels involved, the surgeon’s
skills/dexterity, the use of antifibrinolytics (e.g., tranexamic acid or EACA), and controlled
hypotension.
HOSPITAL STAY
Approximately 5–7 day admission
SPECIAL EQUIPMENT FOR SURGERY
• C-arm fluoroscopy or O-ARM. Require appropriate radiation protection.
• OSI table with Jackson Frames, or Wilson Frames.
• Cell saver
• Bone graft (autolograft, allograft, and BMP)
• Neuromonitoring computer and personnel for monitoring motor-evoked potentials (MEPs),
somatosensory-evoked potentials (SSEPs) and electromyography (EMG).
EPIDEMIOLOGY
Prevalence
In the US: ∼50,000/year are performed
Prevalence
• Adults: 1–15% of the population
• Adolescents: 1–4% of the population (idiopathic disease comprises 60–70% of cases)
Morbidity
• Neurologic deficits: 1–5% with 0.37% incidence of major neurologic complications (up to
11% following PSO); substantial blood loss: 1–5%; pneumothorax: 1–5%; intraoperative
awareness with explicit recall: 0.1–0.2%; visual field defects and vision loss: 0.03–0.1%
• Pulmonary embolism, including venous air embolism (VAE) and fat embolism, postoperative
wound infection, atelectasis and pneumonia, dural lacerations, CSF leaks
• Failure to fuse, hardware fracture, bone graft migration are possible.
Mortality
Rare (0–0.5%)
• Positioning for prone, supine, and lateral approaches can prove challenging and require
meticulous care.
• Patients may have restrictive lung disease and in severe cases pulmonary hypertension or
cor pulmonale.
• Airway management may be affected by limited range of motion and cervical scoliosis and
kyphosis.
• Neuromonitoring. MEPs, SSEPs, and EMG require modification of anesthetic technique to
optimize quality of results. Additionally, intraoperative “wake-up testing” and postoperative
neurologic assessment require techniques that allow for rapid awakening.
• Controlled hypotension may be beneficial in healthy patients to reduce bone bleeding.
Additionally, isovolemic hemodilution can reduce the number of red blood cells (RBCs) lost
and cell saver can decrease exposure to donor blood products.
SYMPTOMS
• Pain, paresthesia, and weakness in lower extremities.
• Lower back pain (LBP)
History
• No improvement with conservative therapy.
• Chronic pain medications
• Comorbidities increase with age
Signs/Physical Exam
Preexisting sensory and motor deficits should be reviewed and documented
MEDICATIONS
Pain patches, pain medications
Labs/Studies
• Electrolytes, CBC, PT/PTT/INR, CXR, EKG, and PFT are routine tests. Type and cross at least
two units of packed RBCs.
• Spine X-ray, MRI, and CT scan are often performed prior to surgery.
• TEE or stress test may be considered depending on comorbidities and/or functional status.
• Restrictive lung disease, respiratory insufficiency, and pulmonary hypertension.
• Cardiomyopathy, congenital heart disease, and cor pulmonale.
• Chronic pain syndrome.
TREATMENT
Premedications
Anxiolysis and analgesia as needed
SPECIAL CONCERNS FOR INFORMED CONSENT
• Smoking cessation. Nicotine inhibits bone-growing cells and reduces successful fusion.
• Patient should be instructed how to correctly use incentive spirometry and PCA.
• Discuss the potential of an intraoperative wake-up test; consider a rehearsal.
ANTIBIOTICS/COMMON ORGANISMS
3rd generation cephalosporin for skin organisms
INTRAOPERATIVE CARE
• Partial or total intravenous anesthesia (TIVA) to optimize neuromonitoring.
MONITORS
• Arterial line may be considered based on anticipated blood loss, comorbidities, and extent of
controlled hypotension.
• Central line may be considered to aid with assessing intravascular volume status as well as
provide postoperative TPN.
• Temperature-sensing Foley catheter.
• SSEPs. Stimulation of a peripheral nerve with subsequent recording of the stimulus over the
sensory cortex allows for the assessment of the posterior spinal cord and provides an
objective assessment of the central and peripheral nervous systems. Both upper and lower
extremity SSEPs should always be monitored. Upper extremity SSEP data would be sensitive
to any upper extremity ischemia due to malposition or inadequate padding in the prone
position. Volatile agents at a MAC >0.5 decrease the amplitude and increase the latency of
the waveforms.
• EMG. Spontaneous EMG is used to identify nerve root irritation during lumbar procedures
(such as decompressions or TLIFs). Triggered EMG is used to evaluate the proper placement
of pedicle screws. Muscle relaxant should be allowed to wear off prior to the start of EMG
monitoring.
• Transcranial electrical motor-evoked potentials (TCeMEPs or MEPs). Stimulation of the
motor cortex through the skull via electrodes placed into the scalp. Responses are recorded
from muscles of the upper extremity and lower extremity assessing the entire motor
pathway from cortex to muscle contraction. TIVA is the optimal technique for MEP
monitoring. A bite block must be placed between the patient’s back teeth to prevent tongue
laceration due to jaw clenching with stimulation.
INDUCTION/AIRWAY MANAGEMENT
• A limited range of motion may preclude the sniffing position; consider having a video
laryngoscope or fiberoptic bronchoscope (awake or asleep) to utilize for the initial attempt
at airway management.
• ETT should be carefully secured to prevent self-extubation particularly in lateral and prone
positioning. Consider No-Sting Skin-Prep or Benzoin to enhance adhesiveness of the tape
followed by Op-Sites to waterproof from sweat, saliva, or other secretions.
• Neuromuscular blockade is contraindicated when EMG or MEPs are monitored.
Succinylcholine (Sux) or small dose of nondepolarizing muscle relaxants may be utilized to
optimize intubating conditions and will wear off quickly. However, succinylcholine should
not be used in patients with neuromuscular (DMD) scoliosis.
MAINTENANCE
• Confirm that the head is supported and kept in the midline/neutral position.
• MEPs and SSEPs have improved reliability with the use of partial or total IV drug
administration. Propofol is often utilized along with volatile/N2O <0.5 MAC, narcotic
(remifentanil, sufentanil), and/or other sedative/analgesic (dexmedetomidine, ketamine).
The goal is to maintain a steady state, particularly during times where injury may occur
(e.g., PSO and instrumentation), and avoid bolusing that may cause significant reductions in
monitoring data. Immediate action should be taken for any significant data change; all
technical, physiologic, and anesthetic factors should be quickly ruled out.
• Critical to maintain an adequate level of anesthesia, as sudden movements can result in
danger to the patient (bucking, coughing).
• Temperature. Convection warming blankets, fluid warmers, and warmed blood products
should be applied and administered. Hypothermia can affect coagulation, hinder
awakening, cause arrhythmias, and increase pulmonary vascular resistance.
• Fluid management. Blood loss may be significant. Autologous blood transfusion strategies
(cell saver, isovolemic hemodilution) and controlled hypotension are often implemented.
Coagulopathies may develop and transfusion with FFP may be necessary.
• “Wake-Up” testing may be performed if neurological monitoring suggests the possibility of
nerve damage, particularly while instrumenting or reducing the curvature.
• Prepare for a fast and smooth emergence for neurologic exam.
• Consider 30° reverse Trendelenburg position to avoid passive aspiration.
FOLLOW-UP
BED ACUITY
• Postoperative care involves acute pain management, removal of drains, neurological
assessment, and monitoring for hematoma.
• Ward/Telemetry or ICU if complex spinal procedure, substantial blood loss, significant
comorbidities, or frequent neurological testing needs to be done.
• Total recovery may take several months. Most patients are out of bed and start
rehabilitation on POD 1, and are discharged home in a week.
Analgesia
• Significant pain may be expected for up to 4 days postoperatively. Implement a multimodal
approach using PCA, anxiolytics, and muscle relaxants to control spasm.
• Thoracic epidural catheter (TEC) placement may be performed intraoperatively by the
surgeon and can significantly aid with the management of postoperative pain.
COMPLICATIONS
See Morbidity
PROGNOSIS
Relief of leg pain in the majority of patients (>80%), and relief of LBP in most of patients
(60–70%).
REFERENCES
1. Buchowski JM, et al. Neurologic complications of lumbar pedicle subtraction osteotomy.
Spine. 2007;32 (20):2245–2252.
2. Padberg AM, et al. Intraoperative electrophysiologic monitoring: Consideration for complex
spinal surgery. Neurosurg Clin N Am. 2006;17:205–226.
3. Raw DA, et al. Anesthesia for spinal surgery in adults. Br J Anaesth. 2003;91(6):886–904.
4. Ornstein E, Berko R. Anesthesia techniques in complex spine surgery. Neurosurg Clin N
Am. 2006;17:191–203.
• Cell salvage
• Somatosensory and motor-evoked potentials (SSEP/MEPs)
CODES
ICD9
• 737.30 Scoliosis [and kyphoscoliosis], idiopathic
• 754.2 Congenital musculoskeletal deformities of spine
ICD10
• M41.9 Scoliosis, unspecified
• M41.20 Other idiopathic scoliosis, site unspecified
• Q67.5 Congenital deformity of spine
CLINICAL PEARLS
• TIVA and avoidance of nondepolarizing muscle relaxants can enhance intraoperative
neuromonitoring. Its goal is to provide early identification of potential neurological injury
to avoid neurological deficits postoperatively.
• Prepare for massive blood loss with adequate fluid replacement with IV fluids (colloid and
crystalloid), blood loss reduction strategies, and transfusion of blood products.
• Ensure a smooth and quick emergence for neurological exam.
SEIZURE DISORDERS
BASICS
DESCRIPTION
• Seizures are symptoms of underlying neurologic disorders that may be
– Genetic
– Traumatic
– Metabolic
– Infectious
– Malignant
– Pharmacologic
– Idiopathic
• Epilepsy syndromes are based on clinical descriptions and etiologies, such as age of onset,
seizure types, EEG features, and other factors such as family history. Seizures occur as part
of an epileptic syndrome; thus, identification of the syndrome helps determine the
appropriate therapy and the prognosis.
• Epileptics may need anesthesia for routine procedures as there is a higher incidence of
individuals with intellectual and developmental disabilities (mental retardation, cerebral
palsy, autism, and psychiatric and behavioral disabilities). Anesthesia and or sedation may
be used to facilitate procedures such as dental restorations, EEGs, and other imaging
studies. Additionally, the incidence of epilepsy increases with the severity of disability.
• Well-controlled epileptics may also present for unrelated surgical procedures. Postoperative
seizures may be seen secondary to missed antiepileptic drugs (AEDs), stress, sleep
deprivation, anesthetic drugs, or metabolic derangement.
EPIDEMIOLOGY
Prevalence
• In the US, 100,000 people have a new onset seizure each year
• Greater in the elderly
Prevalence
• In the US, 2,000,000 persons have epilepsy, of which 300,000 are children under the age of
14.
• Approximately 10% of the population will have at least one seizure at some point in their
life.
Morbidity
• In children it can lead to neurologic impairment and developmental delay.
• Driving and operating machinery should be avoided.
• Coma
Mortality
Uncontrolled, prolonged seizure activity can result in death.
• Seizures are symptoms of underlying disorders that may be genetic, traumatic, metabolic,
infectious, malignant, pharmacologic, or idiopathic.
• Diagnosis and management can be challenging for both the family and healthcare providers,
partly because the incidence of epilepsy is higher in the intellectually and developmentally
disabled population.
• Seizure classifications are based on location, clinical symptoms, spread, and duration.
Appropriate classification of seizure disorders is crucial in providing effective treatment and
prognosis.
• Alterations in GABA neurotransmission have been implicated in epilepsy, and
pharmacotherapy is targeted to affect central nervous system receptors or neurotransmitter
activity.
• Epileptic patients may present for
– Diagnostic procedures. Require preservation of the EEG; epileptic activity required. Many
of these procedures require a cooperative patient, and at times, immobility to obtain
optimal results. The pediatric, as well as neurologically impaired, population often
requires sedation or general anesthesia. Effects of sedatives/anesthetics on the quality of
the diagnostic study must be taken into account.
– Nonrelated and routine procedures. Patients with developmental disabilities are not only
more challenging to treat in the perioperative period, due to a lack of cooperation, but
often have the greatest likelihood of polypharmacy, drug interactions, and unpredictable
sedation efficacy.
• AEDs and anesthetic agents
– Enzyme induction. Antiepileptic medications may upregulate enzymes that are responsible
for drug metabolism and consequent termination of action (e.g., P450). This can result in
rapid metabolism of certain anesthetic drugs and muscle relaxants.
– Side effects. Include drowsiness, sedation, somnolence, and lethargy, which may have an
additive effect when combined with the anesthetic. A thorough evaluation prior to
administration of anesthetics with these factors in mind can help guide the choice of
anesthetics as well as establish appropriate post-sedation monitoring and discharge
criteria.
• EEG and epileptic activity. Anesthetic agents may have proconvulsant effects, anticonvulsant
effects, or pro- and anticonvulsant effects depending on the dose and clinical situation.
SYMPTOMS
Description of seizure type(s), post-ictal symptoms
History
• Seizure history: Frequency, last seizure, precipitating events, loss of consciousness,
treatment efficacy, comorbidities, physical and developmental disabilities/limitations
• Perioperative seizures or complications.
Signs/Physical Exam
• Level of consciousness, awareness, and activity to establish discharge criteria.
• Airway exam. Physical limitations for airway management and operative positioning.
TREATMENT HISTORY
Nonmedication therapy may include a ketogenic diet, vagal nerve stimulator implant, or
craniectomy.
MEDICATIONS
• Epilepsy has many causes, and treatment is based on the diagnosis that is derived from a
compilation of findings. Evaluation of patients with a single, unprovoked seizure must take
into account the likely risk of seizure recurrence, patient age, level of activity, personal
preference, and potential side effects of antiepileptic drugs. Only after a second seizure is
the diagnosis of epilepsy made and routinely treated with AEDs.
• Determine the last dose, symptoms from missed doses.
• AEDs frequently induce the P450 enzyme system, so patients may require increased dose
and frequency of nondepolarizing neuromuscular blockers.
• Gabapentin can compound analgesic effects
• Valproate side effects: Sedation, nausea/vomiting, rashes, scleroderma, systemic lupus
erythematosus, hepatic failure, thrombocytopenia
• Carbamazepine side effects: Anemia, leucopenia, hyponatremia
• Phenytoin side effects: Altered thyroid function
Labs/Studies
Despite potential side effects from AEDs, routine labs are not generally indicated
• Usually related to AED side effects
• Increased incidence of depression and other psychiatric morbidities. In multiple studies,
improvement in quality of life is related to seizure control.
• Reports of increased seizure activity or new onset of seizure type (nontypical seizure)
• Prolonged NPO status (missed AED dose) or concurrent illnesses may increase seizure risk.
CLASSIFICATIONS
Based on
– Location:
– Generalized seizures are due to abnormal activity on both sides of the brain
– Focal (partial) seizures begin in a specific area of the brain and may be motor, sensory, or
both.
• Symptoms:
– Tonic: Stiffening
– Clonic: Rhythmic jerking
– Combined tonic-clonic
– Myoclonic
– Absence: Staring episode
– Atonic: Loss of muscle tone
• Spread:
– Partial seizures that result in a loss of awareness are termed “complex partial”
– If it evolves to include both hemispheres of the brain, it is termed “complex partial with
secondary generalization.”
• Etiology allows for further subdivisions: Idiopathic (genetic), cryptogenic, and symptomatic.
TREATMENT
Premedications
• Benzodiazepines should be avoided for diagnostic procedures.
• Ketamine may activate epileptogenic foci.
• Dexmedetomidine may be administered IV or intranasally for sedation and is devoid of EEG
affects.
• Consider IV preparation of AED if necessary
• Consider a neurology consultation for management of perioperative seizure or anticipated
prolonged NPO status.
Patients and family should be made aware of the potential for perioperative seizures, postictal
delayed awakening, and prolonged postanesthesia monitoring.
INTRAOPERATIVE CARE
• Dependent on the procedure, comorbidities, need for akinesis, and risk for aspiration.
• Diagnostic procedures require avoidance of anticonvulsant anesthetics.
Monitors
• Consider EEG monitoring if there is a high risk of undetectable seizure activity (e.g., use of
muscle relaxation in a high risk patient)
• Seizures are most common during emergence and induction, as rapid changes in brain
concentrations of anesthetic occur.
• Consider the risk of aspiration in patients with severe disabilities; a cuffed endotracheal tube
may be appropriate.
Maintenance
• Anesthetic technique is dependent on the procedure (diagnostic, therapeutic, nonrelated).
• Anticonvulsant anesthetics: Volatile anesthetics, propofol, thiopental, and etomidate.
• Neutral anesthetics: Dexmedetomidine and choral hydrate (sedation procedures)
• Proconvulsant properties
– A rapid rise in sevoflurane.
– Enflurane and methohexital may activate epileptogenic foci.
– Ketamine may result in subcortical epileptogenic stimulation.
– Etomidate and propofol have both been implicated in seizure-like movements.
– High doses of opioids such as remifentanil, alfentanil, sufentanil, and fentanyl are also
associated with seizure activity.
Seizures may occur during emergence due to rapid changes in anesthetic brain
concentrations.
FOLLOW-UP
BED ACUITY
Consider intensive care if the patient has uncontrolled seizures in the perioperative period.
• Consider a neurology consult to manage anticonvulsants if the patient cannot tolerate their
home regimen or if seizure disorder is not controlled.
• If the patient has a seizure, check for glucose and electrolyte derangements. Consider
checking anticonvulsant levels; however, therapeutic levels may not be clinically relevant
and consultation by a neurologist is preferable.
• Discharge: A caregiver who knows the patient’s baseline mental status is helpful for
discharge planning.
COMPLICATIONS
• Perioperative seizure
• Consider postictal unconsciousness if delayed awakening. Consider delaying extubation in
the seizing patient to provide airway protection.
REFERENCES
1. Browne TR, Holmes GL. Epilepsy. N Engl J Med. 2001;344:1145–1151.
2. Drugs for epilepsy. Treat Guidel Med Lett. 2003;1:57–64.
3. Kohrman MH. What is epilepsy? Clinical perspectives in the diagnosis and treatment. J Clin
Neurophysiol. 2007;24:87–95.
4. Modica PA, Tempelhoff R, White PF. Pro- and anticonvulsant effects of anesthetics (Part I
and II). Anesth Analg. 1990;70:303–315, 433–444.
5. Ren WH. Anesthetic management of epileptic pediatric patients. Int Anesthesiol Clin.
2009;47(3):101–116.
6. Smith D, Minshall I. Drug management of epilepsy. Practitioner. 2003;247:19–22, 24, 27–
28 passim.
• Perioperative seizures
• Hypoglycemia
• Anesthesia for neuroradiology
CODES
ICD9
• 345.90 Epilepsy, unspecified, without mention of intractable epilepsy
• 780.39 Other convulsions
ICD10
• G40.909 Epilepsy, unsp, not intractable, without status epilepticus
• R56.9 Unspecified convulsions
CLINICAL PEARLS
• Anaesthetists need to be aware of the common adverse effects of AEDs
• Perioperative seizures occur most commonly during induction and emergence.
• Many anesthetics have both proconvulsant and anticonvulsant properties. Generally, most
anesthetics are anticonvulsant at high doses except opioids.
SEPTIC SHOCK
Anahat Dhillon, MD
Sumit Singh, MD
BASICS
DESCRIPTION
• Sepsis describes a documented infection (culture or Gram stain of a normally sterile body
fluid for pathogenic organism or focus of infection identified by visual inspection) and two
or more manifestations of the systemic inflammatory response syndrome:
– Temperature >38°C or <36°C
– Heart rate >90 beats/min
– Respiratory rate >20 breaths/min or paCO2 <32 mm Hg
– WBC >12,000/μL, <4,000/μL, or >10 immature (band) forms.
• Septic shock is a severe form of sepsis and involves hypotension despite adequate
resuscitation, end-organ hypoperfusion (e.g., lactate >2 mmol/L), and organ dysfunction
(e.g., urine output <0.5 mL/kg). It has features of high output cardiac failure and
distributive shock.
EPIDEMIOLOGY
Prevalence
• ∼50–95 cases per 100,000 annually
• In the US, >750,000 cases/year
Morbidity
Complications include renal failure (50%), disseminated intravascular coagulopathy or DIC
(38%), and acute respiratory distress syndrome (ARDS) (18%).
Mortality
In the US, ∼200,000/year
• Gram-positive bacteria (30–50%): Staphylococcus pyrogenase, S. pneumonia, S. aureus
• Gram-negative bacteria (25%): Escherichia coli, Pseudomonas aeruginosa, Haemophilus
influenza
• Fungal: Candida albicans
• Anaerobes: Clostridium perfringens
• Older individuals (>65 years) have increased comorbidities, impaired immunological
response to infections, and increased exposure to potentially resistant organisms in nursing
homes, all contributing to increased mortality. They account for ∼60% of severe sepsis
cases.
• Immunocompromised patients (neoplasms, AIDS, hepatic or renal failure).
• Compared to community-acquired infection, nosocomial infections have a higher mortality
rate (10% versus 15%).
• Community acquired pneumonia (CAP) patients will develop severe sepsis in 48% and septic
shock in 5% of cases.
• Source of sepsis also determines outcomes, with urosepsis having a 30% mortality rate
compared to 55% if the source was pulmonary, GI or unknown.
• The aim of normal inflammation is to locally contain the spread of infection. However, in
certain cases, the inflammatory process spreads across the locally infected area, invades the
bloodstream, and causes a generalized response, known as sepsis.
• Sepsis is a complex, malignant intravascular inflammation. The lipopolysaccharide of Gram-
negative bacteria and the peptidoglycan of Gram-positive bacteria bind to cell receptors (CD
14, TLR-2,4) and induce production of pro-inflammatory cytokines (tumor necrosis factor α
[TNF α], interleukin-1 [IL-1]), chemokines (ICAM-1, VCAM-1), and nitric oxide. The
endothelium cells express adherence molecules that attract leukocytes and macrophages
that in turn release more cytokines (TNF and ILs). TNF further stimulates production of
other secondary inflammatory mediators, besides being self-stimulating (autocrine).
Activation of the complement system, release of IL-1, 2, 6, 8, 10, platelet-activating factor,
interferons, and eicosanoids result in recruiting more leukocytes and macrophages. These
inflammatory mediators cause local vasodilation, hyperemia, and increased permeability
resulting in protein rich edema. They also contribute to cellular injury. Other proposed
mechanisms of cellular injury are apoptosis (programmed cell death) and ischemic damage.
• Pattern recognition receptors (PRRs) recognize specific structures of microorganisms. In
sepsis response, PRR such as toll-like receptors (TLR) are capable of sensing a wide range of
organisms (bacteria, fungi, viruses and protozoa). Their activation leads to cellular
activation and inflammatory response initiation.
• Some cytokines (IL-6, IL-10) have an anti-inflammatory effect by inhibiting production of
TNF α and IL-1. In a normal effective response to an infectious insult, the pro- and anti-
inflammatory responses balance each other out and the initial infectious insult is overcome.
In certain cases, the initial infectious assault may be so severe and sufficient to produce
sepsis. In another scenario, after the initial insult, the balance between pro- and anti-
inflammatory forces may not be established leading to a massive systemic inflammatory
response, or a period of immune suppression.
• Initiate therapy early. Intubation and mechanical ventilation, invasive monitoring,
laboratory work, antibiotics, and treatment of hypoperfusion.
• Intensive care unit (ICU) bundles may be carried out by the anesthesiologist in the ICU or
continued into the perioperative period. They include
– Identifying a specific anatomic site of infection within the first 6 hours. If intravascular
devices are believed to be the source, they should be removed.
– Broad-spectrum antibiotics should begin within 3 hours of ED admission and within 1 h of
non-ED admission. However, blood cultures should be obtained prior to antibiotic
administration.
– Measure serum lactate
– Hypotension and/or elevated lactate should be treated with IV fluids. If unresponsive,
vasopressors should be implemented to maintain a MAP >65 mm Hg. Achieve a CVP of
>8 mm Hg, central venous oxygen saturation (ScvO2) >70%, or mixed venous oxygen
saturation (SvO2) >65%. This may require pRBC transfusion or inotropy.
– Steroids (hydrocortisone 200–300 mg/day for 7 days) may be used in vasopressor-
dependent shock.
– Consider recombinant human activated protein C (rhAPC). Activated protein C normally
regulates blood clotting, inflammation, cell death, and endothelial integrity. In sepsis the
levels are reduced, and randomized controlled trials suggest that it can decrease mortality,
especially in the first 24 hours in patients with APACHE score >25.
SYMPTOMS
• Fever, rigors, chills
• Abdominal pain (if the source of sepsis is abdominal)
• Mental status changes and confusion (especially if patient febrile or hypoxic)
History
• Look for preceding conditions: Intraabdominal sources (diverticulitis, Crohn disease,
previous abdominal surgery, cholecystitis, subacute appendicitis), urosepsis (pyelonephritis,
nephrolithiasis, congenital urological abnormalities, benign prostate hypertrophy, and
previous urological surgeries).
• Immunocompromised patients, diabetics, systemic lupus erythematosus (SLE), alcoholics,
and steroid-dependent patients are at increased risk of bacteremia and sepsis.
• Suspect IV line infections, especially when other sources of infection have been ruled out.
Central venous lines >1 week are most commonly involved. Arterial lines are rarely
involved and peripheral venous lines are almost never associated.
Signs/Physical Exam
• Hypotension, tachycardia, bounding pulse. Inflammatory mediators such as TNF α, not only
cause a decrease in peripheral vascular resistance but also cause a myocardial depressant
effect (septic cardiomyopathy).
• Early stages: Warm flushed skin. Later stages: Cold, mottled extremities
• Oliguria or anuria
• Hypoxia, tachypnea, respiratory alkalosis
• Hyperthermia or hypothermia
TREATMENT HISTORY
Intubation and mechanical ventilation. There is an increased work of breathing secondary to
increased minute ventilation and airway resistance, and decreased lung compliance.
Additionally, patients may have developed ALI/ARDS.
MEDICATIONS
• Vasopressors: Norepinephrine, dopamine, phenylephrine, vasopressin. No definitive
evidence of superiority has been demonstrated.
• Antibiotics: Broad-spectrums include vancomycin in combination with a 3rd-generation
cephalosporin or carbapenem. If pseudomonas is suspected, vancomycin with two
antipseudomonal agents (e.g., ceftazidime, meropenem, ciprofloxacin, and meropenem) are
used.
Labs/Studies
• Chem 10 to evaluate renal function, CBC plus differential, lactic acid levels
• Arterial blood gases (ABGs) to assess acid base abnormality and oxygenation and any A-a
gradient.
• Mixed venous saturation
• Procalcitonin is an early biomarker of sepsis that has been found to be most sensitive and
specific in recent studies.
• Bedside echocardiography can reveal or rule out cardiogenic causes, as well as guide
resuscitation.
Underlying sources; see above
• Procedures should be limited to those absolutely necessary (source control) and that can
potentially improve survival.
• Prior to the OR, proper resuscitation with IV fluids, vasopressors, and early goal directed
therapy should be done (MAP >65 mm Hg, CVP 8–12 mm Hg, adequate urine output,
correction of acid base abnormality and lactic acidosis, and achieving a mixed venous
oxygen (MVO2%) or ScvO2% >70%).
• Patients in renal failure may need preoperative dialysis catheter placement followed by
dialyses; intraoperative continuous veno-venous hemodialysis (CVVH) may be necessary.
TREATMENT
Premedications
• FFP, platelets, and cryoprecipitate may be considered in coagulopathic or thrombocytopenic
patients.
• Vasopressor drips should be prepared beforehand, in anticipation of hypotension.
• Cautious administration of benzodiazepines and opioids; patients have minimal physiologic
reserve and can get hypotensive or hypoxic.
• H2 blocker or proton pump inhibitors for stress ulcer prophylaxis.
• Altered mental status may preclude consent
• Anesthesia and surgery is extremely high risk
• Need for additional invasive monitoring
• Blood consent
INTRAOPERATIVE CARE
General anesthesia with ETT
Monitors
• Arterial line: BP monitoring, titration of vasopressors, ABGs, glucose, and lactate levels.
Respiratory variations provide a dynamic parameter of intravascular volume assessment and
may be more accurate than CVP.
• Central venous catheter: Pressures and ScvO2 can guide fluid therapy. Pulmonary artery
catheters are not recommended for routine use in sepsis.
• Sufficient IV access for volume resuscitation.
• Core temperature monitoring, as pyrexia of sepsis may be offset by heat loss from the
surgical field.
• Rapid sequence intubation due to decreased gut motility (secondary to hypoperfusion).
Succinylcholine can be used, provided that the patient is not hyperkalemic. Avoid when
source of infection is intraabdominal; succinylcholine may release excessive amounts of K+.
Rocuronium can be used in such cases.
• Induction agent with cardiovascular stability such as etomidate or ketamine can be used.
Etomidate use in sepsis has been debated because of its reversible adrenocortical
suppression. However, no prospective randomized control trial has shown any increase in
adverse effects with a single dose.
• Be prepared to treat hypotension with fluid boluses and/or vasopressors
Maintenance
• Administer antibiotics within 30 minutes of skin incision.
• Consider or continue steroid administration.
• Consider benzodiazepines or scopolamine in patients who cannot tolerate the effects of
volatile agents or hypnotics, to decrease the incidence of awareness under anesthesia.
• Maintain normothermia and normoglycemic (80–150 mg/dL).
• Maintain Hg levels between 7 and 9 g/dL and platelets above 50,000/μL.
• Limit TV (6–8 mL/kg) and plateau pressure <30 cm H20.
Postoperatively mechanical ventilation is often continued into the ICU until the patient is
more hemodynamically stable.
FOLLOW-UP
BED ACUITY
ICU care for monitoring of vital signs, narrowing of antimicrobial therapy as guided by the
culture results, supportive care such as continuation of mechanical ventilation, vasopressors,
dialysis, and early initiation of enteral nutrition.
Infectious disease, nephrology as needed
REFERENCES
1. Angus DC, et al. Epidemiology of severe sepsis in the United States: Analysis of incidence,
outcome, and associated costs of care. Crit Care Med. 2001;29:1303–1310.
REFERENCES
2. Baluch A, et al. Septic shock: Review and anesthetic considerations. Middle East J
Anesthesiol. 2007;19(1):71–86.
3. Dellinger RP, et al. Surviving Sepsis Campaign: International guidelines for management of
severe sepsis and septic shock: 2008. Crit Care Med. 2008;36(1):296–327.
4. Levy M, et al. The Surviving Sepsis Campaign: Results of an international guideline-based
performance improvement program targeting severe sepsis. Intensive Care Med.
2010;36(2):222–231.
5. Schuerholz T, Marx G. Management of sepsis. Minerva Anesthesiol. 2008;74(5):181–195.
CODES
ICD9
785.52 Septic shock
ICD10
R65.21 Severe sepsis with septic shock
CLINICAL PEARLS
• Fluids should be administered in septic shock until there is improvement in perfusion (or
cardiac output).
• Vasopressors and inotropes may be necessary to prevent fluid overload and pulmonary
edema.
SHUNT, INTRAPULMONARY
Eric Bolin, MD
BASICS
DESCRIPTION
• Intrapulmonary shunt (IPS) occurs when blood passes through the lungs without acquiring
oxygen. This results in the return of oxygen-poor venous blood to the left heart that mixes
with well-oxygenated pulmonary venous blood. It may result from
– Ventilation/perfusion abnormalities
– Anatomical arteriovenous anastomosis
• Normally the fraction of blood that passes through the lungs without acquiring oxygen is
very low and therefore has no clinical significance.
• Intrapulmonary shunt (IPS). A right-to-left shunt results in a hypoxic shunt, whereas a left-
to-right shunt does not.
– Ventilation/perfusion shunting describes perfusion without ventilation; this is in contrast
to dead space, which is ventilation without perfusion. A shunt may be relative or absolute;
an absolute shunt occurs when ventilation is zero.
– There are 4 lung zones:
Zone 1 PA > Ppa > Ppv
Zone 2 Ppa > PA > PPV
Zone 3 Ppa > PPV > PA
Zone 4 Ppa > PISF > Ppv > PA
PA = Alveolar pressure, Ppa = pulmonary artery pressure, Ppv = pulmonary venous
pressure, PISF = pulmonary interstitial pressure
In zones 3 and 4, partial or complete alveolar collapse can result in relative or absolute
shunt.
• Intracardiac shunt, while anatomically distinct from IPS, can have the same net impact on
oxygenation and may contribute to shunt fraction. Examples include ventral and atrial
septal defects and a patent foramen ovale. Initially, the relatively higher pressures on the
left side of the heart results in blood being shunted from left-to-right. However, with time,
the increased blood flow through the pulmonary vasculature can result in overload, with
consequent pulmonary hypertension. If the pulmonary pressures become high enough, shunt
reversal may occur (blood flows from the right-to-left), thus converting a nonhypoxic shunt
into a hypoxic shunt. Eisenmenger syndrome describes the combination of increased
pulmonary pressures, cyanosis, and erythrocytosis from shunt reversal.
• Hypoxic pulmonary vasoconstriction (HPV) refers to the normal physiologic constriction of
pulmonary vasculature in response to hypoxia in an attempt to divert blood flow to well-
oxygenated regions of the lung. HPV improves oxygenation by improving V/Q ratios
regionally, and reduces relative shunt. While HPV is an intrinsic physiologic mechanism
that may improve oxygenation, it is important to note that volatile anesthetic agents inhibit
HPV. This may contribute to increased shunt fraction under general anesthesia.
• Shunt fraction/venous admixture. Describes the magnitude of IPS as a percentage of cardiac
output that returns to the left atrium without being oxygenated; it is a physiologic concept.
The shunt fraction/venous admixture may be thought of as the amount of venous blood that
would have to be mixed with optimally oxygenated blood to account for the difference in
oxygen content between the optimally oxygenated blood and the observed oxygen content.
– The formula is derived from a two-compartment model of the lung. In the first
compartment, all lung segments have a V/Q ratio of 1. In the second compartment, all
segments have a V/Q ratio of 0. This formula is generally used with an FiO2 of 100% to
conceptually eliminate lung units with very low V/Q ratios, or relative shunt; at an FiO2
of 1.0, these segments will oxygenate blood well.
– Shunt fraction = QS/QT = (CcO2 – CaO2)/(CcO2 – CvO2) and is a composite of any and
all factors affecting oxygenation. The trend is more important than the absolute value.
With respect to the two compartment model, the shunt fraction can be thought of as the
perfusion of the compartment for which V/Q = 0.
– Normal (physiologic) shunt fraction is ∼2–5% and occurs through anatomic shunts from
the pleural, bronchiolar, and Thebesian veins.
ANATOMY
• Thebesian veins arise in the myocardium and empty into the left atrium.
• Bronchial veins drain small bronchi, septa, and connective tissue in the lungs. Bronchial
circulation returns to the left heart via the pulmonary veins.
• Pleural veins drain the visceral pleura and return to the left heart via the pulmonary veins.
• Processes that may contribute to the development of IPS include
– Atelectasis in the perioperative period is the result of several factors. Anesthetic agents
affect and impair the movement of the diaphragm and intercostal muscles (diaphragm
allows cephaled invasion of the abdomen and the anteroposterior movement of the rib
cage is affected). Supine and Trendelenburg positioning further accentuates these effects.
Mechanical ventilation preferably delivers volume to nondependent lung spaces, whereas
blood flow is greatest in dependent areas. In the postoperative period, pain can lead to
“splinting,” or shallow respiration due to pain; optimal management requires sufficient
pain control without oversedation.
– Acute lung injury. A form of noncardiogenic pulmonary edema that is characterized by
acute hypoxic respiratory failure and bilateral pulmonary infiltrates with resultant
significant V/Q mismatch and resultant hypoxemia. ARDS is a subset of acute lung injury
(2).
– Congestive heart failure. Impaired cardiac pump function can result in “backup” into the
right atrium and pulmonary vasculature. Initially, recruitment and dilation of the
pulmonary vasculature occurs; this is followed by fluid extravasation into the interstitial
space and then entry into the alveoli. These processes impair alveolar expansion.
– Consolidated pneumonia leads to alveoli being clogged with exudative material.
Ventilation of these units is zero, representing a true shunt.
• Hepatopulmonary syndrome (HPS) describes a triad of pulmonary vascular dilation, liver
disease, and a defect in oxygenation. Pulmonary vascular dilation:
– Increases flow through AVMs with a resultant increase in shunt fraction
– Contributes to V/Q mismatching by increasing blood flow without a corresponding
increase in ventilation (3).
• Arteriovenous shunting describes direct vascular anastomoses between pulmonary arteries
and veins. The magnitude of an arteriovenous shunt can be affected by changes in position
and lung volumes.
– Position. In the presence of an asymmetrical cranial to caudal distribution of pulmonary
arteriovenous malformations (AVMs), changing posture may increase shunt fraction. The
Trendelenburg position combined with predominantly basal AVMs will increase blood
flow and shunt.
– Lung volumes. Increases in lung volume increase the resistance in normal pulmonary
blood vessels to a greater extent than AVMs. The result is an increase in blood flow
through AVMs, and hence shunt fraction. This is consistent with increased lung volumes
having no effect on shunt fraction in healthy patients free of AVMs (1).
• Saline contrast echocardiography can be used to diagnosis intracardiac shunting by injecting
agitated saline into the venous circulation. The appearance of bubbles immediately in the
left heart (1–2 cardiac cycles) is consistent with the presence of an intracardiac shunt. The
delayed appearance of bubbles (4–8 cardiac cycles) is consistent with the presence of an IPS
(3,4).
• IPS caused by atelectasis under general anesthesia (V = 0 for atelectatic alveoli,
representing a true shunt) may be improved significantly with strategies and maneuvers
that increase alveolar size and assume a more favorable shape for exposure to pulmonary
vasculature.
– Intermittent postintubation or intraoperative application of high levels of PEEP (up to 15
cmH2O) and a tidal volume up to 18 cc/kg until a peak inspiratory pressure of 40 cmH2O
is reached has been shown to decrease atelectasis. After recruitment, PEEP is maintained
at 5 cmH20 to ensure that recruited alveoli remain open (5).
– Obese patients experience a profound decrease in lung compliance, decreased PaO2, and
increased PaCO2 relative to nonobese individuals. The application of PEEP at 10 cmH20
has been shown to significantly improve pulmonary mechanics and oxygenation (6).
– Noninvasive positive pressure preoxygenation, when combined with a postintubation or
intraoperative recruitment maneuver of 40 cmH20 for 40 seconds, patients exhibited
improved oxygenation and end expiratory lung volumes (7).
• Absolute shunt. Atelectatic alveoli (fully collapsed, fluid filled, proteinaceous filled) are not
ventilated. Thus, hypoxemia from these causes remains unresponsive to increased FiO2;
blood flow is not exposed to alveolar gases and therefore cannot be oxygenated. Conversely,
relative shunt occurs when ventilation is low but greater than zero; it remains responsive to
increased FiO2.
EQUATIONS
• Shunt fraction = QS/QT = (CcO2 – CaO2)/(CcO2 – CvO2) = <5%
– CcO2 = oxygen content of ideal pulmonary end capillary blood
– CaO2 = oxygen content of mixed arterial blood
– CvO2 = mixed venous oxygen content
– Calculation of the shunt fraction via this equation requires a pulmonary artery catheter to
obtain a mixed venous oxygen saturation, limiting the utility of this index.
• Ventilation/perfusion = V/Q = (4 L/min)/(5 L/min) = 0.8.
– Gross normal value for both lungs varies widely for individual lung units.
• Ventilation perfusion ratio = VQI = (1 – SaO2)/(1 – SvO2)
– This formula substitutes saturation values for oxygen content because hemoglobin
concentration is constant (therefore, oxygen content correlates with saturation).
REFERENCES
1. Ueki J, et al. Oxygen and 99mTc-MAA shunt estimations in patients with pulmonary
arteriovenous malformations: Effects of changes in posture and lung volume. Thorax.
1994;49:327–331.
2. Rubenfeld GD, et al. Incidence and outcomes of acute lung injury. N Engl J Med.
2005;353(16):1685–1693.
3. Rodriguez-Roisin R, et al. Hepatopulmonary syndrome – A liver-induced lung vascular
disorder. N Engl J Med. 2008;358:2378–2387.
4. Castro P, et al. Intrapulmonary shunting associated with sildenafil treatment in a patient
with idiopathic pulmonary arterial hypertension. Thorax. 2011 Epub ahead of print.
5. Tusman G, et al. Alveolar recruitment strategy improves arterial oxygentaion during
general anesthesia. Br J Anesth. 1999;82:8–13.
6. Pelosi R, et al. Positive end-expiratory pressure improves respiratory function in obese but
not in normal subjects during anesthesia and paralysis. Anesthesiology. 1999;91:1221–1231.
7. Futier E, et al. Noninvasive ventilation and alveolar recruitment maneuver improve
respiratory function during and after intubation of morbidly obese patients. Anesthesiology.
2011;114:1354–1363.
• Ventilation and perfusion mismatching
• Ventral septal defect
• Atelectasis
CLINICAL PEARLS
• Increased IPS can cause significant hypoxemia during the perioperative period. Shunting
due to atelectasis is a common cause of hypoxemia that can be treated and ameliorated with
appropriate ventilator management.
• Surgery should be avoided or minimized in the presence of conditions or disease processes
that significantly increase shunt fraction and thereby result in hypoxemia. These conditions
include but are not limited to acute lung injury, ARDS, pneumonia, and pulmonary edema.
• Normal physiologic shunt, which is 2–5%, is functionally equivalent to an IPS, and is
reflected in calculations of IPS.
SICK SINUS SYNDROME
Adam M. Stuart, MD
BASICS
DESCRIPTION
• Sick sinus syndrome (SSS) is characterized by abnormalities in the generation of cardiac
impulses from the sinoatrial node (SAN).
– Sinus bradycardia
– Sinus arrest
– Sinus exit block
– SA and AV conduction disturbances
– Chronic atrial tachyarrhythmias
– Alternating episodes of atrial bradyarrhythmias and tachyarrhythmias (tachy-brady
syndrome).
• SSS is categorized into etiologies that are intrinsic or extrinsic to the SAN.
EPIDEMIOLOGY
Prevalence
• Overall incidence has not been quantified
• Accounts for at least 50% permanent pacemaker placement in the US.
Prevalence
• Increases with age (mean age = 68 years)
• Occurs equally in both genders and without predominance in any one race
Morbidity
• Its association with advanced cardiovascular (CV) disease may carry a variety of coexisting
conditions.
• Associated with thromboembolism and/or stroke; chronic atrial fibrillation (a-fib), AV block;
and complications of therapeutic anticoagulation
Mortality
• Increased risk of sudden cardiac death
• Following permanent pacemaker placement, 1–year mortality is 5–10% and 5–year
mortality is 25–30%. This is, in part, attributable to comorbid CV disease.
• Ventricular pacing is associated with higher mortality than atrial pacing alone.
• Pacemakers in patients with tachy-brady syndrome have been shown to ameliorate
symptoms of bradycardia and frequency of a-fib, but not improve survival.
• Patients with only bradycardia have a better prognosis; their mortality is similar to that of
the general population (1).
• Intrinsic etiologies – Most commonly caused by fibrosis of nodal tissue
– Idiopathic (most common cause)
– Cardiac: Chronic ischemia, infarction, myocarditis, pericarditis, cardiomyopathy
– Autoimmune: Amyloid, sarcoid, SLE
– Genetic: Familial SAN disorders, Friedreich’s ataxia, hemochromatosis
– Infectious: Chagas, diphtheria, rheumatic disease
– Neoplasm: Leukemia, metastatic disease
– Pediatric: Congenital abnormalities
• Extrinsic etiologies
– Iatrogenic: Digitalis, calcium channel blockers, beta-blockers, sympatholytics,
antiarrhythmics
– Hypoxia
– Electrolyte imbalance: Hyper/hypokalemia, hypoglycemia
– Hyper/hypothyroid
• Idiopathic fibrosis of the SAN is the most longstanding hypothesis; however, other general
mechanisms have been proposed and researched primarily in animal models. Intrinsic
dysfunction is the result of failure to generate a sinus impulse and/or diminished travel of
an impulse to surrounding myocardium.
• Age-related remodeling of the cardiac extracellular matrix can affect cellular ionic currents
and channels.
• Familial condition has been linked to genetic mutations in genes that encode ion channels,
such as the Na+ channel (SCN5A), funny current (HCN4), and Ca2+ channel = (CASQ2).
• Acute inferior wall myocardial ischemia/infarction is associated with a transient alteration
of neurologic rhythm control.
• Heart failure has demonstrated down regulation of funny current channels.
• Extreme physical conditioning can result in intrinsic changes to the SAN and the cardiac
conduction system from dilation and hypertrophy (2).
• Medical therapies and coexisting medical conditions should be optimized.
• Device interrogation and appropriate preoperative reprogramming should be performed.
• The anesthetic plan should aim for hemodynamic stability, rate control, and adequate
ventricular filling/ejection.
• Preoperative therapeutic anticoagulation must be optimized. Chronic anticoagulation is
recommended in tachy-brady syndrome and chronic atrial fibrillation. Preoperative
therapeutic anticoagulation must be optimized.
SYMPTOMS
• Syncope, dizziness, or lightheadedness
• Palpitations
• Fatigue, poor exercise tolerance
• Dyspnea, orthopnea
History
• History of dysfunction and type
• Coexisting conditions and risk factors
– CAD is common
• Functional status
Signs/Physical Exam
• CV exam
– Irregular rhythm on auscultation or palpation of pulses, bradycardia/tachycardia, JVD,
orthostatic hypotension
– Carotid massage: A sinus pause >3 seconds should elicit concern for SSS.
– A Valsalva maneuver will not cause an increase in the HR (3)
• Extremities
– Cyanosis: Thromboembolism
– Edema from congestive heart failure
• Neurologic
– Focal deficits: Stroke
TREATMENT HISTORY
Permanent pacemaker +/– defibrillator placement. Patients with any form of tachycardia-
related SSS may require rate control with beta-blockers and appropriate prevention of
bradycardia with pacing.
MEDICATIONS
• Medical treatment is utilized in accordance with specific symptoms or rhythm disturbance.
– Warfarin therapy particularly in tachy-brady syndrome
– Negative chronotropic medications (beta-blockers, calcium channel blockers, digitalis)
may be used in select patients with a tachycardic component, but may cause excess
bradycardia, block or arrest and should be used judiciously as chronic treatment.
Pacemaker placement may aid with maximizing therapy.
– Rhythm conversions with procainamide or quinidine are uncommon and unpredictable.
– Theophylline therapy may be employed with dual-chamber pacing (1,3).
Labs/Studies
• Electrolytes, INR, PTT
• EKG: May demonstrate pacing or a variety of manifestations in untreated patients
• Cardiac enzymes in the setting of recent onset arrhythmias
• Pacemaker device interrogation. The type, setting, and manufacturer of the pacemaker
should always be determined. Device interrogation may be appropriate if not performed
recently or there are concerns of malfunction based on the patient’s symptoms.
• Preoperative consultation with cardiology/EP care team does not typically require a full
workup, provided that the patient is regularly followed in clinic.
• CV (as described above)
• Neurologic: Focal deficits as well as generalized CNS deficits related to cerebral
hypoperfusion
• GI and renal dysfunction also as a result of organ hypoperfusion
CLASSIFICATIONS
• Generally SSS is classified by the distinct rhythm and or rate disturbance that is specific to
each patient’s condition.
• Intrinsic versus extrinsic causes (4)
TREATMENT
Premedications
Implanted pacemakers allow for rate control with beta-blockers and Ca+ channel blockers in
the case of tachyarrhythmias. If a pacemaker device is not present, these medications may
exacerbate the underlying conduction disturbance and should be utilized cautiously. Similar
disturbances may result from sympatholytic medications such as clonidine or methyldopa
(1,5).
• Delay of elective surgery in view of new or incompletely investigated arrhythmias
• Thromboembolic or hemorrhagic complications
• Possible need for intraoperative cardioversion and/or pacing.
INTRAOPERATIVE CARE
• Dictated by the procedure and comorbidities, with consideration given to sympatholytic
activity or effect that may uncover or worsen bradycardias.
• Regional and neuraxial methods may be contraindicated in the setting of anticoagulation
therapy.
– Neuraxial techniques may blunt the cardioaccelerator fibers (T1–T4).
Monitors
• Standard ASA monitors with EKG
• Noninvasive BP monitor may be acceptable in hemodynamically stable patients, but the
threshold for arterial catheter placement should be lowered.
• Central venous line and transesophageal echocardiography may also be considered
• No specific induction agents/methods have been established. The sympatholytic effects of
induction agents can produce transient or sustained bradyarrhythmias (5).
• IV lidocaine administration may interrupt sinus node activity causing arrest or severe
bradycardia (6)
• Sympathetic discharge associated with laryngoscopy may elicit tachyarrhythmias in patients
with tachycardia related SSS (5).
• In asymptomatic patients, SSS may be unmasked and require halting the procedure pending
workup.
Maintenance
• General anesthesia with either IV or inhalational administration may be acceptable.
• New onset bradycardia may initially be treated with beta-agonists or antimuscarinics.
• Minimize sympathetic simulation
• Balanced titration of reversal agents
FOLLOW-UP
BED ACUITY
• Routine postoperative care in hemodynamically stable patients with uncomplicated course
• Step down or ICU bed for any hemodynamic instability or new onset sinus node dysfunction
• Anticoagulation as indicated, beta or calcium channel blocker for control of
tachyarrhythmias
• Electrolytes, cardiac enzymes where indicated by new onset sinus dysfunction
• Device reprogramming, cardiology/EP follow-up
COMPLICATIONS
• Cardiac arrhythmias
• Systemic hypoperfusion/ischemia
• Thromboembolism versus bleeding
REFERENCES
1. Adan V, et al. Diagnosis and treatment of sick sinus syndrome. Am Fam Physician.
2003;67:1725–1732.
2. Monfredi O, et al. The anatomy and physiology of the sinoatrial node-a contemporary
review. Pacing Clin Electrophysiol. 2010;33(11):1392–1440.
3. Brignole M. Sick sinus syndrome. J Clin Geriatr Med. 2002;18:211–227.
4. Epstein AE, et al. ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac
rhythm abnormalities: Executive summary: A report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation.
2008;117(21):2820–2840.
5. Atlee JL. Perioperative cardiac dysrhythmias. Anesthesiology. 1997;86(6):1397–1424.
6. Kim KO, et al. Profound bradycardia with lidocaine during anesthesia induction in a silent
sick sinus syndrome patient. J Clin Anesth. 2011;23(3):227–230.
ADDITIONAL READING
• Bradycardia
• Pacemaker cells in the heart
CODES
ICD9
427.81 Sinoatrial node dysfunction
ICD10
I49.5 Sick sinus syndrome
CLINICAL PEARLS
• Patients with signs/symptoms attributable to SSS but without appropriate out-patient
follow-up should receive a complete preoperative workup for elective procedures.
• Temporary pacing may be required in patients with suspected or diagnosed SSS who do not
have implanted pacemakers.
• Sympatholytic therapies, vagal stimulation associated with induction, intubation and
surgical procedures may uncover SAN dysfunction.
• New onset sinus abnormalities and/or arrhythmias should prompt postponement of non-
emergent procedures.
• Asymptomatic sinus bradycardia in older patients may be the only preoperative sign of SAN
dysfunction.
SICKLE CELL DISEASE
Radha Arunkumar, MD
BASICS
DESCRIPTION
Sickle cell disease (SCD) is an inherited hemoglobinopathy characterized by chronic
hemolysis, acute painful vaso-occlusive crises, and end-organ damage
EPIDEMIOLOGY
Prevalence
• Most common in people of African and Mediterranean descent; also common in people from
the Caribbean, South and Central America, Middle East, and parts of India
• Greater than 230,000 affected children are born every year in sub-Saharan Africa.
• In North America and Europe, ∼2,600 and 1,300 affected children are born every year,
respectively (1).
Prevalence
• Prevalence of SCD is highest in sub-Saharan Africa.
• Affects 50,000–100,000 people in the US.
• 1 in every 600 African-Americans has SCD.
Morbidity
• Approximately 30% of patients have severe disease with widespread organ damage and
early death, 60% have a less devastating clinical course, and 10% remain relatively well
most of their life.
• Risk factors for increased perioperative morbidity include increased age, pregnancy, and
preexisting infections.
Mortality
• In the US, the mean age at death for men and women with SCD is 42 and 48 years,
respectively
• Organ failure is a significant cause of perioperative mortality
• Hemoglobin A (HbA) is the predominant hemoglobin in adulthood; it has 2α and 2β globin
chains. A single point mutation in the 6th codon on the α globin chain results in
substitution of valine for glutamic acid and hemoglobin S (Sickle Hb – molecular hallmark of
SCD). This defect creates a new hydrophobic spot on the outer portion of the molecule
(normally hydrophilic and in contact with plasma) (2).
• In both normal and sickle Hb, deoxygenated Hb results in a small hydrophobic patch; thus
in SCD, there is a double hydrophobic spot that seeks out and sticks to other hydrophobic
spots on other Hb molecules. As a result, deoxygenated Hb aggregates into chains; the
tetramers stick to each other and polymerize (form long fibers) instead of remaining
independent.
• Risk factors that favor “sickling”
– Hb deoxygenation secondary to hypoventilation and hypoxemia
– Decreased perfusion secondary to decreased cardiac output, hypotension,
hypovolemia/dehydration, and cardiopulmonary bypass
– Venous stasis secondary to patient immobility, extremity tourniquets, and improper
patient positioning
– Metabolic factors such as acidosis, hypothermia, and infection
– Alcohol binges, high altitudes, and prolonged airline flights also precipitate complications
in SCD patients.
• “Sickling” results in the normally pliable biconcave erythrocyte assuming a rigid sickle
shape on deoxygenation. This causes cell membrane damage, hemolysis, clogging of the
microcirculation, and ischemic organ damage with vaso-occlusive crises.
• Vaso-occlusive processes account for the majority of complications; clinical presentation
depends on the vascular bed affected
• Increased hemolysis
– Decreases the red blood cell lifespan from ∼120 days to ∼15 days, resulting in anemia.
– Disrupts intracellular nitric oxide (NO) metabolism and hence decreases NO
bioavailability. This causes increased endothelial oxidant and shear stress with resultant
endothelial inflammation and exacerbation of vasoconstriction and tissue ischemia (3).
• Oxyhemoglobin curve is shifted to the right (P50 = 31 mm Hg, compared to normal P50 =
27 mm Hg). This reflects the decreased affinity of Hb for oxygen.
Painful crises occur more commonly during pregnancy
• Pathophysiological changes that accompany SCD may necessitate a surgical procedure such
as splenectomy, cholecystectomy, skin grafting for leg ulcers, curettage of osteomyelitic
bone cavities, acute abdomen, orthopedic prosthetic surgery, Cesarean section, etc.
• Since reversal of the sickling process is difficult, the focus is on prevention. Thus, goals for
perioperative care include avoidance of acidosis, hypoxemia, dehydration, venous stasis,
and hypothermia.
• Patients may have increased narcotic requirements from chronic use.
SYMPTOMS
• Pain
• Fever
• Dyspnea, tachypnea
History
• SCD should be considered in patients of African-American descent.
• Exacerbations and hospitalizations
• Evidence of chronic organ damage including lung, kidney, liver, spleen, and brain
Signs/Physical Exam
• Vital signs including room air saturation and pain score
• Dactylitis is inflammation of an entire digit that can result from a vaso-occlusive crisis with
bone infarcts; it is a hallmark of severity of SCD.
• Cardiac assessment
• Respiratory evaluation for obstructive and restrictive lung disease
• Neurologic assessment
TREATMENT HISTORY
• Bone marrow transplant
• Exchange transfusions are used to alter the Hb level rapidly and to replace sickle cells with
normal cells. Thus, it reduces the concentration of sickle cells without increasing the
hematocrit, whole blood viscosity, or iron accumulation (the volume of HbA containing
cells infused is equal to what is removed). However, outcomes studies have not supported
its use.
• Blood transfusions to maintain a hematocrit greater than 30%. The efficacy of this has not
been demonstrated in a randomized trial. The Transfusion Alternatives Preoperatively in
Sickle cell disease (TAPS) is a randomized controlled trial that is currently being undertaken
to compare outcomes with and without transfusion (4).
MEDICATIONS
• Hydroxyurea increases Hb F production and has been shown to decrease pain episodes,
acute chest syndrome (ACS) events, and hospitalizations (5)[A].
• Folate
• Narcotics
• ACE inhibitors
Labs/Studies
• Sickledex test –screening for SCD – addition of reducing substance to peripheral blood smear
under microscope to demonstrate sickling
• Hb electrophoresis – More specific test to demonstrate HbS%
• Evaluation for end-organ damage
– CBC, coagulation studies – Anemia
– Renal function tests – BUN, creatinine, urinalysis for proteinuria, and occult infection
– Liver function tests and bilirubin levels
– EKG
– CXR, ABG, lung function tests
• Immediate preoperative Hb within 24 hours, since it may change rapidly.
• Blood type and screen to rule out alloantibodies from frequent transfusions.
• Central nervous system: Overt stroke is seen in up to 11% of patients before the 3rd decade of
life. Ischemic stroke is more common in the 1st decade, while hemorrhagic stroke occurs
more frequently in the 3rd decade. Risk factors for stroke include low Hb levels, elevated
leukocyte counts, elevated homocysteine levels, low HbF%, hypertension, or recent or
frequent ACS. Cognitive impairment from ischemic brain lesions can occur in the absence of
clinically overt stroke.
• Cardiovascular system: Anemia is compensated with a hyperdynamic circulation, expanded
plasma volume, and dilated cardiomyopathy at an early age.
• ACS: Caused by sequestration of sickled cells, fat embolism, and thrombosis in the
pulmonary vasculature. Frequent cause of hospitalization and leading cause of death. May
present as dyspnea, tachypnea, wheezing, fever, pleuritic pain, or a drop in Hb level. CXR
may reveal a new pulmonary infiltrate.
• Pulmonary: Chronic sickle lung disease is characterized by obstructive and restrictive lung
disease, dyspnea, pulmonary hypertension, and cor pulmonale
• Liver: Chronic hemolysis results in unconjugated hyperbilirubinemia that can manifest as
jaundice and pigmented gallstones.
• Abdominal crisis will require that the clinician rule out an acute abdomen.
• Skeletal system: Microvascular occlusion of bone marrow results in severe pain in the back,
femur, ribs and sternum, necessitating treatment with opioid analgesics. Can result in
dactylitis (early onset in severe disease) or Salmonella osteomyelitis.
• Renal: Dysfunction due to vaso-occlusion causing hematuria, decreased urine concentrating
capacity, glomerular injury, progressive proteinuria
• Spleen: Acute splenic sequestration of blood with life-threatening anemia, painful massive
splenomegaly, and cardiovascular collapse can occur. Over time, splenic atrophy can result
with the loss of splenic function due to vaso-occlusive autoinfarction; patients are more
susceptible to overwhelming bacterial infections that can be fatal.
• Skin: Painful ulcerations around the ankles are very common.
• Painful crisis is the most common reason for hospitalization; results from ischemia and
infarction precipitated by vaso-occlusion
• Other: Priapism, avascular necrosis of the femoral head, retinopathy, vitreous hemorrhage
and hyphema with sudden blindness, hearing loss.
• Dehydration should be corrected
• Preoperative prophylactic transfusion to a HCT goal of 30% is of potential benefit in
moderate and high-risk cases.
• Exchange transfusions may be considered prior to major surgery.
CLASSIFICATIONS
• Homozygous (HbSS): Trait is inherited from both parents
• Heterozygous (HbAS): Trait is inherited from one parent and HbA from the other parent;
sickle cell trait (SCT) patient is a carrier and will not exhibit the manifestations of SCD.
TREATMENT
Premedications
• Anxiolytic and pain medications as appropriate
• Shorter fasting times for pediatric patients
• Possibility of perioperative sickling and crises
INTRAOPERATIVE CARE
• General and regional anesthetics have both been used successfully.
• Neuraxial blocks. Vasodilation and improved pain control may be beneficial. Prophylactic IV
fluids should be administered to avoid hypotension.
Monitors
• Foley catheter may be needed to improve fluid management and resuscitation
• Invasive monitoring as dictated by the surgical procedure or patient’s disease
• Standard induction with drugs titrated to avoid hypotension
• Airway management as appropriate
Maintenance
• Oxygenation: Increased FiO2 and positive end-expiratory pressure may be necessary
• Perfusion: Fluid hydration, β agonists, or anticholinergics
• Transfusion should be based on an individualized assessment of surgical circumstances and
patient’s oxygen delivery.
• Normothermia should be fastidiously maintained; warm intravenous fluids, apply convective
warming devices, and consider warming the room.
• Meticulous positioning is essential.
Decision is based on surgical circumstances and concomitant preexisting complications.
FOLLOW-UP
BED ACUITY
ICU admission for patients with severe disease and undergoing major procedures
• Supplemental oxygen in the PACU and floor may avoid hypoxemia
• Hydrate with IV fluids
• Adequate treatment of postoperative pain with narcotics and/or regional blocks
• Ketorolac may be given (caution in patients with severe pulmonary and renal dysfunction)
• Antiemetics for PONV to avoid dehydration
• Acute pain service consult for pain crisis may be warranted
COMPLICATIONS
• Atelectasis – Chest physiotherapy and pulmonary toilet in the PACU and postoperatively
• Pain crisis: Pain scoring, effective analgesia with opiates, adjuvant analgesics with
nonsteroidals and acetaminophen, possible regional, pulmonary monitoring, psychological
support
• ACS: Oxygen, effective analgesia, incentive spirometry, antibiotics, transfusion, mechanical
ventilation if respiratory failure, steroids and NO may be of possible benefit.
REFERENCES
1. Rees DC, Williams TN, Gladwin MT. Sickle cell disease. Lancet. 2010;376:2018–2031.
2. Schnog JB, Duit AJ, Muskiet FAJ, et al. Sickle cell disease; a general overview. Neth J Med.
2004;62:364–374.
3. Firth PG, Head CA. Sickle cell disease and anesthesia. Anesthesiology. 2004;101:766–785.
4. TAPS RCT http://clinicaltrials.gov/ct2/show/NCT00512577
5. Brawley OW, Cornelius LJ, Edwards LR, et al. NIH Consensus Development Conference
statement: Hydroxyurea treatment for sickle cell disease. Ann Inter Med.
2008;148(12):932–938.
• Hypothermia
• Hemoglobin
CODES
ICD9
282.61 Hb-SS disease without crisis
ICD10
D57.1 Sickle-cell disease without crisis
CLINICAL PEARLS
• Goals for perioperative management include avoidance of hypoxia, acidosis, dehydration,
hypothermia, and venous stasis, as well as providing adequate pain control.
SMOKE INHALATION INJURY
Charles E. Cowles, Jr., MD
BASICS
DESCRIPTION
• Smoke inhalation can result in
– Injury to the airway due to superheated air, steam, or particulate matter
– Systemic toxicities from by-products of combustion
• Patients can present to the anaesthetist for initial airway management, surgery for burns and
other injuries, as well as pain management. Additionally, smoke inhalation injury can result
from operating room or airway fires.
EPIDEMIOLOGY
Prevalence
• Found in 5–35% of patients with burn injuries.
• In the US, there are 700,000 burn injuries per year (1).
Mortality
• Thermal burn injury (all-cause mortality): 25–65%
• Smoke inhalation injury accounts for the majority of fire-related deaths.
• Closed space fire
• Gas, electrical, chemical, steam, or scalding injuries.
• Smoke inhalation injury describes thermal injury to the airways, particulate irritation, and
gaseous-related injury.
– Presentation involves significant airway swelling and edema; and may be delayed
– Animal models suggest that calcitonin gene-related peptide (CGRP) plays a role in
increasing airway hyperemia, transvascular fluid flux, and respiratory malfunction.
Attenuation with an antagonist was shown to decrease edema and alveolar inflammation.
Future efforts may target this gene.
– Interleukin-8 (IL-8) also appears to play a role in the inflammatory pathogenesis. In
animal models, pretreatment with anti-IL-8 demonstrated attenuation of lung
permeability, suggesting another potential therapeutic target.
– Inducible nitric oxide synthase (NOS) also increases the effects of smoke inhalation injury;
inhibition of NOS has been shown to improve pulmonary gas exchange and reduce
pulmonary shunt fraction compared to controls.
• Particulate irritation to the airways can be seen with gas or flame burns. The pathogenesis
involves impaired motility of respiratory cilia. Additionally, it may also dissolve into
harmful substances.
• Gaseous-related Injury
– Carbon monoxide (CO) is a product of incomplete combustion that binds to ferric atoms in
hemoglobin to form carboxyhemoglobin. CO has a 260–300 times greater affinity to
hemoglobin compared to oxygen; thus it “displaces” oxygen and prevents binding and
impairs oxygen delivery to tissues. As a result, tissues resort to anaerobic metabolism with
resultant lactic acid production.
– Hydrogen cyanide is a by-product of burning synthetic polymer materials. Cyanide binds
to ferric ions in the mitochondrial electron transport chain; it prevents the final electron
transfer to oxygen and halts adenosine triphosphate (ATP) production. Tissues resort to
anaerobic metabolism, with resultant lactic acid production.
– Acrolein results from burning wood and petroleum products and causes protein
denaturation along the airways.
– Hydrochloric acid is formed from burning plastics and polyvinylchloride (PVC); it can
cause pulmonary edema and lethal arrhythmias.
– Toluene diisocyanate is produced from burning foam products, furniture, and insulating
materials; it causes severe bronchospasm upon exposure to lower airways.
• Maintain a high index of suspicion for smoke inhalation injury based on history and physical
exam. There should be a low threshold for securing the airway if thermal injury to the
airways is suspected or present. Similarly, CO or cyanide toxicity, if suspected, should be
confirmed and treated.
• In the event of an operating room fire, or rescue scene, make sure as a healthcare provider,
you do not become a victim. Evacuate yourself and the patient from the area of smoke or
fumes before initiating any care.
SYMPTOMS
Coughing, nausea, headache, confusion, somnolence
History
• Type of fire
• Duration of exposure
• Events leading to exposure
• Determine whether the fire was in an enclosed structure such as a building or vehicle
Signs/Physical Exam
• Facial burns, carbonaceous sputum, soot in the mouth, singeing of facial hair, and second or
third degree burns elsewhere on the body correlate strongly with associated airway injuries
(2).
• “Cherry Red” colored skin and mucosal surfaces are very late findings and are often noted
post-mortem.
TREATMENT HISTORY
• Intubation if airway edema is suspected
• High-frequency oscillatory ventilation (HFOV) has been shown to significantly improve
oxygenation in burn injury patients, but not in patients with smoke inhalation injury (3)[A].
• High concentrations of oxygen are required for the treatment of CO toxicity as a bridge
therapy until hyperbaric treatment can be provided. Hyperbaric oxygen therapy is the
delivery of 100% oxygen at increased atmospheric pressures. By providing an
overabundance of oxygen, CO is displaced from hemoglobin molecules.
MEDICATIONS
Hydroxocobalamin for cyanide toxicity; the cyanide antidote kit should be avoided because
nitrites can result in a methemoglobinemia that could be fatal if the patient also has high
levels of carboxyhemoglobin.
Labs/Studies
• Arterial blood gas (ABG) with carboxyhemoglobin level
• Electrocardiogram (EKG)
• Lactate levels (4)
• Acute respiratory failure from burn injury
• Acute renal failure from rhabdomyolysis
• Severe fluid redistribution in burn patients
• Due to significant associated morbidity and mortality, only emergency surgery should be
contemplated in the patient with suspected smoke inhalation.
• Carboxyhemoglobin levels >25% should be strongly considered for hyperbaric oxygen
therapy prior to any operative procedure.
TREATMENT
Premedications
Benzodiazepines and opioids can cause respiratory depression or affect hemodynamics; if
administered, should be done judiciously and with monitoring.
Attempts to obtain consent should be made, as with any emergency case. However, it should
not delay life-saving treatment
INTRAOPERATIVE CARE
• General endotracheal anesthesia is commonly chosen due to the emergent nature of cases
involving smoke inhalation and the need for a secured airway. Thus, regional and neuraxial
blocks as a sole anesthetic are not appropriate.
• Regional anesthesia such as nerve blocks and epidural anesthesia can be considered for
management of pain, but factors such as the patient’s ability to communicate, urgency of
the procedure, and hemodynamic stability should be strongly considered.
Monitors
• Arterial line for frequent blood gas measures and assessment of the pH
• Co-oximetry for detection of CO. The standard pulse oximeter and ABG are not capable of
distinguishing between carboxyhemoglobin and oxyhemoglobin (can yield falsely elevated
oxygen levels).
• If a difficult airway is anticipated, have a fiberoptic bronchoscope, indirect video
laryngoscope (Glidescope), jet ventilator, or surgical airway available. Consider utilizing
advanced techniques during the initial attempt.
• Smaller endotracheal tubes should be available; if burns affect the lips or nose, use of an
extended length, small diameter tube may be considered to accommodate swelling.
• Patients are considered to have a “full stomach” for recent burns; however, rapid sequence
inductions are contraindicated if a difficult airway is suspected. Consideration may need to
be made for an awake fiberoptic intubation.
• Succinylcholine should be avoided if the burn injury occurred >24 hours. The proliferation
of extrajunctional receptors can result in profound hyperkalemia.
• Etomidate is capable of maintaining good hemodynamic stability, but is associated with
adrenal insufficiency. This may be of concern if multiple surgeries are anticipated
Maintenance
• Volatile agents may result in further airway irritability and may even have impaired uptake
and elimination with severe lung injury.
• Fluid management should be guided by the associated burn injury and the time interval
since the burn injury. Patients who have developed lung injury are particularly susceptible
to pulmonary edema from excess fluid administration.
• Hypothermia can be an issue for all burn patients, and is exacerbated by the vasodilatory
effects of general anesthetics. Prevention of heat loss, the use of forced air warming
blankets, and increasing the ambient room temperature of the operating room may help
prevent hypothermia.
Use caution if recent burn injury to airways, as swelling may worsen during the first 24
hours. Consider leaving the patient intubated postoperatively with appropriate sedation.
FOLLOW-UP
BED ACUITY
Burn unit is the most suitable location
• Patient should be managed by a burn specialist and intensivist who is capable of managing
difficult airways and performing repeat bronchoscopies.
• Serial lactate and carboxyhemoglobin can aid with directing therapy in CO and cyanide
toxicity.
COMPLICATIONS
• Smoke inhalation may be an overlooked problem in patients with other trauma or with
distracting burn injuries.
• Hypoxemia is possible from progressive lung injury and systemic toxicities.
• Significant airway edema can occur in the first 24 hours after exposure, even if the initial
presentation appears unremarkable.
REFERENCES
1. all JR.Burns, Toxic Gases, and Other Hazards Associated with Fires: Deaths and Injuries in
Fire and Non-Fire Situations. Quincy, MA:. National Fire Protection Association, Fire
Analysis and Research Division, 2001.
2. Madnani DD, Steele NP, de Vries E. Factors that predict the need for intubation in patients
with smoke inhalation injury. Ear Nose Throat J. 2006;85(4):278–280.
3. Cartotto R, Walia G, Ellis S, et al. Oscillation after inhalation: High frequency oscillatory
ventilation in burn patients with the acute respiratory distress syndrome and co-existing
smoke inhalation injury. J Burn Care Res. 2009;30:199–227.
4. Baud F, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl
J Med. 1991;325:1761–1766.
ADDITIONAL READING
• Center for Disease Control. http://www.cdc.gov/HomeandRecreationalSafety/Fire-
Prevention/fireactivities.htm
• Undersea & Hyperbaric Medical Society. www.uhms.org
• Burns
• Cyanide toxicity
• Hyperbaric oxygen therapy
CODES
ICD9
987.9 Toxic effect of unspecified gas, fume, or vapor
ICD10
T59.814A Toxic effect of smoke, undetermined, initial encounter
CLINICAL PEARLS
• Early endotracheal intubation should be undertaken if airway burns are suspected, even if
the burn injury appears minor.
• Assess for carboxyhemoglobin levels; standard pulse oximetry is not capable of
distinguishing between carboxyhemoglobin and oxyhemoglobin. Early hyperbaric oxygen
therapy is beneficial for CO poisoning.
• Consider cyanide toxicity for cases involving closed spaces or structural fire, which is
treated with hydroxocobalamin and not a standard cyanide kit.
SMOKING
Jagan Devarajan, MD, FRCA
BASICS
DESCRIPTION
• Anaesthetists commonly encounter patients with both short and long term sequelae of
smoking and its associated pulmonary and cardiovascular complications in the perioperative
period.
• An upcoming surgery can provide an opportunity and motivation to quit smoking for ever,
as patients are forced to abstain due to non-smoking policies that are practiced by hospitals.
Thus, if possible, anaesthetists should play a role in counseling preoperatively, and as
healthcare providers, have a responsibility to advise for permanent cessation.
EPIDEMIOLOGY
Prevalence
• Approximately 1 in 5 adult Americans currently smoke.
• Higher in men (23.9%) than women (18%)
Morbidity
Smoking has adverse effects on every organ system in the body and reduces health in general.
It impairs physical fitness, endurance, and general well-being.
Mortality
Approximately 1 in every 5 deaths each year (443,000 deaths) is attributed to either direct or
indirect effects of smoking. More deaths are caused by smoking than that of HIV, illegal drug
use, alcohol behavior, and motor vehicle accidents combined.
• Smoke from tobacco has more than 25 carcinogens, though the most damaging products are
nicotine, tar, and carbon monoxide. The particulate phase contains at least 3,500
compounds, mostly carcinogens and free radicals.
• Tobacco has nicotine (2–5%), sugars (mainly reduced) (8–25%), and moisture (10–14%).
Nicotine stimulates preganglionic autonomic receptors, resulting in the release of epinephrine
from adrenal glands, norepinephrine from nerve endings, and dopamine and endorphins from
the central nervous system. They are responsible for different perceptions and behaviors,
including the euphoria associated with smoking. Hence, it is a highly addictive substance.
Smoking cessation: Ideally smoking should be stopped 8 weeks prior to surgery (patients
should be advised at the surgeon’s office or at the time of scheduling). If that does not occur
or the patient is unable to stop, abstinence should be recommended for at least 24 hours prior
to surgery, or the evening before surgery to decrease the deleterious effects of nicotine and
carbon monoxide.
SYMPTOMS
COPD and cardiovascular symptomatology should be sought.
History
• Pack year history
• Respiratory: Infections, recent COPD exacerbations, dyspnea, increased fatigability.
• Cardiovascular: Evidence of coronary artery disease (CAD) (e.g., previous MI and chest pain)
and peripheral vascular disease (e.g., claudication and rest pain).
Signs/Physical Exam
Respiratory and cardiovascular symptomatology should be sought.
TREATMENT HISTORY
Counseling
MEDICATIONS
• Nicotine replacement therapy
• Bupropion, an atypical antidepressant
Labs/Studies
• Pulmonary function tests (PFTs) would demonstrate an obstructive pattern (decrease in
FEV1 that is greater than the decrease in FVC, and a decreased FEV1/FVC ratio).
• Arterial blood gas can show hypoxia, hypercapnia
• Co-oximetry can measure carbon monoxide levels
• Pulmonary system: Most common cause of lung carcinoma and COPD. Perioperatively,
smoking increases airway irritability, sensitizes the reflex responses to chemical irritants,
and increases mucus production. Bronchial mucus transport during general anesthesia is
further slowed in smokers compared with nonsmokers. Carbon monoxide decreases oxygen
binding to hemoglobin and thus decreases overall blood oxygen content. Smoking is
associated with increased incidences of perioperative laryngospasm, bronchospasm,
episodes of desaturation, development of pneumonia, respiratory failure and unanticipated
ICU admission and requirement of ventilatory support.
• Cardiovascular system. Increases the risk of developing CAD, cerebrovascular disease, and
stroke by 2–4 times. By accelerating atherosclerosis, it indirectly contributes to
perioperative cardiac morbidity and mortality. Carbon monoxide present in smoke can
injure myocardium due to chronic exposure and increases the myocardium’s susceptibility
to viral infections, cardiomyopathy, and CHF. Perioperatively, smoking increases heart rate,
BP, and myocardial contractility, thereby increasing myocardial work and oxygen
consumption. It also increases plasma levels of catecholamines.
• Hepatic system. Induces the liver microsomal enzymes; thus, medications that undergo
hepatic metabolism may require increased dosing (e.g., benzodiazepines and morphine)
• Endocrine system: Increases secretion of antidiuretic hormone resulting in dilutional
hyponatremia
• Hematologic system: Associated with increase in production of hemoglobin, RBCs, WBCs,
platelets, and fibrinogen. Despite an increased incidence of thromboembolic disease in
smokers, the relative risk of deep venous thrombosis (DVT) is not higher than that of
nonsmokers.
• Wound and bone healing. Impairs immune response. Smokers are more likely to develop
postoperative complications related to wound healing such as dehiscence and infection. It
also has been shown to contribute to impairment of bone healing and nonunion of spinal
fusions. In patients undergoing knee and hip replacements, smoking cessation decreased
wound infection from 23% to 4%.
• Mutagenicity. Increases the risk of developing cancer of the lung, oral cavity, kidney,
urinary bladder, cervix, stomach, and uterus.
• Maternal/fetal heath. Increases the risk of infertility, abortions, ectopic pregnancy,
premature rupture of membranes, and placenta previa and abruption. The risk of
prematurity and low birth weight, still birth, and sudden infant death syndrome is higher in
children born to smoking mothers compared to nonsmokers
Acute COPD exacerbation
TREATMENT
Premedications
• Anxiolytic medications can reduce the psychological effects of smoking cessation.
• Bronchodilators in patients who show a reversible bronchospastic component to their
reactive airway disease.
• Antibiotics in those who have active respiratory tract infections.
• Pulmonary toilet. Humidification and chest physical therapy to improve secretion clearance;
incentive spirometry education.
• Steroids may be considered in patients with moderate-to-severe reversible airway disease;
however, their effects are not immediate and need to be weighed against potential risks.
Postoperative pulmonary complications such as respiratory failure, unanticipated intensive
care admission, pneumonia, laryngospasm, bronchospasm, and increased requirement of
postoperative respiratory therapy and aerosol therapy
INTRAOPERATIVE CARE
• Local or regional anesthesia are often preferable to general anesthesia (avoids airway
manipulation, positive pressure ventilation, and unpredictable interactions with opioids).
• Neuraxial techniques for surgical anesthesia. Motor blockade above the T10 level can
markedly decrease the forced expiratory flow in patients with impaired pulmonary function.
• Epidural analgesia for postoperative pain can facilitate deep breathing and coughing and
improves respiratory care.
Monitors
• Pulse oximetry: Beware of overestimation of oxygen saturation due to the presence of
carboxyhemoglobin. May require pulse oximetry with multiple wavelengths to attain
accurate readings.
• Electrocardiogram with ST segment analysis can help detect myocardial ischemia.
• Arterial line. In major surgeries, especially neurosurgical cases, paCO2 measurements are
highly recommended to estimate the paCO2 – EtCO2 gradient (smokers have elevated
gradients).
• Preoxygenation (denitrogenation) with 100% oxygen can negate the effects of increased
closing capacity and carbon monoxide levels.
• Any IV induction agent at adequate dosages is satisfactory. Although thiopental does not
cause bronchospasm, it does not blunt reactivity.
• IV lidocaine is useful during induction to decrease airway reactivity to intubation, or,
alternatively, one can spray lidocaine on the vocal cords before intubation.
• Airway manipulation and surgical stimulation should be avoided during the “excitatory
stages” of anesthesia to decrease the incidence of respiratory-related adverse events.
Maintenance
• Volatile agents are preferred due to their salutary effects on bronchial reactivity. Avoid
introduction of high concentrations of desflurane during induction to prevent breathholding
and laryngospasm. Desflurane stimulates respiratory irritant receptors in chronic smokers
and thereby the sympathoadrenal system, resulting in higher BPs and tachycardia. Nitrous
oxide is not contraindicated in patients without bullous emphysema; however, underlying
respiratory pathology may decrease the patient’s ability to tolerate decreased FiO2.
• Neuromuscular blockade. If utilized, neuromuscular monitoring is mandatory for the
titration of muscle relaxants. Nicotine stimulates nicotinic acetyl cholinergic receptors in
small plasma concentrations resulting in increased requirement of muscle relaxants to
induce and maintain neuromuscular blockade. This effect, however, is not uniform among
all muscle relaxants. Monitoring will help to prevent bucking and bronchospasm during
maintenance.
• Extubation in the excitatory stage of anesthesia can result in laryngospasm, bronchospasm,
and breath holding. Consider a “deep extubation,” if appropriate.
• Nicotine may have antinociceptive effects and decrease the incidence of nausea and
vomiting. However, prophylactic antiemetics should still be considered.
FOLLOW-UP
BED ACUITY
Dependent on surgical procedure, intraoperative events, and the need for postoperative
intubation and mechanical ventilation
• Oxygen therapy usually will be required in the PACU and occasionally on the nursing floor.
• Requirement of analgesics often will be higher due to increased metabolism of drugs and
decreased pain threshold. Patient-controlled analgesia (PCA) is highly recommended.
Regional, epidural, and field blocks should be considered, if appropriate.
• Breathing exercises, physical therapy, and incentive spirometry are mandatory.
• DVT prophylaxis
• Surveillance of wounds to facilitate early detection and treatment of wound infections
• Nicotine patches may be prescribed to prevent nicotine withdrawal. Nicotine patches are not
known to increase wound infections.
COMPLICATIONS
Nicotine withdrawal, inadequate pain control, poor wound healing, DVT, PPC
REFERENCES
1. CDC. Cigarette smoking among adults – United States, 2006. MMWR. 2007;56:1157–1161.
2. Turan A, Mascha EJ, Roberman D, et al. Smoking and perioperative outcomes.
Anesthesiology. 2011.
3. Warner DO. Perioperative abstinence from cigarettes: Physiologic and clinical
consequences. Anesthesiology. 2006;104:356–667.
• Oxygen-carrying capacity
CODES
ICD9
305.1 Tobacco use disorder
ICD10
Z72.0 Tobacco use
CLINICAL PEARLS
• All hospitals are nonsmoking, forcing patients to adopt a nonsmoking behavior, which will
give them the chance to experience the effects of abstinence from smoking and to explore
options for continued cessation in the future.
• Anaesthetists should follow the simple three-step system approach designed by the ASA
Smoking Cessation Initiative Task Force:
– A – Ask a patient about smoking status
– A – Advise smokers to quit, and
– R – Refer smokers to free national telephone quit line
• Anaesthetists should also advise and help smokers to stop smoking during the postoperative
ward rounds. Patients who develop smoking-related complications are shown to be
compliant with the postoperative instructions.
• Pulmonary effects of smoking cessation. Ciliary function improves in 48–72 hours; sputum
production decreases in 1–2 weeks; pulmonary function improves after 4–6 weeks; and the
immune function of alveolar macrophages improves in 6–8 weeks. The incidence of PPC
was not different between patients who continued to smoke until surgery (48%) and those
who quit within 8 weeks before surgery (56%). In contrast, those who quit >8 weeks before
surgery (17%) had a rate of PPCs similar to that of nonsmokers (11%).
• Cardiovascular effects of smoking cessation. Even a short period of abstinence should have
beneficial effects on the cardiovascular system, as the major culprits such as nicotine and
carbon monoxide have short elimination half lives (1 and 4 hours, respectively). At 8 hours,
BP and heart rate decrease. As CO levels return to normal in 12–24 hours, O2 levels and
body temperature increase to normal. At 24 hours, the risk of acute coronary event
decreases. By 1 year, there is a 50% reduction in the risk of CAD. By 5 years, CVA and CAD
risk is reduced to that of nonsmokers.
• This cessation of smoking for 1 or 2 days can produce excessive anxiety, increased secretion
of mucus, as well as a bronchospastic and hypercoagulable state. Nevertheless, these
symptoms can be managed with anxiolytics, bronchodilators, and anticoagulants. By
continuing not to smoke in the perioperative period, patients may benefit in the long term.
SOMATOSENSORY- AND MOTOR-EVOKED POTENTIALS (SSEP
AND MEP)
BASICS
DESCRIPTION
• Evoked potentials are electrophysiologic responses of the nervous system to stimulation of
either sensory or motor pathways.
• Monitoring somatosensory-evoked potentials (SSEPs) and motor-evoked potentials (MEPs)
can aid with assessing the integrity of the brain, brainstem, spinal cord, and peripheral
nervous system during surgeries where these structures are at risk for injury.
• Intraoperative changes in evoked potentials can be due to ischemia, surgical injury, and
physiologic and pharmacologic influences. Physiologic factors include carbon dioxide and
oxygen tension, BP, acid–base balance, hematocrit, and temperature.
• To the anaesthetist, the effect of the various anesthetic agents used is of paramount
importance as to assure proper anesthetic depth and hemodynamics in addition to gaining
proper monitoring conditions.
• SSEP monitoring was first adopted in the 1980s and their advent improved neurological
outcome. However, there were instances where patients would suffer from motor deficits
because SSEPs do not monitor motor pathways.
– Transcranial stimulation developed in the mid-1980s and allowed for integrity assessment
of the motor pathway, but the initial quality of the MEPs was poor.
– The introduction of high frequency multi-pulse stimulation in the early 1990s (and now
post-tetanic MEPs) significantly improved recordings.
• Evoked potentials are a measurement of electrical potentials in response to stimulating the
nervous system via electrical, sensory, or magnetic stimulation.
• SSEPs are used to assess the integrity of the sensory pathway.
– Spinal cord transmission is via the posterior spinal cord and the blood supply is via a pair
of posterior spinal arteries.
– Generation of stimuli is typically via electrodes and electrical current being applied near
peripheral nerves (e.g., median nerve, posterior tibial nerve, and peroneal nerve); the
impulse travels cephaladly along the posterior cord.
– Recordings of the transmitted electrical potential are made at subcortical levels (e.g., neck,
spine, and epidural space) or at the cortical levels from the scalp or cerebral cortex on the
contralateral side.
– The potentials generated in this fashion are small compared to the EEG; therefore
repetitive stimulation and summation, in addition to computer averaging, are used to gain
a stable waveform.
– Amplitude is the peak-to-trough voltage difference. Amplitude changes are expressed as a
percentage change from baseline recordings.
– Latency is the time from stimulation to peak response. It is dependent on the location of
the recording (i.e., it takes more time for the impulse to travel to a subcortical versus a
cortical level). Again, the change in latency is determined by comparing baseline
recordings to later recordings.
• MEPs are used to test the integrity of the motor pathways.
– Spinal cord transmission is via the anterior spinal cord and the blood supply is comprised
of a single anterior spinal artery (arises from the vertebral arteries) that is supplemented
in the caudal cord by anterior segmental medullary arteries and the artery of
Adamkiewicz.
– Generation of the potential occurs transcranially at the motor cortex via electrical or
magnetic stimulation and travels caudally to the peripheral nerves.
– Recordings take place at the spinal nerves, peripheral nerves, or distal muscle level.
– Unlike SSEPs, MEPs have large interpatient variability. Changes in amplitude and latency
from baseline to later recordings have little clinical relevance. Therefore, MEPs most often
are recorded as being either present or absent.
ANATOMY
• SSEPs travel along the following pathway:
– Peripheral stimulus
– Peripheral nerve
– Dorsal root ganglia
– First-order fibers in the posterior column nuclei
– Second-order fibers crossing to the opposite site
– Medial lemniscus to the thalamus
– Third-order fibers to the frontoparietal sensorimotor cortex
• MEPs travel along the following pathway:
– Motor cortex stimulation
– Corticospinal tract
– Anterior horn of spinal cord
– Peripheral motor nerve
There are many diseases and conditions affecting SSEPs and/or MEPs. They include any
physical lesion along the conducting pathway; chronic renal failure, hepatic encephalopathy,
hyperthyroidism, diabetes mellitus, myoclonus epilepsy, stroke, coma; Friedreich’s ataxia,
Guillain–Barré syndrome, leukodystrophies, multiple sclerosis, polyneuropathy, and Reye’s
syndrome.
• SSEP monitoring. The exact criteria of what constitutes clinically relevant changes are
lacking.
– Latency: changes of 7–10% can occur without resultant neurological deficits. Typically an
increase of 50% indicates neurological sequelae.
– Decreased amplitude is considered a more sensitive indicator than increased latency.
• Volatile anesthetics and SSEPs. Inhibit synaptic transmission to a greater extent than axonal
transmission.
– Manifests as dose-dependent decreases in amplitude and increases in latency. In addition,
they can cause morphologic changes in the waveform.
– There is less effect on readings when recordings are made at the cortical level in patients
with good baselines, even at one MAC (and possibly up to 1.3 MAC with sevoflurane and
desflurane) in the majority of subjects, if no nitrous oxide is used.
– There is a greater effect on readings when recorded further away from the generator (e.g.,
at the cortical rather than the spinal level).
• Nitrous oxide and SSEPs:
– Dose-dependent decreases in cortical amplitude with intact latency occur at
concentrations of 60–70%.
– Equipotent levels (in terms of MAC) depress readings greater than volatile anesthetics and
most IV anesthetics.
• IV anesthetics affect SSEPs to a lesser extent than volatile anesthetics.
– Propofol is similar to barbiturates in terms of SSEP modulation. Even large induction
doses of 2.5 mg/kg usually do not produce amplitude changes, but may increase latency
up to 20%. TIVA with propofol/opioid may initially cause significant decreases in
amplitude and increases in latency, but these usually return to baseline after 30 minutes.
– Etomidate will actually increase cortical amplitude up to 400%, but may decrease
subcortical amplitude by up to 50%.
– Ketamine will also increase cortical amplitude, but has no effect on subcortical
waveforms.
– Barbiturates at high doses allow for SSEP recordings, but may increase latency and
decrease amplitude.
– Opioids at high doses have minimal effects. Overall, on an equipotent basis, a
propofol/opioid technique will cause less amplitude reduction and latency increase than
other techniques.
– Benzodiazepines do not have a significant effect; at high doses, they can have a moderate
effect at best.
– Neuromuscular blocking drugs have no influence on SSEPs and may actually improve
recordings by eliminating eletromyogenic artifacts.
– Other drugs such as clonidine, dexmedetomidine, adenosine, and droperidol have a
minimal effect on SSEPs.
• Regional anesthesia diminishes or even eliminates SSEPs depending on the density of the
block.
• Metabolic effects on SSEPs:
– Hypothermia will increase latency, but amplitude changes are variable. SSEPs are
preserved at temperatures where the EEG is isoelectric.
– Hypocarbia decreases latency; it has no effect on amplitude in anesthetized subjects. Mild
hypercarbia has no effect.
– Mild hypoxia (to a paO2 of 48 mm Hg) does not affect SSEPs. However, worsening
hypoxia will decrease amplitude and increase latency.
– Hypotension below the level of autoregulation will decrease amplitude without affecting
latency.
– Hemodilution affects amplitude as follows: Increases at a Hct between 16% and 20% and
decreases at a Hct between 11% and 15%.
• MEP monitoring. The stimulus technique now employs multi-pulse stimulation in order to
increase response amplitudes. In general, MEPs have a large inter- and intrapatient trial-to-
trial variability. Because of this large variability, no specific criteria to warn of impending
injury have been established. Therefore, some will regard MEPs as either present or absent
to make clinical decisions.
• Volatile agents and MEPs:
– Low levels can significantly affect readings.
– Isoflurane can be used up to 0.5 MAC only if multi-pulse stimulation is used.
– Concentrations of 0.75 and 1 MAC will yield adequate responses in only 61% and 8% of
the time, respectively.
– Direct stimulation of the motor cortex will allow for concentrations of up to 1.5 MAC
isoflurane or sevoflurane.
– Measurements at the spinal level allow for higher levels of volatile agents without an
effect on readings (levels up to 1 MAC have minimal effect).
• Nitrous oxide and MEPs:
– Concentrations up to 50% added to agents such as opioids, ketamine, and low-dose
propofol (up to 50 μg/kg/min) will not cause significant myogenic responses if multi-
pulse stimuli are used.
– Higher doses of nitrous oxide will reduce amplitudes.
– Spinally recorded MEPs allow for concentrations of up to 70%.
• IV agents and MEPs:
– Propofol has become the first choice agent when obtaining MEPs because of its rapid
metabolism, titratability, and quick emergence. There is, however, a limit beyond which
propofol will depress MEPs. Infusion rates of 75–100 μg/kg/min will cause MEP
depression in 33–83% of patients. Above this rate, adequate MEPs were obtained in only
60–88% of patients. This depression cannot be overcome by increasing impulse numbers
per stimulation.
– Etomidate is the ideal agent for MEP acquisition. Induction doses of 0.3 mg/kg will
suppress MEPs for 2–5 minutes and then return to baseline. Etomidate infusions of 10–30
μg/kg/min will yield excellent MEPs. Depression of the adrenocortical axis due to
etomidate infusion needs to be carefully weighed against obtaining quality MEPs.
– Thiopental will cause loss of MEPs at total doses of 4–9 mg/kg.
– Methohexital infusions of 100 μg/kg/min with ketamine (20 μg/kg/min) and 25% nitrous
oxide will yield adequate myogenic MEPs even with single train stimulation.
– Under single pulses, methohexital and etomidate infusions will yield better MEPs than
propofol at equipotent doses.
– Ketamine, like etomidate, is an excellent choice for obtaining MEPs. It should be strongly
considered when a subject’s baseline MEPs may be marginal to begin with.
– Opioid infusions have minimal effects on MEPs obtained by multi-train stimulation. Bolus
doses (e.g., fentanyl) can depress MEPs for several minutes. Remifentanil is less
suppressive than other opioids and may be an ideal choice.
– Benzodiazepines cause less depression than propofol or thiopental. Usual doses given as
premedication pose no problems. Infusions of midazolam at 0.1 mg/kg/hr have no effect
on MEPs.
– Partial neuromuscular blockade to a single twitch height of 20–50% of baseline will aid
with surgical exposure, if needed, while still allowing for acquisition of MEPs. Higher
levels of paralysis will increase trial-to-trail variability and reduce amplitude. Less
paralysis will reduce response variation. Patients with preexisting neuromuscular
weakness should not be paralyzed as to avoid loss of MEPs. When using partial paralysis,
twitch height has to be monitored in the same muscle groups used for MEP acquisition.
• Metabolic effects on MEPs:
– Clinically relevant temperatures (32–38°C) have little effect.
– Deliberate hypotension to a mean BP of 60 mm Hg has little effect.
– MEPs during complete ischemia of the lower limbs and the spinal cord can occur after 2
minutes if measured at the myogenic level, but take up to 30 minutes if measured as
spinal potentials.
EQUATIONS
• Amplitude = Peak-to-trough voltage difference.
• Latency = time from stimulus to peak response.
REFERENCES
1. Banoub M, Tetzlaff JE, Schubert A. Pharmacologic and physiologic influences affecting
sensory evoked potentials. Anesthesiology. 2003;99(3):716–737.
2. Kumar A, Bhattacharya A, Makhija N. Evoked potential monitoring in anesthesia and
analgesia. Anesthesia. 2000;55(3):225–241.
3. Kawaguchi M, Hayashi H, Yamamoto Y, et al. Recent advances in monitoring of myogenic
motor-evoked potentials: Development of post-tetanic motor evoked potentials. J Anesth.
2008;22(4):489–492.
4. Lotto ML, Banoub M, Schubert A. Effects of anesthetic agents and physiologic changes on
intraoperative motor evoked potentials. J Neurosurg Anesthesiol. 2004;16(1):32–42.
5. Sloan TB, Janik D, Jameson L. Multimodal monitoring of the central nervous system using
motor-evoked potentials. Curr Opin Anesthesiol. 2008;21(5):560–564.
CLINICAL PEARLS
• Regional anesthesia diminishes or even eliminates SSEPs and MEPs depending on the
density of the block.
• TIVA with agents such as ketamine, etomidate, midazolam, and low infusion rates of
propofol will yield the best MEPs and excellent SSEPs.
• Patients who need MEP monitoring will need to have a soft bite block in place.
• Close cooperation between the anaesthetist, surgeon, and electrophysiologist is needed to
state monitoring goals and create a plan ahead of the procedure to obtain optimal
monitoring results.
• Avoid anesthetics and physiologic changes as much as possible during critical parts of an
operation (e.g., distraction during scoliosis surgery) to avoid confounding factors to the
SSEPs and MEPs.
SPINAL SHOCK
Laura B. Hemmer, MD
Antoun Koht, MD
BASICS
DESCRIPTION
• Spinal shock describes the transient loss of spinal cord function distal to a complete or
incomplete acute spinal cord injury (SCI). It may last several weeks, and possibly months.
• A low systemic vascular resistance (SVR) state (with hypotension) and bradycardia often
coexist with acute SCI. These hemodynamic perturbations are known as neurogenic shock (a
separate entity from spinal shock).
• The presence of spinal shock is important in the determination of injury levels and
prognosis; and it may confound the accurate assessment of neurological status in the post
injury period.
• In the immediate/acute post injury period, priority should be to reduce secondary injury
and prevent an incomplete injury from progressing. In later months, when patients are
likely to present for urological and other procedures, special attention to avoid
complications of hyperreflexive responses may be required.
EPIDEMIOLOGY
Prevalence
In the US, the incidence of SCI is ∼12,000 cases per year (1).
Morbidity
Hypotension is associated with progression of secondary neurologic injury (1).
• The exact definition/model of spinal shock is controversial (2). It is commonly considered to
be a transient physiological interruption of spinal cord function caudal to the injury that
results in areflexia, flaccid paralysis, loss of sensation, and loss of temperature regulation.
Four phases have been proposed:
– Phase 1 (0–24 hours post injury). Absent deep tendon reflexes (DTRs) and flaccid muscles
that are largely due to a loss of supraspinal excitatory input. Impaired sympathetic
innervation also occurs during this phase.
– Phase 2 (1–3 days post injury). Initial reflex return via supersensitivity to
neurotransmitters.
– Phase 3 (4 days to 1 month post injury). Early hyperreflexia via replacement synapse
growth; most DTRs reappear and acute hemodynamic perturbations improve during this
phase.
– Phase 4 (1–12 months post injury). Spasticity and hyperreflexia via continued synapse
growth (axon-length-dependent timeframe) (2).
• SCI interferes with the ability of the spinal cord to autoregulate its blood flow, so perfusion
becomes more pressure dependent (1). Additionally, concomitant injuries and neurogenic
shock may compound hemodynamic perturbations. Secondary ischemic SCI is likely
mitigated with supportive measures.
– Maintain mean arterial BP in the high-normal range (> 90 mm Hg) (1)[B]. Based on
studies in traumatic brain injury, blood pressure support is usually continued for the first
7 days after injury (1)[C].
– Avoid hypoxia (paO2 ≤60 mm Hg) (1)[C].
– Avoid acute anemia (1)[C].
• Special precautions during airway management may be required; discuss the cervical spine
stability/clearance status with the spine surgeon.
• Succinylcholine should be avoided after 48–72 hours of denervation states, as described
below (3)[C].
SYMPTOMS
• Inquire about motor and sensory function and the presence of dyspnea and/or increased
work of breathing.
• In the chronic SCI patient, inquire about hyperreflexia symptoms (e.g., headache or blurred
vision with bowel/bladder distention).
History
Elicit the time and mechanism of SCI, level of cord injury, and rule out concomitant
hypovolemic shock from blood loss and other injuries in the trauma patient.
Signs/Physical Exam
• Perform a routine preanesthesia exam including a careful airway exam and assessment for
cervical spine stability.
• A detailed sensory and motor exam should be performed and documented in the acute post
injury period as a baseline and to compare to the postoperative exam.
TREATMENT HISTORY
• Phase 1–2: Fluid resuscitation, blood product administration, and use of experimental
hypothermia therapy.
• Phase 3–4: Prior anesthetic records, including intubation details, and prior tracheostomy
history.
MEDICATIONS
Phase 1–2: Vasopressors, vagolytics, and use and timing of corticosteroids (controversy exists
regarding efficacy of glucocorticoids) (1).
Labs/Studies
• Basic metabolic panel, complete blood count, coagulation studies
• Type and Screen/Cross, depending on expected blood loss
• EKG (acute higher level SCI can interrupt sympathetic fibers and cause unopposed
parasympathetic activity; bradycardia is common. Other arrhythmias have also been
reported).
• Chest x-ray (pulmonary edema is possible with aggressive fluid administration).
• Serial vital capacity measurements and arterial blood gases to monitor for respiratory
decompensation in nonmechanically ventilated patient with possible SCI-induced
respiratory dysfunction.
• Cardiovascular dysfunction with neurogenic shock. A relative bradycardia may be present
instead of the expected compensatory tachycardia with hypotension (1). This is most
common within the first couple weeks after injury; bradycardia is most prevalent on Day 4
after injury (4).
• Respiratory dysfunction (restrictive pattern) depending on the level of SCI.
• Other traumatic injuries, such as subdural hemorrhage or thoracic, abdominal, and
orthopedic injuries.
Early emergent surgical decompression may be necessary. Unless the patient requires acute
hemodynamic stabilization, emergency surgery should not be delayed.
TREATMENT
Premedications
• For recent trauma, patients are considered to have a full stomach. Drugs should be
administered to decrease gastric fluid volume and increase gastric fluid pH (e.g.,
nonparticulate antacid, H2-receptor antagonist, and gastrokinetic agent).
• If a fiberoptic intubation is planned, consider an antisialagogue to decrease secretions and
improve visualization.
• Determine if methylprednisolone has been administered or is being infused; NASCIS dosing
(controversial) is 30 mg/kg bolus and 5.4 mg/kg/hour maintenance for up to 48 hours post
injury (1).
• Acute SCI patient: Possible prolonged intubation and mechanical ventilation requirements
depending on respiratory dysfunction; possible hemodynamic instability depending on the
degree of neurogenic shock and concomitant injuries may require the placement of invasive
monitors; patient counseling if awake intubation is planned.
• Chronic SCI patient: Possible hemodynamic instability with autonomic hyperreflexia (may
require invasive monitoring).
INTRAOPERATIVE CARE
• General anesthesia for vertebral decompression. Avoid anesthetic techniques that interfere
with the postoperative neurological exam.
• For chronic SCI, consider regional or neuraxial techniques, as appropriate for the planned
surgery.
Monitors
• In the acute post injury phase, placement of arterial lines (continuous blood pressure
monitoring) and central venous catheters (assess preload, help guide fluid management, and
administer vasoactive drugs) is routine (1)[C].
• Pulmonary artery catheterization may be considered depending on the degree of
hemodynamic derangements.
• Neuromonitoring (may include somatosensory and motor evoked potentials and
electromyography) for spine surgery.
• Decompress the stomach and bladder unless contraindicated since SCI can cause gastric
paresis and/or dystonic bladder; organ distension may contribute to autonomic dysfunction.
• Maintain cervical spine immobilization for an uncleared spine. There is no outcome data to
support one intubation technique over another (5)[C].
– Awake fiberoptic intubation with topical anesthesia allows the head and neck position to
remain in a neutral position, maintains protective airway reflexes, and allows for
neurological exam postintubation.
– Direct laryngoscopy with manual in-line immobilization or other techniques can also be
considered.
– Application of cricoid pressure, if clinically indicated, is permissible in cervical spine
injury (5)[C].
• Select a hemodynamically stable induction regimen (e.g., etomidate and ketamine).
• Avoid succinylcholine for muscle relaxation after 48–72 hours of denervation states (risk of
lethal hyperkalemia from up-regulation of muscle nicotinic acetylcholine receptors) (3)[C].
Many anesthesia providers avoid succinylcholine after even shorter durations (24 hours) of
denervation states as a further precaution against hyperkalemia.
Maintenance
• Balanced technique with intravenous and/or volatile agents. Neuromonitoring may require
limiting volatile agents and avoiding neuromuscular blocking agents.
• Acute post injury phase:
– Volume resuscitate to increase preload. Fluids may include crystalloids, colloid, and blood
products. Optimal type of fluid therapy is unknown. However, hypotonic fluids are usually
avoided since they can worsen cellular swelling.
– Administer vasopressors to restore vasomotor tone and inotropes to increase cardiac
output. Choice of therapy depends on the hemodynamic condition of the patient; no
specific algorithm exists to guide choice of therapy.
– Intraoperative blood loss may be considerable and utilization of blood cell salvage is
helpful.
• Prompt emergence is desired to facilitate a neurological exam.
• Extubate when the patient is fully awake, following commands, and able to manage and
protect their airway. Laryngeal edema may be present (especially after long spine surgery
requiring large volume fluid resuscitation in the prone position); consider cuff-leak test
prior to extubation.
• Hypoxemia and endobronchial suctioning may worsen bradycardia from unopposed vagal
stimulation (4).
FOLLOW-UP
BED ACUITY
Invasive hemodynamic monitoring and support in the intensive care unit is usually continued
for 7 days post injury, based on studies in traumatic brain injury (1)[C].
Multidisciplinary care is required including neurosurgery and/or orthopedic surgery, critical
care, physiatry, and social service management.
COMPLICATIONS
• Pulmonary dysfunction: Consider aggressive chest physiotherapy and, if prolonged
intubation/mechanical ventilation is anticipated, consider tracheostomy.
• Venous thromboembolism: Consider mechanical and/or anticoagulant prophylaxis.
• Skin breakdown: Prevent unnecessary pressure points and monitor contact areas.
• Stress ulceration: Initiate prophylaxis with H2-receptor antagonist or proton pump inhibitor.
REFERENCES
1. Gupta R, Bathen ME, Smith JS, et al. Advances in the management of spinal cord injury. J
Am Acad Orthop Surg. 2010;18:210–222.
2. Ditunno JF, Little JW, Tessler A, et al. Spinal shock revisited: A four-phase model. Spinal
Cord. 2004;42:383–395.
3. Martyn JAJ, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic
states. Anesthesiology. 2006;104:158–169.
4. Guly HR, Bouamra O, Lecky FE. The incidence of neurogenic shock in patients with
isolated spinal cord injury in the emergency department. Resuscitation. 2008;76:57–62.
5. Crosby ET. Airway management in adults after cervical spine trauma. Anesthesiology.
2006;104:1293–318.
ADDITIONAL READING
• Fehlings MG, Rabin D, Sears W, et al. Current practice in the timing of surgical intervention
in spinal cord injury. Spine. 2010;35:S166–173.
• Veale P, Lamb J. Anaesthesia and acute spinal cord injury. BJA (CEPD Reviews).
2002;2:139–143.
• Wuermser LA, Ho CH, Chiodo AE, et al. Spinal cord injury medicine. Acute care
management of traumatic and nontraumatic injury. Arch Phys Med Rehabil. 2007;88:S55–
61.
• Neurogenic shock
• Autonomic hyperreflexia/dysreflexia
• Somatosensory and motor evoked potentials (SSEPs and MEPs)
CODES
ICD9
958.4 Traumatic shock
ICD10
T79.4XXA Traumatic shock, initial encounter
CLINICAL PEARLS
• Spinal shock is a transient loss of spinal cord function that can occur after acute SCI.
Neurogenic shock, with hypotension and bradycardia, often coexists with spinal shock.
• Secondary SCI may be mitigated with supportive measures. Avoid hypotension and hypoxia
and maintain elevated mean arterial pressure.
SPIROMETRY
Timothy T. Tran, MD
BASICS
DESCRIPTION
• Spirometry reflects respiratory mechanics. It describes the relationship between maximal
forceful exhaled volume (following maximal inspiration) and time.
– It is safe, inexpensive, and noninvasive.
– Maximal and reproducible patient effort is essential for the accuracy of the test.
• Spirometry, lung volumes, and diffusing capacity (DLCO) constitute pulmonary function
testing (PFTs).
• Spirometry reflects a complex interaction of respiratory muscle strength, elastic properties of
the chest wall and lungs, and airway resistance. For example, forced exhalation reflects the
ability of the expiratory muscles to overcome the outward force of the thorax. Spirometry
cannot measure airway resistance directly, rather it is estimated based on expiratory flows.
• Spirometry testing
– During spirometry, patients are asked to breath normal tidal volumes (Fig.1), inhale
maximally, and then exhale with maximal force (blast) and length of exhalation.
– The generated graph is interpreted to determine key flow and volume parameters (Fig. 2).
FIGURE 1. Spirometry involves having the patient take a maximal inspiration after tidal breathing and then forcefully
exhaling in what is referred to as a “blast exhalation.”
FIGURE 2. Generated graph from spirometry data delineates volumes, volume as a function of time, and flow rates.
• Spirometry parameters. Values are usually expressed as a percentage of normal values.

Normal values are defined as mean ±2 SD based on height, age, gender, and ethnicity.
– Forced vital capacity (FVC): Maximal volume forcibly exhaled following a maximal
inspiration.
– Forced expiratory volume in 1 second (FEV1): Single most important measure to
determine significant obstructive pathology and to gauge its severity.
– FEV1/FVC is the fraction of the vital capacity (VC) that can be exhaled in 1 second. It is a
key metric used to help distinguish between obstructive and restrictive patterns.
Decreased values indicate obstruction whereas a normal or higher than normal ratio and
reduced lung volumes suggest restrictive physiology.
– Forced expiratory flow between 25% and 75% (FEF25-75%) of FVC reflects flow in small
airways; it is not effort dependent. The large variability of normal values limits
applicability.
– Peak expiratory flow (PEF): Used to monitor responsiveness to bronchodilators; flow must
be maintained for at least 10 ms.
ANATOMY
• Inspiratory muscles
– Diaphragm: Innervated by the phrenic nerve (C3–C5). Responsible for one-third of the
tidal volume when upright and two-third when supine. During contraction, the dome
descends (up to 10 cm), elongating the thorax and increasing intra-abdominal pressure.
– External intercostals (intercostal nerves) and accessory muscles (scalene muscles, C4–C8;
and sternocleidomastoid, CN XI) both increase the anteroposterior and transverse
diameters of the chest.
• Expiratory muscles
– During spontaneous ventilation, expiration at rest is passively driven by the elastic recoil.
Inspiratory muscles are relaxed, and no muscles contract.
– During spontaneous ventilation, active expiration (exercise, singing) is generated by the
muscles of the abdominal wall and internal intercostals.
• Spirometry is not a diagnostic test; it reveals respiratory mechanical patterns. These patterns
should be reconciled with clinical diagnosis and other diagnostic tests. Once the specific
diagnosis is known, spirometry is used to quantify the severity of disease and monitor the
progress of therapy.
• Obstructive pulmonary disease (OPD) is characterized by decreased airway flow: Both FEV1
and FEV1/FVC are decreased (FVC is typically normal or increased). The course of disease
and response to therapy is best followed by changes in FEV1 (1)[B].
– Emphysema is characterized by enlargement of the airspaces and obstructive chronic
bronchitis (OCB) is characterized by excessive mucus production in the bronchi. Severity
is assessed per the Global Initiative for Obstructive Lung Disease (GOLD) criteria. Key
differential: DLCO is reduced in emphysema but not in OCB.
– Asthma is characterized by airway obstruction, inflammation, hyperresponsiveness to
triggers, and the following symptoms: Wheezing, dyspnea, cough, and chest tightness.
Diagnostic criteria for asthma: Reduced FEV1/FVC (with no specific ratio); and reversible
airflow impairment, defined as an improvement of >12% (or >0.2 L) in FEV1 or FVC.
Lack of response does not automatically rule out the diagnosis, as some patients require
more aggressive intervention to demonstrate reversibility. Parenchymal gas exchange is
preserved to a greater extent than in emphysema, evident by a normal or increased DLCO.
• Restrictive pulmonary disease is characterized by decreases in FVC and either normal or
increased FEV1/FVC.
– Interstitial disease (e.g., pulmonary fibrosis) causes decreases in lung volumes, with
normal or elevated flow ratios, but decreased DLCO, PaO2, and PaCO2.
– Kyphosis and scoliosis: Depending on severity, may have decreased FVC, FEV1, or both.
– Neuromuscular disorders (amyotrophic lateral sclerosis, multiple sclerosis, Duchenne’s
muscular dystrophy, myasthenia gravis): Reduced FVC often correlates with severity of
disease. Maximal inspiratory and expiratory flows detect muscle weakness.
– Habitus
Obesity: Decreased chest wall compliance and increased large and small airway
resistance result in decreased FVC and FEV1. Also, reduction in volumes and V/Q
mismatching.
Pregnancy: Usually normal spirometry but changes in lung volumes do occur.
• Postoperative pulmonary complications result in prolonged hospital stay and increased
health costs (2)[B].
– Reduced lung volumes due to diaphragmatic dysfunction, splinting from pain, respiratory
depressant effects of narcotics, and impaired mucociliary clearance are the main
mechanisms of pulmonary complications.
– These changes promote postoperative atelectasis, pneumonia, and V/Q mismatches. For
example, after thoracic or upper abdominal surgery, FVC and FRC may be reduced up to
60% and 30%, respectively, and can last for 1–2 weeks. Lower abdominal surgery is
associated with similar changes but to a lesser degree (3)[B].
• Thoracic surgery: Spirometry is indicated in all patients undergoing lung resection, but for
nonlung thoracic surgery it is not always required. (Note: ppo = predicted postoperative)
– Patients with FEV1 >2 L (>80% predicted) tolerate pneumonectomy and those with FEV1
>1.5 L (>60% predicted) can undergo lobectomy (4)[B].
– Increased risk is seen if the FEV1 is <1.5 L; FEV1 <800 mL is generally considered
prohibitive for lung resection; a calculated ppoFEV1 <40% suggests an increased risk,
<30% high risk
– In borderline patients, DLCO and calculated ppoDLCO (Equation 2) refine the above by
assessing parenchymal function; a ppoDLCO <40% is associated with high risk and <20%
with unacceptable risk.
– When FEV1 and DLCO are >80% predicted, no further testing is required. For borderline
values, integrated cardiopulmonary testing (VO2max) may be indicated.
– The difficulty of assigning a specific test value prohibitive for lung surgery stems from
diversity in patient population (age, sex, gender, race) and variable severity of disease of
the remaining lung (e.g., lack of homogeneity of lung disease).
• Perioperative spirometry can aid with risk stratification and planning of risk modification
interventions, with the goal of decreasing complications in at-risk patients. Routine testing
is NOT indicated in asymptomatic or low-risk patients undergoing nonthoracic,
nonabdominal surgery. A thorough history and physical remain the most important tools for
perioperative risk assessment. It may be appropriate for:
– Dyspnea or exercise intolerance of unexplained etiology to differentiate between
pulmonary and cardiac causes
– Chronic obstructive pulmonary disease (COPD) or asthma where clinical evaluation
cannot determine if therapy is optimized
– In general, patients have a high risk for postoperative pulmonary complications when
there is an FVC <50% of predicted; FEV1 <50% of predicted, FEV1 <1 L, or
postoperative FEV1 <40% of predicted; or significant hypoxemia (paO2 <60 mm Hg) or
hypercapnia (paCO2 >45 mm Hg).
• Perioperative risk modification strategies in patients with increased risk of complications (5)
[B] include
– Preoperative optimization:
Asthmatics should have their symptoms controlled prior to surgery, peak flows >80%
predicted, or personal best. Anticholinergics and beta-2 agonists given in meter-dosed
inhalers are effective. Corticosteroids are useful and are not associated with increased
incidence of perioperative infection.
COPD: Symptom and exacerbation control and optimization
– Use regional anesthesia technique if possible to avoid airway instrumentation.
– Consider a thoracic epidural for thoracic or abdominal surgery to optimize postoperative
pain control. This allows for deep breathing, incentive spirometry, and return to early
ambulation.
– Use of nonopioid analgesia when applicable; opioids depress the respiratory drive and can
increase the paCO2.
– Avoid neuromuscular blockade if possible; when utilized, ensure that the patient is fully
reversed.
– Lung protective ventilation strategy includes tidal volumes <8 mL/kg, pressure controlled
ventilation, inspiratory pressure <35 cm H2O, PEEP 4–10 cm H2O, and occasional
recruitment maneuvers should be considered.
– Careful adjustment of the I:E ratio and ventilatory rate can minimize air trapping (ensures
that inspiration starts at FRC).
– Intraoperative delivery of bronchodilators and meticulous pulmonary toilette.
– Bronchospasm can be treated by increasing the depth of inhaled anesthetic, administering
bronchodilators (albuterol, ipratropium); meter-dosed inhalers appear to have better
medication delivery compared to nebulizers.
– Avoidance of irritating agents such as desflurane during induction and emergence helps
prevent bronchospasm.
– Postoperative planning should include adequate monitoring of the environment and the
use of noninvasive or invasive ventilatory support.
EQUATIONS
• Predicted postoperative FEV1: ppoFEV1% = FEV1% × (1–fraction of functional lung tissue
removed)
• Predicted postoperative DLCO: ppoDLCO% = DLCO% × (1–fraction of functional lung tissue
removed). The fraction of functional lung tissue that will be removed can be estimated by
CT or ventilation/perfusion scan.
REFERENCE
1. ayes D, Kraman SS. The physiologic basis of spirometry. Respir Care. 2009;54(12):1717–
1726.
2. Colice GL, et al. Physiologic evaluation of the patient with lung cancer being considered for
resectional surgery: ACCP evidence-based clinical practice guidelines (2nd edn). Chest.
2007;132:161S.
3. hetta A, et al. Changes in lung function and respiratory muscle strength after sternotomy
vs. laparotomy in patients without ventilatory limitation. Eur Surg Res. 2006;28:489–493.
4. Rock P, Rich PB. Postoperative pulmonary complications. Curr Opin Anaesthesiol.
2003;16:123–132.
5. Lawrence VA, et al. Strategies to reduce postoperative pulmonary complications after
noncardiothoracic surgery: Systemic review for the American College of Physicians. Ann
Intern Med. 2006;144:596–608.
ADDITIONAL READING
• Ault ML, Stock MC. Respiratory Function. Clinical Anesthesia. 6th edn. Philadelphia:
Lippincott Williams & Wilkins, 2009.
• West JB. Pulmonary Pathophysiology: The Essentials. 6th edn. Philadelphia: Lippincott
• Asthma
CLINICAL PEARLS
• The use of perioperative spirometry is not based on randomized controlled studies;
therefore, routine preoperative testing is not indicated.
• Spirometry alone is not diagnostic and should not be the sole reason to exclude surgical
candidacy. The history and physical remains the best tool for perioperative risk assessment.
• Spirometry temporarily increases pressures in the thorax, abdomen, cranium, and eyes.
Spirometry causes exertion and should be used with caution in recent MI or angina.
SPLENECTOMY
BASICS
DESCRIPTION
General
• A normal spleen in an adult weighs ∼5 ounces and has dimensions of 5×3×6 inches.
Normal functions include filtration of blood as well as production of immune opsonins and
other complement components.
• Splenectomies are performed for the following indications:
– Spherocytosis
– Metastatic malignancy
– Splenic trauma
– Idiopathic thrombocytopenic purpura (ITP)
– Thrombotic thrombocytopenic purpura (TTP)
– Spherocytosis
– Sickle cell disease
– Lymphoma
– Splenic abscess
– Splenic cyst
– Splenic vein thrombosis
– Cirrhosis of the liver
– Esophageal varices
• Splenectomies may be performed through an open incision or laparoscopically, with the
latter approach preferred as long as the size of the organ is not an issue.
• Open splenectomy involves identifying and dissecting the short gastric vessels, splenocolic
ligament, and inferior pole vessels. The vessels are ligated at the hilum, the spleen is freed
from the diaphragm and then removed from the abdomen. Bleeding is assessed and
controlled and the incision is closed.
• Laparoscopic splenectomy starts with the patient in the reverse Trendelenburg position.
Three or four 10 mm ports are placed into the abdomen. The dissection of the spleen is
carried out as in the open procedure. When the spleen is free, it is either morcellized and
removed in a collection bag or removed whole via an enlarged incision.
• Accessory spleens may be present in up to 20% of patients. In patients undergoing
splenectomy for a hematologic disorder, they may not be cured by splenectomy as
anticipated.
• Alternate techniques for patients in whom surgical splenectomy is contraindicated (due to
significant comorbidities) treatment include radiofrequency ablation (RFA) of the spleen or
splenic artery embolization. Additionally, these procedures may also be performed prior to a
splenectomy to decrease the size or blood supply.
• Partial splenectomy may be performed to retain the important immune functions of the
organ. The goal is to retain at least 25% of the splenic mass of a normal spleen.
Position
• Open: Supine
• Laparoscopic: Semilateral position, left arm extended over head
Incision
• Open: Midline or left subcostal
• Laparoscopic: Four or five 1 cm incisions, one at the umbilicus as the camera port, and the
others in the left upper quadrant for instrumentation.
Approximate Time
• Approximately 45–60 minutes; longer if the spleen is particularly enlarged or the patient has
had previous upper abdominal surgery.
• Laparoscopic cases are longer, up to 2 or 3 hours
EBL Expected
100–300 mL
Hospital Stay
• Open: 5–7 days
• Laparoscopic: 1–3 days
Immunization against pneumococcus, meningococcus, and Haemophilus influenzae should be
performed prior to surgery, if possible.
EPIDEMIOLOGY
Prevalence
• The number of splenectomies have significantly decreased over the past 20 years with the
recognition of morbidities resulting from asplenia. Surgeons are more likely to attempt to
salvage a damaged spleen in order to preserve the patient’s immune function.
• The National Surgical Quality Improvement project indicates that 2,167 procedures were
performed in the US during the years of 2005–2008.
Prevalence
ITP affects ∼90,000 people in the US and Europe and is the most common non-trauma
indication for splenectomy.
Morbidity
• Dependent on the indication for the procedure.
• Morbidity for trauma patients is dependent on other injuries present.
• Open approach is 28.9% and laparoscopic is 11.7%.
• Most common morbidity is atelectasis, present in ∼25% of patients undergoing abdominal
surgery.
Mortality
Operative mortality is <1%.
• Maintain adequate muscle relaxation to facilitate exposure, the creation/maintenance of the
pneumoperitoneum, and the removal of an enlarged spleen through a small abdominal
incision.
• Provide blood component transfusion as needed to maintain hemostasis, particularly platelet
transfusion.
SYMPTOMS
• Left upper quadrant pain or fullness
• Early satiety as the spleen compresses the stomach
History
• Splenic trauma
• Underlying pathology for spleen removal (e.g., sickle cell disease)
Signs/Physical Exam
• Palpation of the enlarged spleen in the right upper quadrant
• Generalized lymphadenopathy may be present if cause is immune related
• Bruit over the left upper quadrant or epigastrium related to splenic congestion
MEDICATIONS
Preoperative vaccination against pneumococcus, meningococcus, and H. influenzae is
indicated.
Labs/Studies
• Ultrasound may confirm an enlarged spleen.
• Nuclear scan may identify an accessory spleen.
• Preoperative CBC is indicated to assess for anemia and platelet count.
May include immunodeficiency or liver dysfunction depending on the procedure indication
TREATMENT
Premedications
Preoperative vaccinations, especially pneumococcal vaccine
• If the planned procedure is laparoscopic, the surgical consent should also include “possible”
open approach, as well.
• A discussion about postoperative pain management should include the possibility of an
epidural, and the associated risk, especially in patients with thrombocytopenia. For
scheduled laparoscopic procedures, a discussion for postoperative placement may be made
in the event that it is converted to an open incision.
• Preoperative antibiotics to cover skin flora are indicated, such as a first-generation
cephalosporin or clindamycin.
• Postoperative antibiotic prophylaxis is controversial. It is generally indicated in children <5
years of age, but not in adults. Other groups such as those with underlying immune
deficiencies may benefit from postoperative oral penicillin prophylaxis, but the data is not
clear.
• Common organisms involved in postoperative infections include
– Encapsulated bacteria
– Staphylococcus aureus
– Gram-negative organisms
– Malaria
– Babesiosis
INTRAOPERATIVE CARE
• Epidural placement for postoperative pain in open procedures, particularly if the
splenectomy is performed as part of a staging laparotomy with a large midline abdominal
incision. Patients with thrombocytopenia (TTP, ITP) or other coagulopathies (liver disease
with varices) may not be appropriate candidates.
Monitors
• Arterial line may be indicated for patients with significant comorbid disease or massive
hypersplenism.
• Standard induction
• A cuffed endotracheal tube is necessary for both open and laparoscopic procedures
Maintenance
• A nasogastric tube should be placed after induction to decompress the stomach, enhance
surgical exposure, and facilitate the isolation of short gastric arteries from the stomach to
spleen.
• Choice of inhalation agent and muscle relaxant to facilitate surgical exposure.
• Insufflation for laparoscopy leads to reduced lung compliance. 15 mm Hg is the typical
intra-abdominal pressure, but this may be decreased if it is necessary to improve
ventilation.
• Reverse Trendelenburg positioning is utilized to allow abdominal displacement with gravity.
This can improve some of the respiratory parameters (peak inspiratory pressures, functional
residual capacity, lung compliance), but decrease cardiac preload.
• Thromboelastography, if available, can be used to guide platelet transfusion
intraoperatively.
EXTUBATION/EMERGENCE
• Standard criteria for extubation.
• In an open splenectomy, the nasogastric tube is left postoperatively to continue gastric
distention. In laparascopic cases, it may not be necessary to leave after extubation (depends
on surgeon’s preference).
FOLLOW-UP
BED ACUITY
• Open splenectomy carries a high risk for postoperative atelectasis and diaphragmatic
dysfunction.
• Overwhelming post-splenectomy sepsis is mostly likely to present in the immediate
postoperative period. It presents as fever, bacteremia, coagulopathy, and progresses rapidly
to shock; thus, requires emergent treatment.
ANALGESIA
• Patient controlled analgesia
• Ketorolac if no other contraindication
• Epidural catheter bolus and infusion
COMPLICATIONS
• Hemorrhage
• Overwhelming post-splenectomy sepsis
• Chronic thrombocytosis
• Portal vein thrombosis
• Pancreatitis
• Left lower lobe atelectasis
• Wound infection
• Subphrenic abscess
• Postoperative hypercoagulable state
• The rate of overwhelming post-splenectomy sepsis in children <5 years of age is significant.
Infants <1 year of age have a 10% risk (highest risk).
• The risk of post-splenectomy sepsis remains high for the first 2 years after the procedure is
performed.
PROGNOSIS
• Generally excellent and mostly related to underlying disease state and injuries.
• Post-splenectomy thrombocytosis is treated with aspirin or hydroxyurea. However, the
benefit is not clear.
• Overwhelming post-splenectomy sepsis carries a mortality rate of 50–70% and is considered
a medical emergency.
• Data indicates that splenectomy may increase the lifetime risk of developing pulmonary
hypertension.
REFERENCES
1. Kyaw MH, et al. Evaluation of severe infection and survival after splenectomy. Am J Med.
2006;119(3):276.
2. Schutze GE, et al. Invasive pneumococcal infections in children with asplenia. Pediatr
Infect Dis J. 2002;21(4):278–282.
3. Watters JM, Sambasivan CN, Zink K, et al. Splenectomy leads to a persistent
hypercoagulable state after trauma. Am J Surg. 2010;199(5):646–651.
• Trauma
• Laparoscopy
CLINICAL PEARLS
• The majority of splenectomies that are performed today are laparoscopic, with chronic ITP
being the most common indication.
• The greatest morbidity results from postoperative sepsis, especially in children.
• Despite the benefits of an epidural for postoperative analgesia, it may be contraindicated in
thrombocytopenic or coagulopathic patients.
SUBCLAVIAN STEAL SYNDROME
Rongjie Jiang, MB, MS
Jeffrey J. Schwartz, MD
BASICS
DESCRIPTION
• Subclavian steal syndrome is a phenomenon of transient cerebral ischemic attacks following
ipsilateral arm exercise in the presence of severe stenosis (>80%) or occlusion of the
subclavian artery proximal to the origin of the vertebral artery.
– During exercise, blood flows retrograde from the ipsilateral vertebral artery to the distal
subclavian artery to supply the arm; in doing so, blood is diverted from the circle of Willis
and can result in transient cerebral ischemia.
• Coronary–subclavian steal syndrome is a rare complication following use of the left internal
mammary artery (LIMA) graft for coronary artery bypass (CABG) in the presence of severe
proximal stenosis in the left subclavian artery. This may produce reversal of blood flow
from the heart to the ipsilateral arm during exercise that leads to angina pectoris.
• Subclavian steal is a flow-related phenomenon.
– At rest, when a proximal occlusion develops in the subclavian artery, the arm becomes
dependent on the collateral vessels from the head, shoulder, and neck, particularly
retrograde flow from the ipsilateral vertebral artery.
– When the arm is exercised, the blood vessels dilate and create a low resistance vascular
bed. More blood flows from the contralateral vertebral artery to the basilar artery and
there is increased retrograde flow into the ipsilateral vertebral artery down to the
subclavian artery to supply the arm.
• Coronary–subclavian steal can happen when patients have a coronary bypass using an in situ
LIMA graft, in conjunction with significant stenosis in the proximal left subclavian. Thus,
retrograde flow can occur and direct the blood away from the heart to the arm.
ANATOMY
• Normally, BPs are similar in both arms. A significant discrepancy raises a possibility of
stenosis in a subclavian artery, or coarctation of the aorta.
• The vertebral arteries arise from the superior aspect of the proximal subclavian artery and
feed into the basilar artery, which is part of the circle of Willis.
• The cerebral collateral conduits are mainly formed by the circle of Willis. It is an arterial
ring surrounding the optic chiasma and hypothalamus.
– Anteriorly, it is formed by the left and right anterior cerebral arteries that arise from the
left and right internal carotid arteries; they are “linked” by the anterior communicating
arteries.
– Posteriorly, it is formed by the division of the basilar artery into the left and right
posterior cerebral arteries.
– Laterally, the left and right posterior communicating arteries join the left and right
posterior cerebral arteries to the internal carotid arteries.
• The internal mammary artery arises from the inferior aspect of the proximal subclavian
artery, opposite the vertebral artery.
• The most common cause of proximal occlusive lesions in the subclavian arteries is
atherosclerosis. The most common sites are the
– Left subclavian artery (62%)
– Right subclavian artery (28%)
– Right innominate artery (10%)
– Other less common causes include
Takayasu disease
Temporal arteritis
Status post surgical repair of coarctation of the aorta
Congenital lesions of the aortic arch or subclavian artery
Status post Blalock–Taussig procedure for tetralogy of Fallot
Compression of the subclavian artery in the thoracic outlet
• Not all retrograde flow through the vertebral artery leads to neurologic symptoms; the
majority of time it is asymptomatic. It usually only becomes symptomatic when occlusive
lesions in the cerebral collateral conduits are present. 80% of patients with subclavian steal
syndrome have contralateral vertebral or carotid disease.
• Neurological symptoms in subclavian steal syndrome usually resolve after discontinuing
exercise of the arm. Common symptoms include
– Vertigo (50%)
– Diplopia (19%)
– Syncope (18%)
– Dysarthria (12.5%)
– Ataxia
– Blurring of vision
– Perioral numbness
– Paresthesia
– Infarction is rare
• Other symptoms:
– Exercise-induced arm pain
– Absent or diminished pulse in the ipsilateral arm and a significantly unequal systolic BP
from one side to the other (>20 mm Hg).
– Bruit in the supraclavicular fossa
• A recurrence of angina in a patient who has had a coronary bypass using a LIMA graft with
presence of stenosis in the proximal left subclavian artery indicates a possibility of
coronary–subclavian steal.
• The most common etiology is atherosclerosis. Thus, subclavian stenosis is associated with an
increased total mortality and cardiovascular disease mortality after adjusting for common
risk factors (2). They share the same risk factors as those with coronary artery disease:
– Advanced age
– Male sex
– Family history
– Cigarette smoking
– Hypercholesterolemia
– Hypertension
– Hyperhomocysteinemia
• Less common etiologies need to be identified if present. They may dictate special anesthetic
planning and special requirements on intraoperative monitoring.
• Diagnostic studies are done not only to confirm the diagnosis but also to ensure patent
proximal common carotid and distal subclavian arteries and to rule out any coexisting
lesions in the collateral pathways.
– Duplex ultrasonography (combined two-dimensional ultrasound and pulse-wave Doppler)
of the neck arteries. A coexisting severe carotid stenosis generally requires that a carotid
endarterectomy be performed first and then a reevaluation of any persistent neurologic
symptoms be made.
– Four-vessel cerebral angiography
– CT angiography
– Magnetic resonance angiography in patients with renal insufficiency
• Conservative treatment includes controlling hypertension, lipid modification, glycemic
control in diabetes, smoking cessation, and antiplatelet treatment with aspirin.
• Surgical treatment is only indicated for symptomatic patients.
– Endovascular angioplasty and/or stenting of the subclavian artery has a success rate of
86–93%. The complication rate is about 3–17%. The restenosis rate is about 0–16% in
stenting after 12–48 months. Stenting requires postoperative aspirin and clopidogrel for
6–12 months to reduce the risk of restenosis.
– Extrathoracic carotid–subclavian bypass (using a prosthetic conduit) requires a brief
period of complete clamp of the carotid artery for anastomosis that is usually well
tolerated. An intraluminal shunt is necessary only if there are significant lesions in the
contralateral common or internal carotid arteries.
– Extrathoracic subclavian transposition (subclavian to carotid anastomosis) requires more
extensive dissection compared to carotid–subclavian bypass. Phrenic nerve injury or the
thoracic duct injury is possible.
– Axillary-axillary bypass can be done when there is significant ipsilateral carotid disease.
The prosthetic graft is usually placed underneath the skin overlying the sternum. A
sternotomy after an axillary-axillary bypass would put the graft at risk.
– Subclavian endarterectomy requires thoracotomy and is rarely performed.
• Postoperative monitoring:
– Bleeding in the access site
– Neurological status (cerebral ischemic events from thrombosis of the target vessel or distal
embolization up the carotid or vertebral arteries)
– Check BP in both arms
• To prevent coronary–subclavian steal syndrome, it is crucial to rule out any high-grade
proximal stenosis in the left subclavian artery before LIMA is considered as a graft (3). At a
minimum, bilateral upper extremity noninvasive BP should be checked. A difference of 15
mm Hg identifies all patients with subclavian stenosis of >50% (4). If present, stent the
subclavian artery prior to CABG, then use an in situ LIMA graft. In an emergent setting, a
free LIMA graft to LAD appears to be a reasonable choice (1).
GRAPHS/FIGURES
FIGURE 1. Blockage of the subclavian artery proximal to the vertebral artery. During exercise, blood vessels in the arm
dilate (decrease resistance). Blood from the cerebral vasculature flows preferentially in the direction of decreased
resistance and retrograde down the vertebral artery. This results in “steal”.
REFERENCE
1. ogers JH, Calhoun RF. Diagnosis and management of subclavian artery stenosis prior to
coronary artery bypass grafting in the current era. J Card Surg. 2007;22(1):20–25.
2. Aboyans V, Criqui MH, McDermott MM, et al. The vital prognosis of subclavian stenosis. J
Am Coll Cardiol. 2007;49(14):1540–1545.
3. Hwang HY, Kim JH, Lee W, et al. Left subclavian artery stenosis in coronary artery bypass:
Prevalence and revascularization strategies. Ann Thorac Surg. 2010;89(4):1146–1150.
4. Osborn LA, Vernon SM, Reynolds B, et al. Screening for subclavian stenosis in patients who
are candidates for coronary bypass surgery. Catheter Cardiovasc Interv. 2002;56(2):162–
165.
5. Osiro S, Zurada A, Gielecki J, et al. A reivew of subclavian steal syndrome with clinical
correlations. Med Sci Monit. 2012;18(5):RA57–RA63.
6. choa VM, Yeghiazarians Y. Subclavian artery stenosis: a review for the vascular medicine
practitioner. Vasc Med. 2011;16(1):29–34.
ADDITIONAL READING
• Burlhan E, Soma F, Iared W. Angioplasty versus stending for subclavian artery stenosis.
Cochrane Database Syst Rev. 2011; 5(10):CD008461.
• Circle of Willis
• Peripheral artery disease
CODES
ICD9
435.2 Subclavian steal syndrome
ICD10
G45.8 Oth transient cerebral ischemic attacks and related synd
CLINICAL PEARLS
• A difference of 15 mm Hg in bilateral upper extremity brachial artery BP readings identifies
all patients with subclavian stenosis of >50%.
• The majority of patients with proximal subclavian stenosis are asymptomatic even when
there is retrograde flow from the ipsilateral vertebral artery. It requires only conservative
management.
SUBSTANCE ABUSE AND PREGNANCY
BASICS
DESCRIPTION
• The sequelae of substance abuse superimposed on the physiological changes of pregnancy
can have serious consequences to both the mother and fetus.
• Commonly abused substances in pregnancy include cocaine, amphetamines, opioids,
marijuana, alcohol, and tobacco. Opioid abuse includes morphine, meperidine, heroin,
fentanyl, and methadone.
• Alcohol use is a leading cause of preventable birth defects and developmental disabilities in
the US.
• There is a need for prevention strategies for at-risk parturients. Psychological and social
comorbidities must be thoroughly evaluated in this subset of parturients
EPIDEMIOLOGY
Prevalence
• There has been an increase in substance abuse during pregnancy over the past three
decades.
• The incidence of fetal alcohol syndrome (FAS) is 3.7 cases per 10,000 live births.
Prevalence
• Prenatal illicit drug abuse is estimated at ∼5% in the US. However, it may be significantly
higher than estimated due to inadequate reporting.
• Smoking is estimated to be <10%. Of note, 90% of opioid-dependent women are also heavy
smokers.
• Alcohol abuse in the parturient population is about 12% and binge drinking occurs in ∼3%
of pregnancies.
• FAS ranges from 0.5 to 2 cases per 1,000 live births.
Morbidity/Mortality
• The Health Resources and Services Administration (HRSA) suggests a 40% increase in the
risk of death during the first year of life in infants with frequent smoke exposure.
• Fetal alcohol exposure is the leading cause of preventable birth defects and developmental
disorders in the US.
• Heavy alcohol intake increases the overall neonatal mortality by 18%.
• Women who use drugs such as cocaine during pregnancy have more than twice the risk of
delivering a preterm, low birth weight baby than those who do not. They are also five times
more likely to have a baby with a birth defect.
• Neonatal abstinence syndrome (NAS) is seen in up to 94% of neonates with intrauterine
opioid exposure; it is present in up to 60–80% of neonates exposed to maternal methadone.
• Drug use varies by race/ethnicity with nonwhite women being twice as likely as Caucasian
parturients to use illicit drugs.
• A strong predictor of alcohol and tobacco use during pregnancy is their use prior to
pregnancy.
• Lack of prenatal care, history of premature labor, and tobacco use are associated with
substance abuse.
• There is a high rate of psychiatric illnesses in substance-dependent women including anxiety
(32%) and depression (30%).
• There is a strong correlation between childhood abuse in mothers and later drug
dependence.
• The mechanism of action depends on the substance abused.
• Alcohol abuse affects every organ in the body. It affects several neurotransmitters including
GABA, glutamate, serotonin, and dopamine resulting in its euphoric, anxiolytic, and
sedative effects. Long-term ingestion results in an increase in glutamate receptors, which on
alcohol withdrawal result in an excitatory state.
– FAS involves a spectrum of symptoms including characteristic facial appearances, growth
restriction, neurotoxicity, and cardiovascular abnormalities. There is no safe level of
alcohol consumption. Regardless of the gestational period, these adverse effects can occur.
• Tobacco exposure leads to tissue destruction and cellular changes that contribute to organ
damage. It dramatically increases the prevalence of cardiovascular and pulmonary disease
processes higher than in the mother.
– Consequences include hypotrophic placenta, placental vasoconstriction leading to
spontaneous abortion, fetal growth restriction, and low birth weight.
– Nicotine crosses the placenta reaching fetal concentrations 15% higher than those of
mother. It is also transferred via breast milk.
• Cocaine blocks the presynaptic uptake of sympathomimetic neurotransmitters like
norepinephrine, serotonin, and dopamine resulting in prolonged adrenergic stimulation. It is
lipophilic and rapidly diffuses through the placenta.
– Fetal complications result from maternal vasoconstriction leading to uteroplacental
insufficiency, acidosis, and hypoxia. Cocaine is teratogenic as well.
– Maternal complications include premature labor, placental abruption, uterine rupture,
cardiac arrhythmias, cardiac ischemia/infarction, stroke, and death.
• Amphetamines are indirect sympathomimetic drugs that cause euphoria, appetite
suppression, and increased alertness. It may be difficult to distinguish from cocaine
intoxication. Maternal complications of ingestion include premature labor, placental
abruption, uterine rupture, cardiac arrhythmias, cardiac ischemia/infarction, stroke, and
death.
• Marijuana has a complex mechanism of action with an unpredictable clinical picture. There
is no evidence of teratogenicity reported. However, low birth weight, delay in cognitive
development, and complications during labor have been reported.
• Opioid abuse can result in NAS that is characterized by a variety of symptoms including
fevers, poor sucking, stuffy nose, excessive crying, yawning, tremor, hyperexcitability,
sneezing, vomiting, and diarrhea in the fetus. The IV mode of administration increases the
mother’s risk of endocarditis, malnutrition, cellulitis, skin abscesses, hepatitis, and HIV
infections.
• The anesthetist does not have an extensive role in the prevention of parturient substance
abuse; however, they should be aware of treatment and prevention modalities that may
affect the patient’s peripartum care.
• Abstinence is ideal; however, most opioid-dependent women cannot remain drug free
throughout pregnancy. This may result in relapse with cycles of intoxication and
withdrawal that leads to fetal distress.
– Methadone maintenance is the gold standard in opioid-dependent parturients, although
the drug is not approved for use during pregnancy.
– Evidence shows that parturients on methadone have higher follow-up rates, improved
prenatal care, and reduced fetal morbidity and mortality.
– Buprenorphine maintenance therapy has been shown to be safe in the mother and fetus
and may be an alternative for the treatment of opioid-dependent women in pregnancy.
• Psychosocial intervention and counseling play an important role. This includes establishing
an appropriate living environment and settling financial problems.
• Psychiatric medications may be appropriate; there is a high rate of psychiatric illnesses in
substance-dependent women including anxiety (32%) and depression (30%). SSRIs are
widely used to treat major depression and anxiety in this population. Such patients should
be carefully monitored for serotoninergic toxic effects.
• Tobacco abstinence of 4–6 weeks decreases postoperative respiratory morbidity to
nonsmoker levels.
• History: Most parturients with a history of drug abuse deny it. A lack of prenatal care,
history of premature labor, and smoking should evoke a high index of suspicion for
substance abuse.
• Signs and symptoms depend on the type of substance abused, route of administration, and
frequency of use.
• Cocaine: Tachycardia, hypertension, cardiac arrhythmias; confusion, hyperreflexia, fever,
dilated pupils, proteinuria, edema, and seizures.
• Amphetamines: Confusion, hyperreflexia, fever, dilated pupils, proteinuria, edema, and
seizures.
• Alcohol withdrawal: Tremors, hypertension, confusion, agitation, hallucinations, nausea,
tachycardia, and arrhythmias. Acute withdrawal occurs after 6–48 hours of abstinence.
Delirium tremens can occur from 2 to 10 days after the last drink.
• Acute marijuana use: Tachycardia, nasal, or conjunctiva congestion.
• Opioid overdose: Respiratory depression, miotic pupils, lethargy, and sedation.
• Opioid withdrawal: Mydriasis, restlessness, tachycardia, tachypnea, hypertension,
lacrimation, rhinorrhea, yawning, and piloerection. Withdrawal symptoms usually occur 4–
6 hours after the last opioid dose and peak at 48–72 hours.
• Alcohol screening tools.
– T-ACE: Tolerance, Annoyed by criticisms, having felt the need to Cut down, Eye opener in
the morning.
– TWEAK: Tolerance, Worry by family member, Eye opener, Amnesia, Kut down.
• Maternal urine toxicology screening can be used to identify the recent use of illicit
substances. Cocaine metabolites are seen in maternal urine for 24–60 hours after drug
administration.
• Analysis of fetal urine may serve as a marker as well.
• Differentiating between the symptoms of substances abused is difficult when multiple
substances are involved.
• In the presence of cognitive decline or focal deficits, gross structural brain disorders like
head trauma or spontaneous bleeds must be ruled out.
• Hypertension, proteinuria and convulsions seen in cocaine or amphetamine intoxication
may be mistaken for preeclampsia or eclampsia. Liver and kidney dysfunction may be
present in preeclampsia, whereas, a positive urine toxicology screen can help distinguish
cocaine or amphetamine abuse.
• Symptoms of alcohol/benzodiazepine withdrawal may resemble cocaine or amphetamine
intoxication.
TREATMENT
• IV access may be difficult; central vein access may be required.

• Standard ASA monitors (pulse oximetry, NIBP, EKG, temperature monitoring) for laboring
epidurals may be necessary.
• Invasive monitors including an arterial line, central venous pressure and/or pulmonary
artery catheter (rarely) may be indicated in parturients with a high risk of bleeding,
uncontrolled hypertension, or severe hypotension.
• Regional anesthesia
– Preferred in smokers secondary to the pulmonary effects of tobacco that include increased
secretions, decreased ciliary motility, impairment of gas exchange, and bronchospasm.
– Infection may preclude placement.
– Adequate fluid resuscitation is essential prior to placement.
– Direct-acting sympathomimetics (phenylephrine) may be necessary to treat hypotension.
Depleted catecholamine stores (seen with chronic cocaine and amphetamine use) can
result in a resistance to ephedrine (indirect method of action).
– Emergent delivery of the neonate may be necessary in cases of fetal and maternal
instability.
– Aspiration prophylaxis should be implemented.
– Be prepared to treat hypertension, cardiac arrhythmias, and myocardial ischemia.
– Drugs and fluids should be carefully administered in the setting of cardiac failure or
hepatic dysfunction; consider invasive monitoring.
– Marijuana use compounded with volatile agents may result in profound myocardial
depression.
– Acute intoxication with CNS depressants (benzodiazepines, alcohol, and opioids) requires
a reduced amount of anesthetic.
– Acute intoxication with CNS stimulants (cocaine or amphetamine) requires an increased
amount of anesthetics.
• Altered pain perception may result from changes in the opioid receptors and endorphin
levels.
• Hypertension and chest pain from cocaine or amphetamine use may be treated with
nitroglycerin, labetalol, and/or hydralazine. Propranolol is contraindication secondary to
the potential of unopposed alpha-adrenergic stimulation following beta-adrenergic
blockade.
• Treatment of alcohol withdrawal includes benzodiazepines and alpha-2 agonists such as
clonidine.
• A resuscitation cart should be placed adjacent to the operating room.
FOLLOW-UP
• In the postpartum period, the patient should be monitored for signs of substance
withdrawal. Appropriate therapy with antihypertensive agents, benzodiazepines, and alpha-
2 agonists may be required.
• The neonate is monitored closely in the neonatal intensive care unit for symptoms of
withdrawal.
REFERENCES
1. Howell EM, Heiser N, Harrington M. A review of recent findings on substance abuse
treatment for pregnant women. J Subst Abuse Treat. 1999;16(3):195–219.
2. Keegan J, Parva M, Finnegan M, et al. Addiction in pregnancy. J Addict Dis.
2010;29(2):175–191.
3. Kuczkowski KM.Anesthetic implications of drug abuse in pregnancy. J Clin Anesth.
2003;15(5):382–394.
4. Kuczkowski KM.The effects of drug abuse on pregnancy. Curr Opin Obstet Gynecol.
2007;19(6):578–585.
5. Winklbaur B, Jung E, Fischer G. Opioid dependence and pregnancy. Curr Opin Psychiatry.
2008;21(3):255–259.
• Cocaine abuse
• Alcohol abuse
CODES
ICD9
• 648.30 Drug dependence of mother, unspecified as to episode of care or not applicable
• 648.40 Mental disorders of mother, unspecified as to episode of care or not applicable
• 649.00 Tobacco use disorder complicating pregnancy, childbirth, or the puerperium,
unspecified as to episode of care or not applicable
ICD10
• O99.320 Drug use complicating pregnancy, unspecified trimester
• O99.310 Alcohol use complicating pregnancy, unspecified trimester
• O99.330 Smoking (tobacco) complicating pregnancy, unsp trimester
CLINICAL PEARLS
• Substance abuse in the pregnant woman has an unfortunately high incidence. It requires
tailoring of the anesthetic management to the needs of the individual high-risk patient.
• A preanesthetic plan with nonjudgmental questioning is essential.
• Breast-feeding is encouraged in patients on methadone or buprenorphine maintenance. It
can potentially decrease NAC severity.
SUPERIOR LARYNGEAL NERVE
Peter K. Yi, MD
BASICS
DESCRIPTION
• The superior laryngeal nerve (SLN) provides sensory innervation to a portion of the oral
pharynx and motor innervation to the cricothyroid muscle, whose primary function is to
tense the vocal cords.
• The SLN is an important nerve to block in order to achieve adequate anesthesia for
instrumentation of the airway (e.g., awake fiberoptic intubation).
• Branch of the vagus nerve
• The SLN, itself, is made up of two branches:
– Internal: Provides sensation to the base of the tongue, epiglottis, and arytenoids
– External: Provides motor innervation solely to the cricothyroid muscle
ANATOMY
• The SLN separates from the vagus nerve at the base of the skull and travels along with the
internal carotid artery to the superior pole of the thyroid gland (2).
• It divides into the internal and external branches at the level of the hyoid bone.
• The internal branch of the SLN is usually larger and enters the thyrohyoid membrane before
innervating the larynx.
• The smaller external branch of the SLN travels along the lateral border of the inferior
pharyngeal constrictor muscle. It then descends in an anterior-medial direction and courses
along with the superior thyroid artery. As the external branch of the SLN and the superior
thyroid artery enter the thyroid capsule, the external branch takes a more medial direction
to innervate the cricothyroid muscle.
• Because of its sometimes discreet location under the inferior pharyngeal muscle fascia, the
external branch of the SLN may be severed during (3)
– Thyroid lobectomies
– Parathyroidectomies
– Anterior approaches to the cervical spine
– Neck dissections
– Carotid endarterectomies
• Since the majority of motor innervation to the vocal cords is by the recurrent laryngeal
nerve, damage to the external branch of the SNL does not result in complete vocal cord
dysfunction. It could however result in
– Decreased voice quality
– Decreased voice strength
– Easy tiring
– Hoarseness
– Possible increased risk for aspiration; the cricothyroid muscle functions to maintain
tension and elongation of the vocal cords.
• The SLN provides sensation from the inferior portion of the epiglottis to the vocal cords.
Thus, blocking the nerve with local anesthetic agents can be useful for:
– Awake fiberoptic intubation
– Awake bronchoscopy or esophagoscopy
– Transesophageal echocardiography in critically ill patients who cannot be sedated
– Treatment or prevention of laryngospasm or stridor especially in the pediatric patient
population
– Supplement to total IV anesthesia for airway procedures such as rigid bronchoscopy.
• SLN block technique (1):
– The hyoid bone, located superior to the thyroid cartilage and inferior to the angle of the
mandible, is palpated and displaced laterally to identify the greater cornu at each end
while the neck is extended (see Figure).
FIGURE 1. Anatomical depiction of superior laryngeal nerve block technique.
– A 25-gauge needle is advanced toward the cornu of the hyoid with one hand, while the
other hand applies contralateral pressure at the opposite end.
– The needle is advanced until the tip contacts the hyoid bone and then is walked off
laterally and posteriorly passing the thyrohyoid membrane to a depth of 1–2 cm.
– The needle is aspirated to ensure that the placement is not intravascular or in the pharynx
– 1–3 cc of local anesthetic is injected. The identical procedure is repeated on the other side.
• Alternate approach:
– Identify the superior ala of the thyroid cartilage and insert the needle toward the superior
margin of the cartilage.
– The needle is then walked superiorly off the cartilage through the thyrohyoid membrane.
– The needle is aspirated and ∼2–3 cc of local anesthetic is injected. This is then repeated
on the opposite side.
• Risks of SLN blocks (4):
– Hypotension and bradycardia have been reported.
– Inability to protect the airway and potential for aspiration
– Local anesthetic systemic toxicity; small amounts of intravascular injections can readily
cause CNS side effects due to the close proximity to the brain.
– Edema or airway obstruction if inserted too deeply; insertion into the thyroid cartilage at
the level of the vocal cords may cause edema and airway obstruction.
– Hematoma formation; maintain pressure should this occur.
• Laryngospasm is an exaggeration of the normal glottic closure as a result of stimulation of
the vocal cords via the SLN. It is triggered by the presence of blood, secretions, or surgical
debris during light anesthesia. It is more common during upper airway procedures and in
children.
– Manifests initially as stridor and can lead to complete airway obstruction.
– Management involves removing the offending stimulus with suctioning, positive pressure
ventilation to open the airway, and/or small doses of IV anesthetic or muscle relaxant
(typically succinylcholine due to its quick onset and very short duration of action).
REFERENCES
1. Furlan JC. Anatomical study applied to anesthetic block technique of the superior laryngeal
nerve. Acta Anaesthesiol Scand. 2002;46(2):199–202.
2. Furlan JC, Brandao LG, Ferraz AR, et al. Surgical anatomy of the extralaryngeal aspect of
the superior laryngeal nerve. Arch Otolaryngol Head Neck Surg. 2003;129(1):79–82.
3. Furlan JC, Cordeiro AC, Brandão LG. Study of some “instrinsic risk factors” that can
enhance an iatrogenic injury of the external branch of the superior laryngeal nerve.
Otolaryngol Head Neck Surg. 2003;128(3):396–400.
4. Wiles JR, Kelly J, Mostafa SM. Hypotension and bradycardia following superior laryngeal
nerve block. Br J Anaesth. 1989;63(1):125–127.
• Laryngospasm
CLINICAL PEARLS
• The SLN can also be blocked “noninvasively”
– The tongue is retracted and held with gauze.
– A local anesthetic-soaked gauze is placed in a right angle forcep and held at the pyriform
sinuses bilaterally for ∼5 minutes.
• Unlike partial damage to the recurrent laryngeal nerve (innervation to the single abductor
posterior cricoarytenoid), damage to the SLN does not cause airway obstruction and stridor.
To that extent, neuromonitoring of the SLN is not routinely performed during surgical
procedures. However, damage can be significant to patients who rely on their voice for their
occupation.
• Damage to the SLN presents as loss of tension of the vocal cord with a wavy appearance on
laryngoscopy or bronchoscopy.
SUPPLEMENTAL OXYGEN
John J. Freely Jr., MD
Christopher A. Skorke
BASICS
DESCRIPTION
• The primary goal of oxygen therapy is to prevent or correct hypoxemia and/or tissue
hypoxia.
• Efficient and rapid oxygen delivery (DO2) is a vital component in the care of critically ill or
injured patients. Certain disease processes including myocardial infarction, acute lung
injury, ARDS, pulmonary fibrosis, cardiogenic pulmonary edema, cyanide poisoning, and
carbon monoxide inhalation all require supplemental oxygen.
• In general, supplemental oxygen is indicated for adults, children, and infants (older than 1
month) when the PaO2 is <60 mm Hg or the SpO2 is <90% while breathing room air.
Oxygen therapy is indicated in neonates if the PaO2 is <50 mm Hg, SaO2 <88%, or
capillary PO2 is <40 mm Hg.
• During general anesthesia, supplemental oxygen is required to prevent declines in the PaO2
that can result from decreased functional residual capacity (FRC) and hypoventilation.
• The clinical status of the patient and the desired dose of oxygen will determine the choice of
the DO2 system. Patients vary considerably in their response to oxygen; additionally, there
are several potential hazards associated with its use. Careful monitoring is required to avoid
the consequences of hyperoxia.
• A continuous supply of oxygen is fundamental to normal cellular function and aerobic
metabolism.
• The transfer of oxygen from alveolar air to pulmonary capillary blood is affected by the
PaO2 in the alveoli, its ability to diffuse across the alveolar capillary membrane, and the
matching of alveolar ventilation to capillary perfusion.
• Delivered oxygen partial pressure (PiO2) is equal to the barometric pressure at one
atmosphere times the fraction of oxygen. At room air it can be calculated as follows: 760
mm Hg × 0.21 = 149.7 mm Hg. At a fraction of inspired oxygen (FiO2) of 1.0, it is
calculated as follows: 760 mm Hg × 1.0 = 760 mm Hg. Upon entering the airway, the gas
is humidified and the inspired oxygen tension is reduced by the added water vapor (PH2O is
47 mm Hg at 37°C). Thus it can be calculated as follows: PiO2 = [(Pbaro − PH2O) × FiO2]
• Alveoli. The inspired gases are mixed with residual alveolar gas from previous breaths;
oxygen is also taken up and carbon dioxide is added.
– Alveolar oxygen tension (PAO2) can be estimated using the alveolar gas equation: PAO2 =
PiO2 – (PaCO2/RQ), where the PaCO2 = arterial CO2 tension and RQ = respiratory
quotient. Large increases in PaCO2 (>75 mm Hg) readily produce hypoxia (PaO2 <60
mm Hg) at room air but not at high inspired O2 concentrations.
– The PAO2 can also be quickly estimated in millimeters of mercury (mm Hg) by
multiplying the percentage of inspired O2 concentration by 6. For example at 50%, the
PAO2 is 6 × 50 mm Hg or 300 mm Hg.
• Gradient. The PaO2 in the alveoli for a patient breathing room air (∼100 mm Hg) exceeds
that of mixed venous blood (40 mm Hg) and mitochondria (<10 mm Hg). This gradient is
the driving force for DO2 from the alveoli to the tissue.
• Adequate tissue oxygenation requires that oxygen content and delivery exceed consumption.
Sufficient oxygen content is dependent on normal arterial oxygen tension (PaO2) and
hemoglobin concentration. DO2 to tissues necessitates appropriate blood volume, heart rate,
and cardiac function. Tissue ischemia and hypoxia may occur with circulatory impairment
or failure, even if the oxygen content is normal.
– Arterial oxygen content (CaO2) is the sum of oxygen dissolved in solution plus that carried
by hemoglobin and is expressed by the following equation: CaO2 = 1.34(Hb) (SaO2) +
(0.003) (PaO2), where Hb is the hemoglobin concentration, SaO2 is the arterial
oxyhemoglobin saturation, and PaO2 is the partial pressure of oxygen in arterial blood.
Normal CaO2 is ∼20 mL O2/dL.
– DO2 is the amount of oxygen that is transported from the lungs to the microcirculation
and is dependent on the cardiac output (Q) and the CaO2. DO2 can be compromised by a
reduction in any component (cardiac output, hemoglobin concentration, or SaO2);
however, a decrease in one component may be offset by an increase in another to
maintain DO2.
– Oxygen consumption can be calculated indirectly from the Fick equation: VO2 = Q ×
(CaO2–CvO2), where the arteriovenous content difference represents the quantity of O2
extracted by the peripheral tissues. When DO2 is reduced, VO2 usually remains normal
because of increased oxygen extraction (mixed venous O2 saturation decreases); thus VO2
remains independent. With further reductions in DO2, a critical point is reached, beyond
which VO2 becomes directly proportional to DO2. This supply-dependent O2 state typically
is associated with progressive lactic acidosis caused by cellular hypoxia.
• Oxygen administration systems are best classified according to their ability to provide
adequate flow levels and a range of FiO2. Patient compliance, the presence and type of
artificial airway, and the need for humidification are other considerations in selecting a type
of oxygen therapy.
• Nasal cannulas provide oxygen into the nasopharynx and it mixes with room air.
– Rate: 1–4 L/min
– FiO2: 0.25–0.4; concentration varies depending on the patient’s respiratory rate, tidal
volume, and extent of mouth breathing
– Advantages: Comfort and the ability to eat and speak
– Disadvantage: Low maximum inspired concentrations of oxygen and the unpredictability
of what amount of oxygen is truly being delivered to the patient. Rates >4 L/min can dry
the mucous membranes and are discomforting to the patient.
– Cautions: Oxygen should be humidified. Flow rates in newborns and children >2 L/min
are usually not recommended due to inadvertent administration of positive airway
pressure at higher flow rates.
• Simple masks fit loosely over the nose and mouth.
– FiO2: 0.3–0.6
– Advantages: Higher oxygen concentrations can be delivered compared to nasal cannula;
useful in mouth breathing
– Disadvantages: Not precise
– Caution: There is some accumulation of CO2 from rebreathing, which may pose a risk in
CO2 retainers.
• Partial rebreathing masks consist of a simple mask with a reservoir attached. The term
partial refers to the portion of the patient’s expired tidal volume that refills the reservoir
bag.
– FiO2: 0.5–0.6
– Advantages: Conserves oxygen supply, particularly during transport
– Disadvantages: The lack of a tight seal and valves allows for mixing of room air and the
inability to provide an FiO2 of 1.0.
– Cautions: If the oxygen supply is insufficient to prevent collapse of the reservoir,
entrainment of room air through the exhalation ports can occur.
• Nonrebreathing masks consist of a mask and reservoir modified with two valves.
– FiO2: 0.4–1.0 depending on the flow rate
– Advantages: Exhaled air egresses out of the one way valves, thus allowing for higher
fractions of oxygen that can be inspired from the reservoir bag. In spontaneously
breathing patients, this technique most reliably supplies the highest oxygen concentration.
– Disadvantages: Lacks a tight seal and allows the potential for mixing of room air; cannot
provide pressure support or PEEP
– Cautions: A key factor to the successful application of this mask is to use a sufficient flow
of oxygen so that the reservoir bag is partially filled during inspiration.
• Oxygen hoods and tents are enclosure systems primarily used for infants or neonates who
require prolonged administration of oxygen. Oxygen hoods are clear plastic cylinders that
cover an infant’s head. Oxygen tents are clear plastic shells that cover an infant’s head and
upper body.
– Rate: Hoods 10–15 L/min; tents >10–15 L
– FiO2: Hoods 0.8–0.9; tents 0.5
– Advantages: More easily tolerated than nasal cannula or masks
– Disadvantages: Cannot exactly control FiO2 or deliver positive pressure ventilation
– Cautions: Retinopathy of prematurity (ROP)
• Ventilation bags are usually used to provide oxygen and assisted ventilation, either with a
mask or through an artificial airway. These are high flow fixed performance systems.
– Rate: High flows
– FiO2: Close to 1.0
– Advantages: Useful for transport of intubated and mechanically ventilated patients. Face
mask positive pressure ventilation can potentially prevent intubation in some situations.
– Disadvantages: Cannot measure pressures that are being delivered. Positive pressure
ventilation via a face mask may result in stomach insufflation and does not protect the
airway from aspiration.
ANATOMY
• Oxygen is carried in the blood in two forms: Dissolved and combined with hemoglobin.
• The oxyhemoglobin dissociation curve describes the relationship between PaO2 and
hemoglobin.
• Hemoglobin has the dynamic ability to bind and release oxygen and this capability is
modulated by pH, CO2, 2,3-diphosphoglycerate, temperature, and fetal hemoglobin. Under
normal physiological circumstances, this promotes oxygen uptake in the pulmonary arteries
and unloading into the tissues.
• Five possible causes of a reduction in PaO2:
– Low inspired oxygen tension
– Alveolar hypoventilation
– Diffusion impairment
– Ventilation/perfusion (V/Q) mismatching
– Shunt
• Supplemental oxygen is effective in prolonging the survival of patients with COPD that have
a resting PaO2 <60 mm Hg; it also mildly improves a patient’s subjective feelings of
dyspnea. However, hypoventilation is a complication often seen in this patient population
who also are chronic CO2 retainers. These patients are somewhat dependent on a relative
hypoxemia, due to an altered respiratory drive. In addition, oxygen-mediated release of
hypoxic vasoconstriction can result in greater blood flow to areas that are poorly ventilated,
worsening the shunt. Elevation of arterial oxygen tension to relatively normal levels can
cause severe hypoventilation in these patients.
• Absorption atelectasis can occur in patients on oxygen therapy. High concentrations of
oxygen in poorly ventilated alveoli are prone to atelectasis when nitrogen (which serves as
an alveolar “filler") is washed out of the lungs. The pulmonary capillaries readily take up
alveolar oxygen (uptake greater than intake), leading to alveolar collapse.
• Oxygen toxicity. Lung damage can occur with prolonged high concentrations of oxygen.
Toxicity is dependent on both the inspired PaO2 and the length of exposure. The alveolar
oxygen tension rather than the arterial oxygen tension is more important in the
development of lung toxicity. Generally speaking, 100% oxygen for <24 hours is
considered safe, but concentrations >50% for prolonged periods of time are undesirable as
they may lead to toxicity. Oxygen toxicity is believed to be due to intracellular generation
of highly reactive oxygen metabolites or free radicals. These metabolites are cytotoxic
because they readily react with cellular DNA, sulfhydryl proteins, and lipids. The injury to
the lung is indistinguishable from ARDS. Pulmonary capillary membrane permeability
increases, and the membrane is thickened secondary to proliferation of type II alveolar cells.
Pulmonary O2 toxicity in newborn infants is manifested as bronchopulmonary dysplasia.
• ROP is a neovascular retinal disorder that is common in premature infants. Initially, the
hyperoxic stage impairs normal vascularization of the retina. The retina is particularly
sensitive to this effect, because of the high rate of blood flow to the choroidal circulation.
The hypoxic stage follows and is the result of high oxygen requirements by the retinal
vasculature being unmet. As a result, hypoxia-inducible factor and vascular endothelial
growth factor are consequently released. These factors result in “neovascularization" with
abnormal proliferation from the retina to the vitreous. Neovascularization can cause fluid
leak, hemorrhage, and retinal scar formation with traction of the retina. In severe cases,
traction can lead to detachment and blindness.
• Oxygen is highly combustible and has the potential to cause fires and explosions. Caution
must be taken when the fire triad (ignition source, oxidizer, fuel) can develop (e.g., sedation
cases with supplemental oxygen for procedures above the xiphoid that use electrosurgical
instruments).
• The concept of O2 stores is vital in anesthesia. During apnea, the vital flux of O2 is
interrupted, and existing stores of O2 are consumed by cellular metabolism. When these
stores are depleted, hypoxia and subsequent cell death follow.
• Normal O2 stores are limited to what is present in the lungs (FRC), bound to hemoglobin,
and dissolved in blood. To that extent, the oxygen contained within the FRC is the main O2
store. Following ventilation with 100% O2, FRC contains a much greater content of O2 as
compared to a patient breathing room air. This increase in O2 stores delays hypoxemia
following apnea and ultimately forms the basis for preoxygenation (or denitrogenation)
prior to induction of anesthesia.
EQUATIONS
• PiO2 = (Pbaro – PH2O) × FiO2; where PiO2 is the partial pressure of oxygen that after
mixing with water vapor, Pbaro is the atmospheric pressure, PH2O is the partial pressure of
water vapor found in the airway, and FiO2 is the fraction of inspired oxygen.
• PAO2 = PiO2 – [PaCO2/RQ]; where PAO2 is the partial pressure of oxygen in the alveoli,
PaCO2 is the partial pressure of carbon dioxide in the artery, and RQ is the respiratory
quotient.
• CaO2 = 1.34(Hb)(SaO2) + (0.003/PaCO2); where CaO2 is the oxygen content in the
arteries, Hb is hemoglobin, SaO2 is the arterial oxygen saturation, and 0.003 is oxygen’s
solubility coefficient.
• DO2 = Q × CaO2; where DO2 is the oxygen delivery to organs/tissue, Q is the cardiac
output.
• VO2 = Q × (CaO2 – CvO2); where VO2 is the oxygen consumption by tissues, CvO2 is the
oxygen content in the veins.
REFERENCES
1. Bateman NT, Leach RM. ABC of oxygen. Acute oxygen therapy. BMJ. 1998;317:798.
2. Bradley JM, Lasserson T, Elborn S, et al. A systematic review of randomized controlled
trials examining the short-term benefit of ambulatory oxygen in COPD. Chest.
2007;131:278.
3. Durrington HJ, Flubacher M, Ramsay CF, et al. Initial oxygen management in patients with
an exacerbation of chronic obstructive pulmonary disease. QJM. 2005;98:499.
4. Jensen AG, Johnson A, Sandstedt S. Rebreathing during oxygen treatment with face mask.
The effect of oxygen flow rates on ventilation. Acta Anaesthesiol Scand. 1991;35:289.
5. Myers TR. American Association for Respiratory Care (AARC). AARC Clinical Practice
Guideline: Selection of an oxygen delivery device for neonatal and pediatric patients—
2002 revision and update. Respir Care. 2002;47:707.
6. Stoller JK, Panos RJ, Krachman S, et al. Oxygen therapy for patients with COPD: Current
evidence and the long term oxygen treatment trial. Chest. 2010;138:179.
7. SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network,
Carlo WA, Finer NN, et al. Target ranges of oxygen saturation in extremely preterm infants.
N Engl J Med. 2010;362:1959.
8. Tanni SE, Vale SA, Lopes PS, et al. Influence of oxygen delivery system on the quality of
life of patients with chronic hypoxemia. J Bras Pneumol. 2007;33:161.
9. Vallet B. Perioperative oxygen therapy and oxygen utilization. Curr Opin Crit Care.
2010;16:359–364.
• Oxygen toxicity
• Partial pressures
CLINICAL PEARLS
• Supplemental oxygen is often utilized perioperatively to avoid the harmful effects of
hypoxemia in the setting of benzodiazepines, opioids, residual volatile agents, or
neuromuscular blocking agents.
• It is important to assess the need as well as the characteristics of each DO2 system.
SUPRACELIAC/SUPRARENAL AAA REPAIR
Ali R. Abdullah, MBChB
Ibetsam Hilmi, MBChB, FRCA
BASICS
DESCRIPTION
General
• An aneurysm is defined as a permanent dilation of a blood vessel that is at least 1.5 times
the diameter of the expected normal value; it can be fusiform or saccular in morphology.
• Abdominal aortic aneurysms (AAAs) can be either above the renal arteries (suprarenal) or
below (infrarenal). Compared to infrarenal AAA repair, suprarenal repair is associated with
greater:
– Hemodynamic effects
– Blood loss
– Risk of spinal injury
– Renal insufficiency
– Conversion to open repair from endovascular
• Following dissection and exposure of the aneurysm, the patient is heparinized. Cross-
clamping of the aorta is performed distal to the aneurysm, followed by clamping of the
aorta above the renal arteries. Once the graft is sutured into place, the proximal and distal
suture lines are examined for bleeding.
• Heparin reversal may be performed after discussion with the surgeon; protamine 1mg for
every 100 U of heparin.
• While open repair is still indicated in certain cases (e.g., lack of an adequate implantation
site for the stent), endovascular repair is commonly performed. Open repair is associated
with
– Increased 30-day mortality
– Increased morbidity: Longer hospital stay and postoperative pulmonary, cardiac, and renal
complications
– Increased blood transfusion requirement
– Increased analgesia requirement
Position/Incision
Supine with upper abdominal incision
Approximate Time
• <6 hours
• Cross-clamping may last for 30–60 minutes
EBL Expected
• >250 mL
• Common surgical complications – bleeding, coagulopathy, prolonged cross-clamp time, and
visceral injuries
Hospital Stay
• 5–10 days for open repair
• Ruptured aneurysms may require a longer hospital stay.
• Cell salvage
• Rapid infuser
EPIDEMIOLOGY
Prevalence
• AAA is present in 5.9 per 100,000 people.
• Increased incidence with age due to exposure to risk factors and decreased aorta
compliance.
• In the US, AAAs are more common in white males than black males.
Prevalence
• <1% in the population under 50 years old.
• By the 7th decade of life, prevalence >5%
Morbidity
Acute rupture, paraplegia, postoperative sepsis, respiratory failure, renal dysfunction, MI, and
heart failure.
Mortality
Male/female mortality ratio 4/5
• Patient population often with multiple comorbidities that require concurrent management in
the perioperative period.
• Anticipate large hemodynamic swings and optimize changes in blood pressure and
tachycardia to maintain perfusion to vital organs.
• Implement measures to protect renal function.
• Spinal cord protection may involve distal aortic perfusion, CSF drainage, and systemic/local
hypothermia.
SYMPTOMS
• Often asymptomatic.
• Abdominal pain is a common complaint.
• Acute rupture can present with severe, sudden abdominal pain, and/or hemorrhagic shock.
History
• Detect any coexisting disease; risk factors include smoking, hypertension, hyperlipidemia,
family history, age, and diabetes mellitus.
• Etiology includes atherosclerosis (90%), hereditary disorders (e.g., Marfan’s), traumatic,
inflammatory, or as a sequelae of chronic aortic dissections.
Signs/Physical Exam
HTN, tenderness in abdomen or lower back, throbbing mass in abdomen, audible thrill in
abdomen on auscultation.
MEDICATIONS
Beta-blockers. By decreasing BP and heart rate, they are effective in reducing the sheer force
on the aortic wall and may reduce the incidence of aneurysmal rupture. Additionally,
initiation prior to major vascular surgery may reduce morbidity and mortality; optimal dose,
particular drug, duration of time, and target heart rate have not been elucidated.
Labs/Studies
• Electrolytes, renal panel, Hg, coagulation studies.
• Abdominal US/CT scan for diagnosis and monitoring of size.
• Cardiac evaluation: EKG; stress testing. A coronary angiography may be performed for high
risk patients or a stress test that suggests ischemia.
Peripheral vascular disease, coronary artery disease, renal insufficiency, COPD, diabetes
mellitus, morbid obesity, transient ischemic attacks, or previous cerebrovascular events.
TREATMENT
Premedications
• Beta-blockers; titrate to heart rate
• Anxiolytics, and analgesia
• Initiation of statins
• Blood consent
• Potential for postoperative intubation, spinal cord injury, myocardial events
• Epidural catheter consent if no contraindications to placement. Traumatic placement may
necessitate delaying the procedure (intraoperative heparin)
Cefazolin 1–2 g IV; if cephalosporin allergy, any other broad- spectrum antibiotic
INTRAOPERATIVE CARE
• Epidural catheter placement for open procedures if coagulation studies are within
acceptable limits and antiplatelet therapy does not contraindicate. Consider a paraverterbral
block in the presence of an INR >1.5.
Monitors
• Two large bore IVs
• Arterial line; consider preinduction placement
• Central venous catheter for CVP monitoring and venous access
• Pulmonary artery catheter and transesophageal echocardiography (TEE) if comorbidities
warrant
• Foley catheter
• Motor-evoked potentials (MEPs) to assess anterior spinal cord perfusion
• BIS to monitor depth of anesthesia
• A slow, controlled induction should be performed to ensure an adequate depth of anesthesia
and minimize hypertensive and tachycardic responses during laryngoscopy and intubation
– Choose quick onset/offset agents (e.g., esmolol, nitroglycerine)
– In patients at risk for pulmonary aspiration, carefully weigh the risks versus benefits of a
rapid sequence induction (HTN, tachycardia)
• Muscle relaxation. Baseline MEPs are usually attained after induction. If needed and not
contraindicated, succinylcholine should be utilized. Alternatively, short duration
nondepolarizing agents may be needed but should be communicated and discussed with the
surgeon and neuromonitoring team
• Epidural analgesia is advantageous for postoperative pain; it is often prudent to wait until
after the aorta is unclamped and hemodynamics has stabilized to bolus the epidural and
begin an infusion.
Maintenance
• Balanced anesthetic with volatile agent or IV techniques; avoid muscle relaxants if MEPs are
measured.
• Cross-clamping:
– Preload: Increased secondary to venous redistribution.
– Afterload: Increased by the clamp; more profound than with infrarenal clamps.
Compensatory vasodilation occurs above the clamp. May be poorly tolerated in patients
with left ventricular dysfunction (increased tension/myocardial oxygen consumption).
Myocardial ischemia and left ventricular failure can result if not properly anticipated.
Treat aggressively with vasodilators (nitroprusside, nicardipine, propofol).
– Heart rate: Reflex bradycardia may be seen.
– Contractility will increase in a normal heart; patients with cardiac disease may not be able
to compensate.
– SVR: Increases distal to the clamp to maintain perfusion; vasodilators can impair distal
perfusion pressure.
• Unclamping of the aorta: Release and activation of a wide range of bioactive mediators (e.g.,
proinflammatory cytokines, nitric oxide) leads to systemic vasodilatation with relative
hypovolemia and myocardial depression.
– Preload: Decreases as vasodilated arterial beds fill with blood; volume loading should be
performed prior to unclamping.
– Afterload is abruptly decreased. Consider initiating phenylephrine or norepinephrine drip
a few minutes prior to anticipated release of cross clamp or bolusing, as needed.
– Contractility: Washout of metabolites from lower extremity ischemia may impair inotropy
and necessitate the use of inotropes.
– Pulmonary artery pressure can increase from hypercarbia, acidosis, and ischemic
metabolites.
– Frequent ABG testing should be performed to diagnose and treat lactic acidosis from
splanchnic hypoperfusion, hypocalcemia, or other electrolyte imbalances.
• Spinal cord ischemia can result from interruption to its blood supply secondary to a variable
and unpredictable anatomy of the collateral intercostal and lumbar arteries (especially the
artery of Adamkiewicz).
– Lumbar CSF drains are placed preoperatively. Drainage of CSF can increase cord perfusion
(dependent on mean arterial pressure minus CSF pressure/venous pressure in the epidural
veins).
– Methylprednisolone 30 mg/kg before and after aortic occlusion may result in improved
spinal cord protection.
– Minimize clamp time to <30 minutes.
– Lower limb MEPs provide indirect monitoring of compromised cord perfusion.
– Other strategies: Maintain a high systemic arterial pressure, low systemic venous pressure,
and adequate right heart venous return; correct acidosis; and avoid hypoxia.
• Coagulopathy. Can cause, (or result from), excessive surgical bleeding, intraoperative
heparin, or multiple transfused cell salvage units (washing and processing depletes
coagulation factors).
• Renal protection. Adequate hemodynamics, volume, and inotropy. Mannitol 0.5 g/kg prior
to cross clamping, sodium bicarbonate infusions, and fenoldapam/dopamine may be used,
but their efficacy is controversial.
• Avoid sympathetic stimulation during extubation/emergence.
• Continue antihypertensive medications during extubation/emergence and ensure adequate
analgesia prior to extubation; if an epidural catheter is in place and the patient is
hemodynamically stable, the infusion may be started.
• Neurological function should be assessed as soon as possible.
FOLLOW-UP
BED ACUITY
ICU
ANALGESIA
• Maybe difficult to titrate in the intubated ICU patient.
• Continue regional anesthesia in the postoperative period and only remove if no signs of
coagulopathy are present (check the TEG and/or INR, PTT and platelet count)
COMPLICATIONS
• Hypotension could be a sign of intraabdominal or retroperitoneal bleeding.
• Postoperative care may be complicated by the presence of comorbidities such as CAD,
COPD, and CRF.
• Complications include MI, neurological deficits, spinal cord ischemia, renal failure, sepsis,
respiratory failure, and ventilator dependency.
REFERENCES
1. Blanchard JF. Epidemiology of abdominal aortic aneurysms. Epidemiol Rev.
1999;21(2):207–221.
2. Chang CK, Chuter TA, Reilly LM, et al. Spinal arterial anatomy and risk factors for lower
extremity weakness following endovascular thoracoabdominal aortic aneurysm repair with
branched stent-grafts. J Endovasc Ther. 2008;15(3):356–362.
3. DREAM Study Group. Long-term outcome of endovascular repair of abdominal aortic
aneurysm. NEJM. 2010;362:1881–1889.
4. El-Sabrout RA, Reul GJ. Suprarenal or supraceliac aortic clamping. Tex Heart Inst J.
2001;28:254–264.
5. Jacobs MJ, Mess W, Mochtar B, et al. Spinal cord blood supply in patients with
thoracoabdominal aortic aneurysms. J Vasc Surg. 2002;35(1):30–37.
6. Jean-Claude JM, Reilly LM, Stoney RJ, et al. Pararenal aortic aneurysms: The future of
open aortic aneurysm repair. J Vasc Surg. 1999;29:902–912.
7. Kahn RA, Stone ME, Moskowitz DM. Anesthetic consideration for descending thoracic
aortic aneurysm repair. Semin Cardiothorac Vasc Anesth. 2007;11:205.
• Somatosensory and motor-evoked potentials
• Endovascular aneurysm repair (EVAR)
• Somatosensory and motor evoked potentials (SSEPs/MEPs)
CODES
ICD9
ICD10
CLINICAL PEARLS
Preserve myocardial, pulmonary, renal, and CNS perfusion. Postoperative renal failure ranges
form 12–31% and is the most common factor seen in early mortality.
SUPRAGLOTTIC DEVICES
BASICS
DESCRIPTION
• Supraglottic devices are blind-insertion airway support devices that sit above the glottis.
They
– Allow for spontaneous and/or limited positive pressure ventilation
– Are used as planned or rescue airway devices
– Are available mostly as disposable devices
– Are generally latex free
• Commonly utilized devices on the market include the
– Laryngeal mask airway (LMA)
– Combitube
– King LT-D/LTS-D (suction capability)
• Indications: Supraglottic devices are appropriate when mask ventilation is desired but
endotracheal intubation is not necessary.
• Advantages:
– Compared to mask ventilation, it is more secure, allows “hands-free" ventilation, and
decreases spillage of volatile agents into the operating room.
– Avoidance of laryngoscopy (and muscle relaxation)
– Avoidance of tracheal stimulation in cases where general anesthesia is desired (e.g.,
reactive airway disease).
– Decreased postoperative sore throat
– Part of the difficult airway algorithm (2). May facilitate ventilation in patients that cannot
be ventilated with a mask. Additionally, it can serve as a conduit for tracheal intubation,
especially in a difficult airway situation. An endotracheal tube, tube exchanger, Aintree,
or fiberoptic bronchoscope can also be passed, depending on the device.
• Placement: Following induction, the device is inserted blindly into the pharynx and rests
above the vocal cords. The apertures are positioned to deliver fresh gas flow directly over
the laryngeal inlet.
• LMA
– Four main components: Soft cuff, airway tube, inflation balloon, and connector
– The cuff is designed to conform to the contours of the hypopharynx with its lumen facing
the laryngeal opening.
– The airway tube has a single large-bore lumen; an appropriately sized endotracheal tube
can be passed through it.
– Sizing varies by manufacturer and is usually weight based.
– Used in the difficult airway algorithm in a “cannot intubate, cannot ventilate” situation.
• Combitube (1)
– Four main components: Two cuffs, double lumen, two inflation balloons, and two possible
connections
– The distal cuff is low volume and can hold up to 15 mL of air; the proximal cuff is larger
and can hold up to 85 mL of air. They are designed to seal the upper airway and isolate
the trachea from the esophagus.
– It is inserted blindly and the distal cuff enters either the trachea or esophagus; the lumen
used for ventilation depends on the location in which it was placed.
– If the distal cuff is inserted in the trachea, then the distal lumen delivers air directly into
trachea. If the distal cuff is inserted into the esophagus, multiple apertures located in
between the distal and proximal cuff serve to deliver air over the laryngeal inlet.
– Only available in adult sizes 37 Fr and 41 Fr; cannot be used in the pediatric population.
• King LT-D/LTS-D
– Four main components: Two cuffs, single lumen tube, a single inflation balloon, and
connector
– It is inserted blindly, with the lumen entering the esophagus (size and angle favor
posterior passage). The two cuffs (one for the oropharynx and the other for the esophagus)
are inflated simultaneously; the cuffs are high volume and low pressure.
– Multiple ventilation holes are located between the cuffs; they are positioned to deliver air
over the laryngeal inlet.
– The single lumen allows passage of a bronchoscope or tube exchanger to emerge through
a “ramp” in the pharyngeal cuff that is directly over the laryngeal inlet. This allows for
tube exchange or examination.
– The King LTS-D has a double lumen/side port that allows passage of suction, a tube
exchanger, or a fiberoptic scope that would emerge at the distal end (esophagus) and
would not disrupt ventilation.
– Sizing is based on height
ANATOMY
• LMA
– The cuff area should be lubricated with plain jelly to reduce friction against the hard
palate. The use of lidocaine jelly may cause postoperative numbness that distresses
patients.
– The cuff can be fully, partially, or not inflated during insertion.
– Insertion is commonly performed with the head extended using the dominant hand.
– The cuff is pressed upward toward the hard palate.
– Care should be taken not to “drag” the tongue; this may be achieved by displacing the
tongue from the hard palate with fingers from the nondominant hand (or providing a chin
lift), a tongue depressor, or even a laryngoscope.
– The LMA should be advanced past the epiglottis; final position should be in the
hypopharynx above the vocal cords. The ventilation outlet is midline, directly over the
glottic opening.
– A “good fit” is confirmed by assessing tidal volumes and the pressure where a leak is
detectable.
– Removal may be performed with the cuff fully, partially, or not inflated. Some advocate
not deflating in order to “pull out” secretions
FIGURE 1. Laryngeal mask airway. Single-lumen, single-cuff, single-balloon inflation
• Combitube (1)
– Insertion should occur with the cuffs deflated and lubricated with plain jelly.
– Using the dominant hand, the device is placed blindly and gently, without force, to a
depth where the upper incisors are between the two black lines on the device. The tongue
should not be “dragged;” consider above-mentioned techniques as appropriate.
– The distal cuff is inflated with 10–12 mL and ventilation is performed via the distal
connector while listening for gurgling sounds over the epigastrium or bilateral breath
sounds over the lungs.
– If breath sounds over the lungs are heard, the tube has entered the trachea; the distal cuff
should remain inflated and ventilation is performed via the distal lumen, as with a
standard endotracheal tube.
– More commonly, gurgling sounds are heard over the epigastrium, indicating that the tube
has entered the esophagus. Inflate both cuffs to prevent air from escaping through the
esophagus or back out the oropharynx/nasopharynx. Ventilate via the proximal lumen.
Fresh gas flow is delivered through the multiple apertures situated above the distal cuff.
FIGURE 2. Combitube. Double-lumen, double-cuff, double-balloon inflation
• King LT-D
– Insertion should occur with the cuffs deflated and lubricated with plain jelly.
– The device is inserted blindly with the dominant hand into the esophagus until the upper
incisors are between the black lines on the device. The nondominant hand is used to hold
the mouth open and apply a chin lift as needed. Some advocate for introduction using a
lateral approach, followed by rotation back to midline once the tip is behind the base of
the tongue
– The distal cuff inflates in the esophagus and the proximal cuff inflates at the base of the
tongue.
– It may be necessary to gently pull back while assessing ease of ventilation and tidal
volumes. Readvancement cannot be performed with the cuffs inflated.
– To utilize the gastric lumen in the King LTS-D, the suction catheter needs to be lubricated.
FIGURE 3. King LT-D. Single-lumen, double-cuff, single-balloon inflation
• Relative contraindications for supraglottic devices include
– Risk of aspiration: Because these devices sit above the vocal cords and do not isolate the
trachea from the esophagus, patients are not protected from aspiration. Endotracheal
intubation is preferable for patients who are pregnant or in patients at risk for aspiration.
– Major abdominal or thoracic surgery
– When high-inspiratory pressures are required for ventilation: Supraglottic devices are not
ideal for laparoscopic procedures or Trendelenburg position because it may be difficult to
administer adequate positive pressure ventilation. Additionally, decreased respiratory
system compliance can be seen in patients with obesity and restrictive pulmonary disease.
– Patient positioning influences the seating and seal. Supraglottic devices should not be used
for cases in the prone position. Leak and cuff pressures are altered in the LMA with
changes in head extension and mouth opening.
• Potential difficulties:
– “Poor seating” or malpositioning, resulting in poor seal and large leak.
– Dental trauma
– Bleeding
– Sore throat.
– Hiccups
– Vagal response
• Laryngospasm: Because supraglottic devices sit above the vocal cords, they do not protect
against laryngospasm. Laryngospasm can occur at any time when there is an inadequate
depth of anesthesia.
• Because the trachea is not manipulated, the use of a supraglottic device makes
bronchospasm and coughing on emergence less likely. The sympathetic stimulation with
direct laryngoscopy is also avoided.
• General anesthesia must be induced before insertion, but laryngoscopy and muscle
relaxation are not necessary.
• Patient is able to breathe spontaneously, through a wider lumen than an endotracheal tube.
• In addition to being used electively, they are also part of the difficult airway algorithm (2).
When laryngoscopy fails and ventilation is not effective, an LMA (or other supraglottic
device) can be placed blindly.
• The amount of air to be placed in the supraglottic device and the optimal cuff pressure are
controversial. Placing the amount of air recommended by the manufacturer may avoid
overinflation and excessive cuff pressures.
• Some devices include a built-in bite block. Otherwise, a prepared bite block or gauze may be
used to prevent biting down.
• Some devices include a port for nasogastric tube placement. Otherwise, placement of such a
tube may be difficult or impossible without compromising the seal.
• The LMA is useful to assist with intubation. With the LMA-Aintree technique, an LMA is
placed and ventilation is confirmed (3). An Aintree Intubation Catheter (AIC) is
fiberoptically guided through the LMA into the trachea. The LMA and fiberoptic scope are
removed while the AIC is left in place. The endotracheal tube is passed over the AIC and the
AIC is removed.
REFERENCE
1. Urtubia RM, Aguila CM, Cumsille MA. Combitube: A study for proper use. Anesth Analg.
2000;90:958–962.
2. Practice guidelines for management of the difficult airway: An updated report by the
American Society of Anesthesiologists Task Force on Management of the Difficult Airway.
Anesthesiology. 2003;98: 1269–1277.
3. Turk M, Gravenstein D (2007). Aintree Intubation Catheter Technique in Unanticipated
Difficult Intubation. Retrieved March 10, 2011 from University of Florida Department of
Anesthesiology, Center for Simulation, Advanced Learning and Technology, Virtual
Anesthesia Machine Web site: http://vam.anest.ufl.edu/ airwaydevice/aintree/index.html.
4. Bein B, Scholz J. Supraglottic airway devices. Best Practice & Research Clinical
Anaesthesiology. 2005;19(4):581–593.
• Laryngospasm
CLINICAL PEARLS
• Supraglottic devices are useful in “cannot intubate, cannot ventilate” situations.
• They do not protect the trachea from aspiration of gastric contents or laryngospasm (4).
• The Combitube has an increased incidence of sore throat, dysphagia, and upper airway
hematoma when compared to LMAs and endotracheal tube. Esophageal rupture is a rare
complication that has been reported, thus known esophageal disease is a contraindication.
SURGICAL SITE INFECTIONS, PREVENTION
Edward C. Nemergut, MD
BASICS
DESCRIPTION
A surgical site infection (SSI) is a bacterial infection of the skin or underlying tissue that
results from a surgical wound. This definition was established in 1992 when the Centers for
Disease Control (CDC) revised its definition of “wound infection” to prevent confusion
between the infection of a surgical incision and the infection of a traumatic wound.
EPIDEMIOLOGY
Prevalence
• The overall incidence of SSI is ∼3%; however, the incidence varies greatly for each
operative procedure, surgeon, hospital, and country.
• Depending upon the series, SSIs are the second or third most common nosocomial infection
after urinary tract infections and lower respiratory infections, respectively.
• “Contaminated” procedures are typically associated with the highest incidence of infection.
In the CDC’s Study on the Effect of Nosocomial Infection Control (SENIC), the wound
infection risk in patients undergoing colon surgery ranged from 9% to 27%
• “Clean” procedures are typically associated with a lower incidence of infection.
• In the US, there are ∼500,000 SSIs each year.
Morbidity
• Highly dependent on the site of infection and the depth of the tissues infected. For example,
deep sternal wound infection after cardiac surgery is associated with high morbidity;
whereas skin infection after a superficial lipoma resection is associated with lower
morbidity. Nevertheless, most SSIs are superficial, but contribute greatly to the morbidity
and mortality associated with surgery.
• In the US, mean estimates of prolonged hospitalization vary from 5 to 20 days per infection.
A review of the incidence and economic burden of SSIs in Europe estimated that the mean
length of extended stay attributable to SSIs was 9.8 days.
• SSI also leads to a longer ICU stay and a five-fold increase in the need for hospital
readmission.
• Costs are higher after discharge because many patients recovering from wound infections
are usually discharged before the wound closes entirely, and thus require dressing changes
and home nursing visits. Patients may also require long-term IV antibiotics and the
consequent need for central line access.
Mortality
Like morbidity, mortality is highly dependent on the site of infection and the depth of the
tissues infected. For example, the mortality associated with deep sternal wound infection after
cardiac surgery ranges from 6% to 30%, with a mean around 13%.
• Type of surgery
• Character and magnitude of bacterial contamination
• Hypothermia
• Hyperglycemia
• The presence of foreign bodies in the wound
• Hypovolemia
• Patient immune function or immunosuppression
• Inappropriate or inadaquate antimicrobial prophylaxis
• The National Nosocomial Infection Surveillance System (NNISS) can help quantify risk based
on the type of surgery, American Society of Anesthesiologists’ physical status rating, and
surgical duration.
• Wound contamination
– Even with perfect surgical technique, clean surgical wounds will inevitability become
contaminated with bacteria. The ability of a patient to prevent contamination from
becoming an infection is dependent on an intact immune response. The first few hours
after surgery represent the critical period; wherein the course from contamination to
infection is either blunted or progresses (even if the infection may not manifest for several
days).
• Immune response
– The body’s first line of defense against bacterial pathogens is nonspecific killing by
neutrophils, an oxygen-dependent process. Oxidative killing depends on the production of
the bactericidal superoxide radical from molecular oxygen, catalyzed by the enzyme
NADPH oxygenase. It is not surprising that the risk of infection is related to the oxygen
tension in the wound and infection. In one study, tissue oxygen measured in the patient’s
upper arm only 75 minutes after colorectal surgery predicted development of
postoperative SSI, although infections were typically diagnosed more than a week later.
• Optimization
– The prevention of infection revolves around optimizing wound physiology. Adequate
tissue perfusion provides ample oxygen substrate and neutrophils.
– In order to be effective, antibiotics must be present in the skin and subcutaneous tissues at
adequate concentrations prior to surgical incision.
• The Surgical Care Improvement Project (SCIP) partnership is a multi-year national campaign
in the US focused on substantially reducing surgical mortality and morbidity, including the
incidence of SSIs. Some recommendations are more applicable to surgeons (e.g., appropriate
hair removal), whereas others are more applicable to anaesthetists.
• Appropriate timing and selection of antibiotics
– Timely administration of antibiotics is necessary for effective infection prophylaxis so that
adequate tissue concentrations are present at the time of surgical incision. Most
recommendations suggest that IV antibiotics should be administered between 15 and 60
minutes prior to incision.
– It is also important to select antibiotics that cover the bacteria most likely to cause
infection in a given procedure. In general, a first-generation cephalosporin (e.g., cefazolin)
is appropriate for most clean procedures. For contaminated procedures, a second-
generation cephalosporin (e.g., cefoxitin) may be appropriate. Beta-lactam allergic
patients require special considerations.
– As anaesthetists are typically responsible for the administration of antibiotics, they should
be familiar with all current guidelines.
• Optimize wound physiology. Adequate tissue perfusion provides ample oxygen substrate and
neutrophils.
• Maintenance of normothermia (>36°C)
– In a 1996 study of patients undergoing colorectal surgery, patients randomized to
hypothermia were three times more likely to develop a SSI compared to patients
randomized to normothermia. Additionally, the duration of hospitalization was prolonged
by 2.6 days in the hypothermia group.
• Control of hyperglycemia
– In patients undergoing cardiac surgery, perioperative hyperglycemia is strongly associated
with SSIs. That said, the risks of aggressive glucose control must be measured against the
significant risks associated with hypoglycemia. Recommendations may be patient-specific
and disease-specific; however, most data suggests that glucose should be controlled with
an IV insulin infusion to keep levels below 180 mg/dL.
• Hyperoxia
– The use of normobaric hyperoxia (∼80%) has been shown to decrease the risk of SSI
during surgery and the immediate postoperative period. Of note, in all trials
demonstrating efficacy, hyperoxia was continued for a minimum of 2 hours after the
conclusion of surgery.
– It is unknown if normobaric hyperoxia used only during the intraoperative period is
associated with decreases in the risk of SSI. A meta-analysis of the results found it
reasonable to conclude that hyperoxia has a beneficial, albeit limited, effect on the
incidence of SSI.
• CDC criteria, revised in 1992, for incisional SSI are an infection at the incision site within 30
days after surgery as defined by any of the following items:
– Purulent drainage from the incision or drain located above the fascial layer
– Organism isolated from a fluid culture in a closed wound
– Surgeon deliberately opens wound (unless the wound culture is negative)
– Surgeon’s or attending physician’s diagnosis of infection
• The CDC criteria for deep surgical wound infections are an infection related to surgery
occurring at the operative site within 30 days of surgery involving tissues or spaces at or
beneath the fascial layer and any of the following:
– Purulent drainage from the drain placed beneath the fascial layer
– Wound spontaneously dehisces or is deliberately opened by the surgeon when the patient
has a fever (>38°C) and/or localized pain or tenderness, unless the wound culture is
negative
– An abscess or other evidence of infection seen on direct examination, during surgery, or
by histopathologic examination
– Surgeon’s diagnosis of infection
TREATMENT
SSIs are typically treated with a combination of antibiotic and/or surgical drainage.
FOLLOW-UP
• Scheduled antibiotics are often necessary

• Return to the operating room for a “wash out” in certain incidences.
REFERENCES
1. Haley RW, Culver DH, Morgan WM, et al. Identifying patients at high risk of surgical
wound infection. A simple multivariate index of patient susceptibility and wound
contamination. Am J Epidemiol. 1985;121(2):206–215.
2. Houbiers JG, et al. Transfusion of red cells is associated with increased incidence of
bacterial infection after colorectal surgery: A prospective study. Transfusion.
1997;37(2):126–134.
3. Jonsson K, Jensen JA, Goodson WH III, et al. Assessment of perfusion in postoperative
patients using tissue oxygen measurements. Br J Surg. 1987;74(4):263–267.
4. Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of
surgical-wound infection and shorten hospitalization. Study of wound infection and
temperature group. N Engl J Med. 1996;334(19):1209–1215.
5. Mauermann WJ, Nemergut EC. The anesthesiologist’s role in the prevention of surgical site
infections. Anesthesiology. 2006;105(2): 413–421.
6. Mauermann WJ, Sampathkumar P, Thompson RL. Sternal wound infections. Best Prac Res
Clin Anaesthesiol. 2008;22(3):423–436.
7. Murray BW, Huerta S, Dineen S, et al. Surgical site infection in colorectal surgery: A review
of the nonpharmacologic tools of prevention. J Am Coll Surg. 2010;211(6):812–822.
8. Nichols RL. Preventing surgical site infections: A surgeon’s perspective. Emerg Infect Dis.
2001;7(2): 220–224.
• Hypothermia
• Hyperglycemia
CODES
ICD9
998.59 Other postoperative infection
ICD10
• T81.4XXA Infection following a procedure, initial encounter
• T81.4XXD Infection following a procedure, subsequent encounter
• T81.4XXS Infection following a procedure, sequela
CLINICAL PEARLS
• Although generally thought to be a surgical complication, the incidence of SSIs is lower
when anaesthetists take an active role in infection prevention. Studies have shown that
when anaesthetists administer antibiotics, on time administration occurs 92% of the time.
• Keep patients warm.
• Check and control blood glucose in patients prone to hyperglycemia.
• Consider normobaric hyperoxia if there is no contraindication.
SYNCHRONIZED ELECTRICAL CARDIOVERSION
Susan Kaplan, MD
BASICS
DESCRIPTION
General
• Synchronized electrical cardioversion is the delivery of a brief pulse of external electrical
direct current (DC) across the chest wall to convert certain abnormal rhythms to a normal
sinus rhythm (NSR) in elective or emergent scenarios. It is utilized for (1):
– Atrial fibrillation (elective treatment is the most common indication).
– Reentry supraventricular tachycardia (SVT)
– Atrial tachycardia
– Monomorphic ventricular tachycardia (VT) with pulses
• Elective cardioversion (CVN) is generally performed by a cardiologist or electrophysiologist
in a controlled setting.
• Urgent or emergent CVN may be performed in the perioperative period by the anaesthetist.
• A biphasic, synchronized discharge is delivered via paddles or self-adhesive electrodes (pads
or patches).
– Current flow is either in the anterolateral (AL) or anteroposterior (AP) direction.
– Electrode positioning: Parasternal and inferoapical for AL, parasternal and left
infrascapular for AP.
– Electrodes should be firmly adherent to chest wall with sufficient conductive gel to
prevent skin burns or improper current dispersion.
– If a pacemaker or internal cardioverter defibrillator (ICD) is present, electrodes should be
positioned 15 cm from the device (2), preferably in the AP position
• Energy requirements for DC CVN vary depending on the underlying rhythm (Biphasic
mode).
– Atrial fibrillation: 120–200 J; if initial shock fails, increase sequentially (200 J then 360 J)
(1)
– Atrial flutter: 50–100 J (2)
– Monomorphic VT with pulse: 100 J; if initial shock fails, increase sequentially (200 J then
360 J) (1)
• Synchronization and discharge occur with the R or S wave of the QRS complex to avoid
energy delivery during the relative refractory period of the myocardium (apex of T wave)
that can result in malignant ventricular arrhythmias
• Common surgical problems
– Inadequate anticoagulation (international normalized ratio (INR) <2.0–3.0)
– Atrial thrombus evident on transesophageal echocardiography (TEE) precluding DC CVN
– Impaired transthoracic impedance
Increased body mass index
Emphysema
Insufficient contact between electrodes and chest wall
– Inability to convert to NSR
– Bradyarrhythmias
– Sinus tachycardia, multifocal atrial tachycardia, digoxin toxicity
– Inadequate anticoagulation
– Presence of atrial thrombus
– Pulseless VT, ventricular fibrillation (VF)
Position
• Supine, arms tucked at sides
• May be performed in the operating room (OR), emergency room (ER), on a stretcher or
hospital bed
Incision
• None
• Paddles or self-adhesive electrodes
Approximate Time
• Seconds for electrical discharge
• Several minutes if multiple discharges are required
• Anesthesia time 5–10 minutes
EBL Expected
None
Hospital Stay
• Elective CVN is generally performed on an outpatient basis; observation for several hours
after procedure
• Semiurgent, emergent CVN is performed in the OR, or at the bedside
• ECG/defibrillator with synchronized discharge
• Paddles (and conductive gel) or self-adhesive electrodes
EPIDEMIOLOGY
Prevalence
Not available
Morbidity
• Soreness or pain over chest wall, especially with repeated electrical discharges
• Arrhythmias
• Device malfunction if pacemaker or ICD present
• Oral trauma
• Skin burns (insufficient conductive gel)
Mortality
Rare
• Amnesia and analgesia are required for a short duration of time.
• Patients with significant cardiac disease and functional impairment may deteriorate rapidly,
even with reduced dosing and careful titration of sedation medications.
• Precautions should be taken to avoid patient self-injury during electrical discharge.
• Despite elective CVNs being performed frequently in remote locations (outside the OR), the
same medications and equipment that are standard to the OR should be available
• Emergent DC CVN may be life-saving in the perioperative setting in patients with unstable
arrhythmias.
SYMPTOMS
• Palpitations, irregular heart beat
• Shortness of breath, chest pain
• Fatigue, reduced exercise tolerance
• Lightheadedness, dizziness, syncope
• Some patients asymptomatic
History
• Date of onset, frequency, duration of symptoms
• Previous history atrial flutter, AF, VT
• Cardiac and noncardiac diseases, cardiovascular risk factors (ischemia, myocardial infarct,
valvular disease, coronary artery disease)
• Alcohol, caffeine, drug, smoking history
• Previous interventions (pacemaker, ICD, CVN, ablation procedures)
• Medication changes or dosing changes
Signs/Physical Exam
Irregularly, irregular pulse
MEDICATIONS
• New onset AF (<48 hours): Risk of thromboembolism is low; anticoagulation is not
typically required before or after CVN
• Paroxysmal AF (terminates spontaneously within 7 days, often within 24 hours)
– Full anticoagulation
– If INR <2.0–3.0, a TEE should be performed to rule out thrombus.
– If no thrombus is evident, heparin must be started prior to CVN.
– Anticoagulation should be continued for 4 weeks after CVN.
– Anticoagulants include warfarin (most commonly prescribed), aspirin, heparin, low
molecular weight heparin, and clopidogrel.
• Persistent AF (>7 days); same treatment as paroxysmal AF
• Additional medications are usually prescribed in patients with long-standing AF to prevent
stroke or other embolic events, atrial remodeling, or tachycardia-induced cardiomyopathy
(3).
• Rate control medications
– Beta-blockers
– Calcium channel blockers
• Rhythm control medications
– Flecainide, propafenone
– Sotalol, dofetilide, ibutilide
– Amiodarone, dronedarone
– Verapamil
– Quinidine
Labs/Studies
• ECG
– Atrial fibrillation: Irregularly, irregular R-R intervals, absence of P waves
– Atrial flutter: Saw tooth pattern
– SVT
– Atrial tachycardia
– Monomorphic VT
• Coagulation profile
• Chest radiograph to detect underlying cardiopulmonary pathology
• Transthoracic echocardiography to identify underlying heart disease, dilated atria, atrial
thrombus
• 24-hour electrocardiographic monitoring or event recorder to diagnose paroxysmal AF
• Electrolytes, CBC, INR
• Renal, hepatic, and thyroid function
• In urgent, emergent situations, acquisition of above should rarely preclude treatment.
• Structural or valvular heart disease, hypertension, coronary artery disease
• Obesity, obstructive sleep apnea, diabetes
• Hyperthyroidism
• Stroke, thromboembolic disease of the heart, lungs, kidneys, limbs
TREATMENT
Premedications
• Benzodiazepines for anxious patients
• Heparin infusion when appropriate
• Anti-arhyrhmic infusions when appropriate
• Emergency intubation or CPR if malignant ventricular arrhythmias or asystole occur and are
unresponsive to medications
• Possible oral trauma
INTRAOPERATIVE CARE
A continuum between deep sedation and general anesthesia
Monitors
• Functioning IV (18, 20 gauge) with crystalloid infusion; in patients with severe cardiac
disease, judicious fluid administration
• Supplemental oxygen via nasal cannula or face mask (simple, nonrebreather) in
spontaneously breathing patients
• If airway obstruction or apnea:
– Jaw thrust
– Positive pressure ventilation
– In rare circumstances, urgent placement of endotracheal tube (ETT) or laryngeal mask
airway (LMA) in patients who cannot be mask ventilated.
• Induction agents titrated to loss of eyelid and glabellar reflexes
– Propofol most commonly used
– Etomidate may be substituted in patients with an ejection fraction (EF) <30–40%
• Opiates may be added in patients with drug dependency
• Elective intubation (LMA, ETT) in select patients (e.g., known difficult airway, aspiration
risk).
Maintenance
• Procedure is typically of such a short duration that no additional medications are needed
unless a repeat CVN must be performed.
• Emergency medications should be available and ready for immediate administration (e.g.,
atropine, ephedrine, phenylephrine, epinephrine)
• Emergence and response to commands occurs as induction medications redistribute to
peripheral compartments.
• Generally 5–7 minutes, longer with repeated dosing for multiple shocks.
FOLLOW-UP
BED ACUITY
• Elective CVN
– Outpatients
– Observation to assure normal recovery from anesthesia
– Treatment of postoperative problems such as nausea and vomiting
• Semiurgent, emergent CVN
– Observation to assure normal recovery from anesthesia, maintenance of NSR
– Treatment of patients with unstable hemodynamics
ANALGESIA
• Not generally required
• Fentanyl or ketorolac for pain, soreness
COMPLICATIONS
• Procedure related
– Failed conversion to NSR
– Bradyarrhythmias, reoccurrence AF
– R-on-T phenomena, malignant ventricular arrhythmias, asystole (rare)
– Accidental shock to healthcare personnel
• Anesthesia related
– Prolonged sedation
– Hypoxia or inability to mask ventilate
– Postoperative nausea and vomiting
– Aspiration
– Tongue, lip laceration if patients bite down during electrical discharge
PROGNOSIS
• Success rate is 90% when AF <1 year duration (5) and no underlying heart disease; 50%
when arrhythmia present >5 yrs or atrial diameter >5 cm (2).
• Adult monomorphic VT with pulse responds well to a single shock at 100 J (1).
REFERENCES
1. Link MS, Atkins DL, Passman RS, et al. Part 6: Electrical therapies: Automated external
defibrillators, defibrillation, cardioversion, and pacing. 2010 American Heart Association
Circulation. 2010;122(suppl 3):S706–S719.
2. Sucu M, Davutoglu V, Ozer O. Electrical cardioversion. Ann Audi Med. 2009;29(3): 201–
206.
3. Lafuente-Lafuente C, Mahe I, Extramiana F. Management of atrial fibrillation. Br Med J.
2010;340:40–45.
4. Khoo CW, Lip GYH. Acute management of atrial fibrillation. Chest. 2009;135:849–859.
5. Cakulev I, Efimov IR, Waldo AL. Cardioversion. Past, present, and future. Circulation.
2009;120: 1623–1632.
ADDITIONAL READING
• Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management
of patients with atrial fibrillation: A report of the American College of Cardiology/American
Heart Association Task Force on practice guidelines and the European Society of Cardiology
Committee for Practice Guidelines (Writing Committee to Revise the 2001 guidelines for the
management of patients with atrial fibrillation): Developed in collaboration with the
European Heart Rhythm Association and the Heart Rhythm Society. Circulation.
2006;114(7):E257–354.
CLINICAL PEARLS
• Elective CVN of atrial fibrillation (<1 year) has a 90% success rate with a single electrical
discharge of 100–200 J. This value decreases to 50% when AF is present for longer than 5
years.
• Induction agents should be titrated slowly, especially in patients with a low EF.
• Protect the patient from self-injury as well as yourself from accidental shock.
• In the perioperative setting, early DC CVN may be life-saving in patients with unstable
arrhythmias.
• Malignant ventricular arrhythmias and asystole are rare after CVN, but be prepared to treat.
• Synchronized electrical cardioversion is NOT effective in focal and multifocal atrial
tachycardias.
SYNCHRONIZED INTERMITTENT MANDATORY VENTILATION
(SIMV)
Lan Chi Tran, MD
BASICS
DESCRIPTION
• Synchronized intermittent mandatory ventilation (SIMV) is a time-cycled mode that
provides a minimum level of ventilation, while allowing the patient to breathe
spontaneously between preset mechanical breaths. It allows for three different types of
breaths and prevents “breath stacking”:
– Controlled or mandatory breath; a backup rate is set to prevent apnea or hyperventilation
– Assisted (synchronized) breaths for spontaneously initiated breaths that fall within the
synchronization window. Limits barotrauma from high peak pressures that could arise if a
preset breath is delivered when the patient is maximally inhaled (breath-stacking) or
forcefully exhaling (dyssynchrony).
– Spontaneous breaths that occur outside the synchronization window (can be pressure
supported).
• SIMV was originally developed as a weaning mode; however, it is now popularly used as a
primary mode of ventilation in the intensive care unit (ICU). In the operating room, under
general anesthesia, it has also garnered popularity. Benefits can include
– Improved patient comfort
– Decreased “breathing against the ventilator” from asynchrony or “bucking;" this can
theoretically decrease the need for sedation and muscle relaxants (1,2)[B].
– Decreased hyperventilation; prevents respiratory and left-shift of the oxygen-dissociation
curve (decreased O2 unloading to tissue).
• Parameters that need to be set:
– FiO2
– Positive end-expiratory pressure (PEEP)
– Method of support; preset tidal volumes (SIMV-Vol), pressure control level (SIMV-PC), or
pressure support (SIMV-PSV)
– Sensor sensitivity
– Backup respiratory rate (RR)
– Trigger window
– I:E ratio
• Full and partial ventilator support. Full ventilator support is provided when patients are
apneic, sedated, or paralyzed. Partial ventilator support is provided when the patients are
spontaneously ventilating.
• Interactive components of SIMV. Timing windows are used to give a mechanical breath
during a pause in the patient’s respiratory cycle; should a spontaneous breath take place,
the preset breath is synchronized to it. A spontaneous breath is detected by a flow sensor at
the opening of the airway (at endotracheal tube [ETT] adaptor). The flow sensor is triggered
by changes in airway pressure, airflow, and respiratory movements. Flow cycling
(responsible for switching from expiration to inspiration) stops ventilator-derived breaths
when spontaneous inspiration terminates and improves synchronization because the patient
modulates the length of inspiration. These components function to prevent breath stacking.
• Patient-triggered versus ventilator-triggered breaths. Spontaneous breaths that fall within
the timing window are supported or synchronized. Spontaneous breaths that occur outside
the synchronization window are not supported unless pressure support ventilation (SIMV-
PSV) is added.
• Work of breathing (WOB). Spontaneous breaths incur energy and work. If they are not
supported, it can result in increased WOB, tachypnea, abnormal breathing patterns, and
respiratory fatigue (3,4)[A]. The addition of SIMV-PS serves to support the spontaneous
breath, decreases work, and reduces shallow breaths that can result in atelectasis and
shunting. Thus, WOB is inversely proportional to inspiratory pressure support. However, it
does not abolish the breathing effort made by the patient; the WOB is equivocal to other
controlled modes (2)[B].
• Settings
– FiO2: As with most modes of ventilation, this needs to be selected. Patients are often
started at an FiO2 of 1.0 with downward titration to avoid oxygen toxicity and decreased
surfactant production.
– PEEP: Reduces atelectasis during expiration and results in improved oxygenation, lung
volume (by increasing functional residual capacity), and lung compliance. Optimal PEEP
is calculated based on the level at which static compliance is highest (generally 5–12 cm
H2O). Avoid PEEPs >12–15 cm H2O that can result in overdistention of alveoli and
decreased cardiac output.
– Method of support (tidal volume versus pressure control). In tidal volume support (SIMV-
VC), a volume is set for each ventilator delivered or synchronized breath. Peak inspiratory
pressure (PIP) varies as lung compliance changes; and sudden drops in compliance can
lead to barotrauma. In pressure control (SIMV-PC), a pressure is set for each ventilator
delivered or synchronized breath; it prevents high PIP and thus prevents barotrauma.
However, the tidal volume may change if lung compliance is dynamic. There can be a
wide range of breath-to-breath tidal volumes and risk of hypocarbia. Inspiratory pressure
support (SIMV-PS) is usually set at 30–50% of the difference between the PIP and PEEP; it
aids with overcoming resistance imposed by an ETT and ventilator circuit for spontaneous
patient breaths.
– Sensor sensitivity is the amount of negative inspiratory force needed to trigger a breath
from the ventilator. It is usually set at −1 to −2 cm H2O.
– Backup RR is typically at 8–12 breaths/minute. A higher rate decreases expiratory time
and risks air trapping and auto-PEEP.
– Trigger window is the proportion of expiratory pause that the ventilator waits for an
inspiratory effort. A spontaneous breath during this window will be “synchronized” and
supported.
– I:E ratio is typically set at 1:2. For obstructive airway disease, breath stacking, or auto-
PEEP, it is often changed to 1:2.5 to 1:4. Consider an inverse I:E ratio in poorly compliant
lungs or ARDS.
ANATOMY
During SIMV, depth and rate of spontaneous ventilation is driven by the patient’s intrinsic
ventilatory drive, and respiratory muscle effort.
Adverse effects are similar to other modes of mechanical ventilation:
• Ventilator-associated pneumonia (VAP)
• Oxygen toxicity: Prolonged exposure to FiO2 >0.5 can result in alveolar membrane injury
from prolonged exposure to hyperoxia. The pathogenesis is believed to be secondary to
excess oxidant production, lipid peroxidation, protein oxidant damage, and cell death.
• Absorption atelectasis can occur at higher inspired oxygen fractions. In poorly ventilated
alveoli, uptake/absorption of oxygen by blood exceeds replenishment and alveoli “collapse”
(shunting).
• Bronchopulmonary dysplasia. Chronic lung injury can be seen in neonates exposed to
positive pressure ventilation and hyperoxia. Toxic factors cause injury to small airways and
microvasculature, thus interfering with alveolar septation. SIMV has been shown to be
associated with a lower risk of chronic lung injury in neonates (3)[B].
• Barotrauma/volutrauma. Inappropriate ventilator settings, plateau pressures >30 cm H2O,
peak pressure >40 cm H2O. Lower risk with SIMV compared to other controlled modes of
ventilation.
• Acute lung injury (ALI). High distending pressures in alveoli can increase vascular filtration
pressure and microvascular permeability to protein as well as produce pulmonary capillary
stress fractures and surfactant inactivation. Mucous flow can be impeded and lung rupture
may occur. Mechanical damage leads to leakage of fluid, protein, and blood into the tissue
and air spaces.
• V/Q mismatch. Alveolar distension can compress vessels and result in decreased alveolar
perfusion.
• Decreased cardiac output. Increased intrathoracic pressure from positive pressure ventilation
can decrease filling in the compliant right heart. This can result in decreased cardiac
preload, which is exacerbated in the setting of hypovolemia.
• Increased WOB and risk of respiratory fatigue if used without pressure support (5)[A].
• Intraoperatively, SIMV can be used to ensure a minimal level of ventilation in spontaneously
breathing patients whose RR and effort will decrease after administration of narcotics,
sedatives, and volatile agents. It is a useful tool during emergence and allows a smooth
transition from full ventilator support to partial ventilator support to unsupported
spontaneous breathing. Weaning can be achieved by
– Reducing the backup RR and/or the tidal volumes (decrease volume or pressure settings).
Requires patient to take on greater proportion of breathing.
– Decreasing ventilation to raise the paCO2 (permissive hypercarbia) above apneic threshold
and stimulate spontaneous breathing.
– Conversely, increasing ventilation or SIMV rate (overbreathing) lowers the paCO2 below
the resting paCO2 (apneic threshold) and depresses ventilatory drive.
• In the ICU, SIMV is commonly used to wean patients off mechanical ventilation. Studies in
adults have not shown statistical differences in weaning duration, use of sedation, weaning
fatigue, length of ICU stay, or mortality compared to other controlled modes (IMV & A/C)
(1,2,5)[A]. Weaning can be achieved by
– Decreasing the initial set rate to ∼2–4 breaths/minute every 12 hours as tolerated
(monitor the rapid shallow breathing index and arterial blood gases) until a rate of 2–4
breaths/minute.
– Adding PS (∼5–8 cm H2O) to overcome the resistance imposed by the ETT, ventilator
tubing, and circuit valve.
– Extubation can be considered if the patient is tolerating a backup RR <4/minute for
>120 minutes.
• Overall lower peak pressures with SIMV compared to other controlled modes in neonates
has been shown to decrease chronic lung injury (3)[B].
EQUATIONS
• Tidal volumes depend on pulmonary status:
– Normal Adult: 8–10 mL/kg of ideal body weight.
– ARDS/ALI: 5– 8 mL/kg of ideal body weight, plateau pressure <30 cm H2O
• Ideal body weight:
– Male: 50 + 0.91 (height in cm – 152.4)
– Female: 45.5 + 0.91 (height in cm – 152.4)
• Minute ventilation at rest: TV × RR. (Normal adult: 5–8 L/min)
• Lung compliance = ΔVolume (L)/ΔPressure (cm H2O)
GRAPHS/FIGURES
FIGURE 1. Pressure versus time for the three different types of breaths seen with synchronized intermittent mandatory
ventilation (SIMV).
REFERENCE
1. Giuliani R, et al. Patient-ventilator interaction during synchronized intermittent mandatory
ventilation. Effects of flow triggering. Am J Respir Crit Care Med. 1995;151:1–9.
2. Vitacca M, et al. Assessment of physiologic variables and subjective comfort under different
levels of pressure support ventilation. Chest. 2004;126:851–859.
3. Reyes ZC, et al. Randomized, controlled trial comparing synchronized intermittent
mandatory ventilation and synchronized intermittent mandatory ventilation plus pressure
support in preterm infants. Pediatrics. 2006;118:1409–1417.
4. Patel DS, et al. Work of breathing during SIMV with and without pressure support. Arch
Dis Child. 2009;94:434–436.
5. Ortiz G, et al. Outcomes of patients ventilated with synchronized intermittent mandatory
ventilation with pressure support: a comparative propensity score study. Chest.
2010;137:1265–1277.
• Assist-controlled ventilation
• Mechanical ventilation
• Ventilator associated pneumonia
• Positive end-expiratory pressure
• Work of breathing
CLINICAL PEARLS
• SIMV delivers backup ventilation (rate and tidal volumes) in a manner that does not
compete with the patient’s spontaneous efforts.
• Suitable to general anesthesia where the ventilator can provide minimal minute ventilation
or augment spontaneous effort in patients whose RR and efforts decrease with
administration of anesthetic agents/narcotics.
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
SECRETION (SIADH)
Adam Romanovsky, MD
BASICS
DESCRIPTION
• The syndrome of inappropriate antidiuretic hormone (SIADH) causes an inability to excrete
free water. It manifests as hypoosmolality and hyponatremia; total body sodium does not
change.
• SIADH presents as hyponatremia with normal total body sodium (Na+)
EPIDEMIOLOGY
Incidence
Most common cause of hyponatremia in hospitalized patients.
Prevalence
Exact prevalence is uncertain
Morbidity
• Hyponatremia is associated with an increased duration of hospital stay and a higher rate of
discharge to a long-term care facility.
• May have added morbidity due to underlying illness (e.g., malignancy).
Mortality
Hyponatremia is associated with increased all-cause mortality in hospitalized patients.
• Medications/drugs
– Narcotic analgesics
– Antipsychotics
– Selective serotonin reuptake inhibitors
– Tricyclic antidepressants
– NDMA agonists (e.g., ecstasy)
– Cyclophosphamide
– Carbamazepine
– ADH analogues (vasopressin, desmopressin, oxytocin)
• CNS disorders
– Meningitis, encephalitis, brain abscess
– Stroke
– Intracranial hemorrhage
– Post-transsphenoidal pituitary surgery
– Intracranial tumor
• Malignancy
– Lung
– Genitourinary tract
– GI tract
– Lymphoma
• Pulmonary disease
– Pneumonia
– Tuberculosis
– Parenchymal abscess
– Empyema
• Other
– Pain
– Nausea
– Stress
– HIV infection
– Hereditary
– Idiopathic
PATHOPHYSIOLOGY
• ADH is synthesized in the hypothalamus and is secreted from the posterior pituitary gland.
It is normally released in response to an increase in serum osmolality, which is sensed by
hypothalamic osmoreceptors. Release is also stimulated by activation of baroceptors in the
aortic arch, carotid sinus, and left atrium as a result of low blood pressure and low cardiac
output.
• ADH binds to V2 receptors in the renal medullary collecting ducts leading to increased free
water reabsorption (e.g., solute-free) via aquaporin-2 channels. This excess retention of
solute-free water leads to hyponatremia by dilution of the patient’s serum sodium; the total
body sodium does not change.
• The SIADH describes the secretion of ADH independent of plasma osmolality or volume
status. This results in
– Increased free water reabsorption
– Decreased serum sodium concentration
– No change in total body sodium
– Slightly increased body fluid volume
– Increased urine osmolality
– Decreased urine volume
– No change in urine sodium excretion
• Identify and manage acute symptomatic hyponatremia before proceeding with the
operation.
• Prevent an excessive rise in sodium concentration in patients with documented chronic
hyponatremia (>48 hours) as it can lead to osmotic demyelination (central pontine
myelinolysis). Correction should not exceed 0.5 mEq/L/hr
• Avoid intraoperative exacerbation of hyponatremia by using IV fluids that are hypotonic to
the patient’s urine. Worsening hyponatremia may lead to cerebral edema, seizures, and
possibly death.
SYMPTOMS
Hyponatremia: Ranges from asymptomatic to nausea, headache, lethargy, altered mental
status, seizures, and coma.
History
Underlying cause
Signs/Physical Exam
• Assessment of mental status
• Assessment of volume status
• Examination for features of underlying cause
TREATMENT HISTORY
Free water restriction
MEDICATIONS
• Loop diuretics (e.g., furosemide)
• Demeclocycline
• ADH antagonist therapy (tolvaptan or conivaptan
Labs/Studies
• Serum [Na+] <135 mEq/L
• Serum osmolality <280 mOsm/kg
• Urine [Na+] is dependent on the patient’s sodium intake as sodium excretion is not
impaired (typically >40 mEq/L).
• Urine osmolality is inappropriately high in the context of low serum osmolality. Exact
osmolality depends on the degree of excess ADH activity; typically >300 mOsm/kg and
may be significantly higher.
• Serum creatinine and urea (typically normal)
• Serum cortisol
• Serum thyroid stimulating hormone
Underlying causes can be pulmonary, CNS, or malignancy
• Delay elective surgeries if the [Na+] <130 mEql/L to complete full workup and treatment.
• Symptomatic hyponatremia (e.g., cardiac arrhythmias and mental status changes)
• Proceeding with urgent or emergent surgery in these patients must be done with caution
CLASSIFICATIONS
• Hyponatremia is divided into acute (present for <48 hours) or chronic (present for >48
hours or if uncertain of the time of onset).
TREATMENT
Premedications
Benzodiazepines and opioids should be avoided in patients with an altered level of
consciousness.
INTRAOPERATIVE CARE
When possible, regional anesthesia may be preferred to facilitate monitoring of clinical
manifestations in patients with neurologic abnormalities.
Monitors
• Arterial line or central venous access can be useful for frequent blood sampling. Long
operations may require frequent checks of serum sodium to ensure stability and guide fluid
management.
Symptomatic patients, especially those with cerebral edema, are at risk of increased
intracranial pressure during intubation.
Maintenance
• No specific technique has been shown to be superior to the other. Volatile anesthetics may
lead to increased intracranial pressure from “uncoupling” of cerebral blood flow and oxygen
consumption.
• For hemodynamic support, avoid vasopressin or use with caution as it can worsen
hyponatremia; acts as exogenous ADH.
• Fluid choice should be guided by frequent surveillance of serum sodium and urine
osmolality. Any fluid with lower osmolality than urine may lead to exacerbation of
hyponatremia.
– Normal saline (0.9% NaCl) and lactated Ringer’s solution have an electrolyte-based
osmolality of 308 and 272 mOsm/kg, respectively. For many patients with SIADH, these
fluids will be hypotonic in comparison to their urine. Therefore, use of these fluids (which
are generally considered isotonic) may lead to worsening hyponatremia. This underscores
the importance of frequent monitoring of serum Na+ in these patients.
– Hypertonic saline may be necessary in symptomatic or severe hyponatremia. This should
be done with caution so as to avoid a rapid rise in serum sodium.
Increased confusion and decreased level of consciousness may preclude safe extubation.
POSTOPERATIVE CARE
BED ACUITY
• Most patients can be managed safely in a regular floor bed unless precluded by an abnormal
level of consciousness.
• For symptomatic patients or those with rapid shifts in serum sodium, close observation
should begin in the postoperative recovery unit and continued in an intensive care unit.
• Repeat serum electrolytes (SIADH can be exacerbated by postoperative pain and nausea)
• Consider nephrology consultation
COMPLICATIONS
• Worsening hyponatremia may lead to cerebral edema, seizures, and possibly death.
• Rapid increase in serum sodium in chronic hyponatremia can lead to osmotic demyelination.
REFERENCES
1. Ellison DH, Berl T. The syndrome of inappropriate diuresis. New Engl J Med.
2007;356:2064–2072.
2. Hannon MJ, Thompson CJ. The syndrome of inappropriate antidiuretic hormone:
Prevalence, causes and consequences. Eur J Endocrinol. 2010;162:S5–S12.
3. Sterns R, Cappuccio J, Silver S, et al. Neurologic sequelae after treatment of severe
hyponatremia: A multicenter perspective. J Am Soc Nephrol. 1994;4:1522–1530.
4. Wald R, Jaber BL, Price LL, et al. Impact of hospital-associated hyponatremia on selected
outcomes. Arch Int Med. 2010;170(3):294–302.
• Hyponatremia
• Crystalloids
• TURP syndrome
CODES
ICD9
253.6 Other disorders of neurohypophysis
ICD10
E22.2 Syndrome of inappropriate secretion of antidiuretic hormone
CLINICAL PEARLS
• Do not ignore hyponatremia; SIADH requires a comprehensive workup.
• IV fluid choice is patient and situation specific. The administration of fluid that is hypotonic
to the patient’s urine can worsen hyponatremia; therefore, hypertonic saline may be
necessary.
SYSTEMIC LUPUS ERYTHEMATOSUS
BASICS
DESCRIPTION
• Systemic lupus erythematosus (SLE) has a complex pathogenesis with a link to
autoimmunity against various native cellular components.
• A diagnosis of SLE is made when patients meet 4 of the 11 criteria simultaneously or in
succession. Criteria include:
– Rash: Malar or discoid
– Photosensitivity
– Oral ulcers
– Serositis (pericarditis, pleuritis)
– Arthritis
– Renal disorders (proteinuria, renal casts)
– Neurological disorders (seizures, psychosis)
– Hematological disorders (anemia, leukopenia, thrombocytopenia)
– Positive anti-DNA antibody, anti-Sm antibody, antiphospholipid antibody
– Positive antinuclear antibody
• The multiple organ and system involvement has variable clinical presentations; optimal
perioperative care by the anaesthetist requires a thorough understanding and awareness.
EPIDEMIOLOGY
Incidence
Ranges from 2 to 7.6 cases per 100,000 persons per year
Prevalence
• National Health Survey reports a prevalence of 53.6/100,000.
• Ten times more common in women than men with a predilection for women of child-
bearing age
• Nine times more common in Afro-Caribbean females
Morbidity
• In a multicenter study of 1,000 patients followed over a 10-year period: Arthritis 48%;
malar rash 31%; active neuropathy 28%; neurologic involvement 19%; Raynaud’s
phenomenon 16%; serositis 16%; thrombocytopenia 13%; and thrombosis 9%
• Myocardial ischemia is 50 times more likely to develop in women aged 44–55 years
compared to healthy women as shown in the Framingham Offspring study.
Mortality
• 10-year survival from the time of onset: 92%.
• 20-year survival from the time of onset: 68%.
• The exact etiology remains unknown. There appears to be a link to race, multiple
susceptibility gene loci, hormones, and environmental factors.
• Women of child-bearing age
• African American women
• Use of exogenous hormones
• History of hypertension
• Type I/II sun-reactive skin type
• Family history of SLE
• Smoking
PATHOPHYSIOLOGY
• It is hypothesized that abnormal apoptosis and intolerant lymphocytes are responsible for
the disease’s manifestations.
– Increased apoptosis may result from DNA methylation and is accompanied by plasma and
nuclear antigen display on cell surfaces.
– Normally, lymphocytes do not target these intrinsic antigens; however, abnormal
lymphocyte signaling results in targeting of these cell surface antigens.
– Antibody-antigen immune complexes form that can lodge in the microvasculature and
cause complement activation. These complexes also become deposited on renal and skin
basement membranes.
• Assess for the severity of disease, including acute flares and end-organ damage. Careful
attention should be paid to the cardiovascular, pulmonary, and renal systems.
• Assess and evaluate for the need of “stress dose” steroids in patients with chronic steroid
use.
SYMPTOMS
• Chest tightness
• Cough
• Tachypnea
• Neuropathic pain
History
• Review disease course and presence of end-organ damage.
– ER visits and hospitalizations
– Treatment history
– Triggers
• A discussion with the patient’s rheumatologist (or note) can provide accurate information on
the history of the disease, course of the illness and current therapies.
Signs/Physical Exam
• Cardiovascular system exam
– Murmurs may indicate valvular disease
– Diminished heart sounds, friction rub may indicate pericarditis
• Pulmonary exam
– Diminished or inaudible breath sounds or coarse breath sounds may indicate pleural
effusions, interstitial lung disease or pneumonia
• Check for atlanto-axial subluxation signs
TREATMENT HISTORY
• Hemodialysis or renal transplant for chronic renal disease.
• Pericardiocentesis or pericardial window for history of tamponade.
• Mechanical valve replacement for Libman-Sacks vegetations; prosthetic valves are
susceptible to valvulitis relapse.
MEDICATIONS
• Cyclophosphamide: Cardiotoxicity
• Azathioprine and methotrexate: Hepatotoxicity
• Methotrexate: Pulmonary fibrosis; when combined with NSAIDS can result in acute renal
failure and pancytopenia
• Mycophenolate: Pancytopenia
• Long term steroids: Hyperglycemia, hypercholesteremia, osteoporosis, and hypertension
• NSAIDS, aspirin: Peptic ulcers, platelet inhibition
• Hydroxychloroquine: Retinotoxicity, cardiotoxicity, neurotoxicity
Labs/Studies
• CBC to rule out anemia, thrombocytopenia, leukopenia. If anemic, consider hemolysis
workup.
• Electrolytes, particularly in patients with lupus nephritis.
• Liver function tests to investigate autoimmune hepatitis or drug hepatotoxicity.
• Coagulation factors. An elevated PTT may be seen in patients with lupus anticoagulant.
• Antibody and complement levels, if present, should be compared to previous values.
• Antiphospholipid antibody indicates an increased risk of thrombosis.
• Chest radiography can reveal interstitial lung disease, pneumonia, or pleural effusions.
• EKG can reveal increased risk of myocardial ischemia, acute right heart failure, or PVCs.
• Echocardiogram may be indicated if signs of endocarditis or valvular disease exist.
• Neurologic
– Increased risk of cerebrovascular disease, even in the absence of classic risk factors
– Migraine or tension headaches are common
• Cardiac
– Pericarditis, pericardial effusion, tamponade.
– QT prolongation may result from hydroxychloroquine therapy.
– Common arrhythmias include sinus tachycardia, atrial fibrillation, and atrioventricular
block
– Libman-Sacks vegetations are verrucous non-infective vegetations that can be seen on
echocardiogram in ~1 in 10 SLE patients.
• Pulmonary
– Common parenchymal manifestations include interstitial lung disease, diffuse alveolar
hemorrhage, and acute lupus pneumonitis.
– In patients with pericarditis, there is an association with pleural effusions.
• Acute flare
• Serositis (pericarditis/pleuritis)
• Pneumonia
TREATMENT
Premedications
• Stress dose steroids may be indicated if the patient has been treated for more than 2 weeks
within the past 6–12 months to avoid manifestations of adrenal insufficiency. Steroids with
glucocorticoid and mineralocorticoid activity should be administered.
• Patients with a history of thrombosis may warrant therapeutic anticoagulation. Discuss with
the hematologist and surgeon prior to starting.
• Aspiration prophylaxis should be considered
• Appropriate antibiotic therapy is warranted secondary to the increased risk for infection
Discuss the need for invasive monitoring, if applicable
INTRAOPERATIVE CARE
Neuraxial and regional anesthesia may be contraindicated in patients that have a baseline
coagulopathy, are being anticoagulated, or need to be anticoagulated in the immediate
Monitors
• Consider arterial line in high-risk surgeries (patient population with increased cardiac risk)
• Laryngeal mask airways (LMAs) sit supraglotically and may minimize airway manipulation
and edema. Post-intubation subglottic stenosis is a potential in patients with active SLE,
even after brief periods of intubation.
• Endotracheal tubes
– A rapid sequence intubation (RSI) may be indicated in patients with gastroesophageal
reflux (present in 11–50% of patients)
– Laryngeal edema, subglottic stenosis, and vocal cord paralysis can make laryngoscopy and
intubation difficult
– Oral mucosal ulceration may be present in one-third of patients; laryngoscopy should be
performed gently
• Muscle relaxation
– Increased doses of nondepolarizing muscle relaxants may be needed. One study
demonstrated that there is a 20% dose increase for vecuronium, 45% for pancuronium,
and 37% for atracurium
– Succinylcholine may have a prolonged duration of action in patients taking
cyclophosphamide (a pseudocholinesterase inhibitor). Succinylcholine is metabolized in
the plasma by pseudocholinesterase enzyme.
Maintenance
• Proper positioning with padding can prevent peripheral nerve compression and fractures of
osteoporotic bones
• Eye protection and lubrication can prevent corneal abrasions. Sjögren’s syndrome
predisposes to corneal abrasions.
• Drug interactions with immunosuppressants
– Nitrous oxide may worsen bone marrow suppression.
– Muscle relaxants (see above)
• Lupus nephritis
– Maintain adequate urine output with proper fluid resuscitation (frequent monitoring and
adjustments to fluids).
– Avoid hypotension
– Avoid nephrotoxic drugs
• Avoid Raynaud’s phenomenon by
– Maintaining normothermia
– Humidifying and warming inspiratory gases
Cricoarytenoid arthritis may cause airway obstruction following tracheal extubation.
POSTOPERATIVE CARE
BED ACUITY
• Vigilance for airway obstruction
• Consider supplemental oxygen (nasal cannula, face mask); incentive spirometry to reduce
atelectasis
• Thromboprophylaxis includes early mobilization and pharmacologic anticoagulation
COMPLICATIONS
Drug-induced SLE may result from treatment with procainamide, hydralazine, isoniazid,
penicillamine, and alpha-methyl dopa.
REFERENCES
1. Ben-Menachem E. Review article: Systemic lupus erythematosus: A review for
anesthesiologists. Anesth Analg. 2010;111(3):665–676.
2. http://www.niams.nih.gov
3. Manson JJ, Rahman A. Systemic lupus erythematosus. Orphanet J Rare Dis. 2006;27(1):6.
4. www.lupus.org
• QT prolongation
CODES
ICD9
710.0 Systemic lupus erythematosus
ICD10
M32.9 Systemic lupus erythematosus, unspecified
CLINICAL PEARLS
• Perioperative management of SLE patients should be tailored to the individual patient.
• Assess severity of disease and organ involvement in order to plan an appropriate anesthetic
technique.
• Patients with SLE may present for procedures specific to the disease (renal transplants,
pericardial windows) or for nonrelated procedures (pregnancy).
SYSTOLE
Srikantha L. Rao, MBBS, MS
Niraja Rajan, MB, BS, FAAP
BASICS
DESCRIPTION
• In simple terms, systole is the time during which the ventricles contract and eject blood. It is
followed by diastole (a period of relaxation), and a set of these events in both the atria and
ventricles comprises a cardiac cycle.
– The sino-atrial (SA) node, also known as the cardiac pacemaker, spontaneously and
rhythmically initiates each cardiac cycle. The action potential at the SA node is
propagated through both atria (atrial contraction – P wave on EKG) and then through the
atrio-ventricular node (PR interval on EKG), His bundle and Purkinje system to both
ventricles (QRS complex on EKG). Ventricular repolarization is seen as the T wave on the
EKG.
– Isovolumic contraction. During the first phase of left ventricular (LV) systole, the ventricle
begins contraction with the mitral and aortic valve closed leading to a rapid increase in
intraventricular pressure but no change in volume.
– Ejection phase: The second phase of systole begins with the opening of the aortic valve
(ventricular pressure exceeds the aortic pressure) and ends when the ventricle has stopped
contracting, although ejection is still taking place (the aortic valve is still open).
– Diastole: Marks the onset of ventricular relaxation. Ejection into the aorta continues until
the left ventricular pressure drops below the aortic pressure and the aortic valve closes.
• Physiologic systole begins at the start of isovolemic contraction and ends at the peak of
ventricular ejection. Clinical systole (by echocardiography) begins with mitral valve closure
and ends with aortic valve closure.
• Systole and diastole require energy. During diastole, ventricular relaxation occurs by the
removal/uptake of calcium from troponin C and into the sarcoplasmic reticulum. The
factors that affect systolic function, preload, afterload, heart rate and contractility overlap
the effects of calcium on the ventricle.
• The amount of blood ejected by the ventricle with each contraction is the stroke volume
(SV). Normal SV in an adult man is 70–80 mL. SV is determined by preload, afterload, and
contractility. The description below pertains to LV systolic function. The amount of blood
ejected by the heart per minute is the cardiac output (CO).
• Preload
– Is the load on the ventricle before contraction and is determined by ventricular volume.
– It is the end-diastolic myocardial fiber length and is represented by the end-diastolic
volume (EDV); normally around 120 mL.
– Cardiac muscle develops most of its force over a small range of shortening near its
maximal length. Thus, within limits, increases in preload (rise in EDV) will increase the
SV and systolic pressure.
– Factors affecting preload include venous return (including venous tone), total blood
volume, intrathoracic pressure, body position, and atrial contraction.
– Surrogate measures of LV volume used to estimate EDV are pulmonary capillary wedge
pressure (PCWP) or central venous pressure (CVP).
• Afterload
– Is the load on the ventricle at the start of a contraction. In simple terms, afterload is the
impedance to ejection of blood.
– Most of the resistance to ejection is from the systemic vascular resistance (SVR).
– An increase in afterload decreases ventricular ejection.
– Ventricular wall stress (tension) is a concept that incorporates both preload and afterload.
Arterial blood pressure, vascular compliance and volume, and wall thickness all factor
into tension. It can be calculated by LaPlace’s law: Tension = (change in pressure)
(ventricular radius)/(wall thickness ×2).
• Contractility
– Is the muscle’s ability to generate work (contract, develop pressure, generate a contractile
force) from a set end-diastolic fiber length.
– Increased contractility refers to a greater velocity of contraction (Vmax) reaching a higher
peak force. This definition is useful at the subcellular level to measure contractility in
isolated papillary muscle.
– Another measure of contractility, the rate of pressure development (dP/dt), is not used
clinically.
– Ejection fraction (EF) is a clinically useful index of contractility.
• Both systolic and diastolic function can be assessed using pressure-volume curves that can
be obtained during cardiac catheterization.
• Coronary blood flow
– 75% of total coronary blood flow occurs during diastole. During systolic contraction, there
is an increase in tissue pressure that impedes arterial flow; blood is redistributed from the
subendocardial to the subepicardial layer of the LV. Systole has minimal impact on
coronary flow to the right ventricle (RV).
– Coronary blood flow at rest is about 250 mL/min (4–5% of CO) or 75 mL/100 g/min,
assuming the adult heart weighs 300 g and the CO is 5 L/min.
– The myocardial oxygen consumption at rest is 8–10 mL/100 g/min, about 10% of the total
body consumption of oxygen.
– In the coronary circulation, near maximum oxygen extraction (75% of arterial oxygen
content) occurs during rest. Hence, an increase in coronary blood flow is necessary when
myocardial oxygen consumption occurs.
– Heart rate, LV wall stress, and contractility determine myocardial oxygen consumption.
ANATOMY
• The heart consists of two atria and two ventricles that circulate blood in series; the RV
pumps through the low-resistance pulmonary circulation, while the LV pumps through the
high-resistance systemic circulation.
• The RVs and LVs differ in their shape, size, and pressure against which they contract.
• The LV is ellipsoidal in shape with the muscle fibers arranged longitudinally in the
subepicardium and subendocardial layers, and circumferentially in between these two
layers. The LV ejects blood with a corkscrew type of motion with the apex moving toward
the base. Wall motion of regions supplied by branches of the coronary artery can be
individually assessed semi-quantitatively by echocardiography.
• The RV is crescent-shaped with an inflow and outflow region that contract sequentially to
eject blood into the low-pressure pulmonary circulation. 3-D echocardiography is becoming
useful in quantifying RV systolic function.
• The atrial systole contributes 25–30% of the volume toward ventricular filling, and the SV
could significantly decrease in the absence of this atrial contraction during cardiac
dysrhythmias and could also be compounded by impaired relaxation of the ventricles, for
example, during atrial fibrillation in older patients.
• Electrical activity of the heart is monitored using the ECG, while the mechanical events are
monitored using the arterial and pulmonary BP or echocardiography.
• A pulmonary artery catheter has been traditionally used to estimate CO by thermal dilution.
Assuming a normal LV systolic and diastolic function, EDV is estimated from left ventricular
end-diastolic pressure (LVEDP). In disease states where ventricular compliance is abnormal,
LVEDP correlates poorly with CVP/PCWP.
• With transesophageal echocardiography (TEE), EDV can be directly measured, as well as
estimate the EF.
• The majority of intravenous induction agents decrease BP via venodilation (decreased
preload) and/or vasodilation (decreased afterload).
• Isoflurane, desflurane, and sevoflurane used for maintenance of anesthesia (1–1.5 MAC),
decrease SV by 15–30%. An increase in heart rate caused by these inhaled agents may
minimize the decrease in CO.
• Positive-pressure ventilation (PPV) leads to raised intrathoracic pressure leading to reduced
venous return, in turn reducing SV and thereby BP. The onset of positive pressure
ventilation is associated with a greater decrease in RV function compared to LV function;
however, with time, the reduction in RV output will decrease LV output. During PPV, the
SV varies with inspiration and exhalation. When this variation is >15%, it may be
indicative of relative hypovolemia and volume responsiveness.
• Newer pulse contour analysis monitors allow estimation of LV SV from systemic arterial
pressure waveforms.
• Stand-alone monitors exist that use esophageal Doppler probes to estimate SV. These probes
measure the velocity (peak and mean) of blood in the descending thoracic aorta, and by
integrating it over the ejection time, obtain the velocity time integral (VTI). VTI multiplied
by the cross-sectional area of the aorta (assuming a diameter, given the patient’s age,
gender, and height and weight) provides the SV with every beat. A similar method may be
used to estimate SV using TEE.
EQUATIONS
• In a normal-sized human with a heart rate (HR) of 70–80 beats per minute, cardiac output
(CO) is 5–6 L/min.
– CO = SV × HR
• Cardiac index (CI) is CO indexed to bodies of varying sizes, expressed using body surface
area (BSA)
– CI = CO/BSA
• SVR = (MAP – CVP)/CO × 80
– MAP is mean arterial pressure
– CVP is central venous/right atrial pressure
– Normal SVR is 900–1,500 dynes.sec.cm−5
• LV wall stress = (Pressure × Radius)/(2 × Wall thickness)
• EF = (EDV – ESV)/EDV
– EF is ejection fraction
– ESV is end-systolic volume
– EDV is end-diastolic volume
– SV is stroke volume
REFERENCES
1. Hunter WC, Janicki JS, Weber KT. Mechanical properties of the ventricle during systole.
Fed Proc. 1980;38(2):169–174.
2. Meller J, Herman MV, Teichholz LE. Noninvasive assessment of left ventricular function.
Adv Intern Med. 1979;24:331–357.
3. Shoucri RM. Studying the mechanics of left ventricular contraction. IEEE Eng Med Biol
Mag. 1998;17(3):95–101.
• Cardiac output
• Cardiac output, methods to measure
• Diastole
• Afterload
CLINICAL PEARLS
• Systole and diastole are both energy-requiring processes.
• Adequate and judicious IV hydration before induction of anesthesia is recommended,
especially in the older patient, to minimize the cardiovascular effects of the induction drugs
and PPV.
• When compared to other methods, an increase in CO achieved by optimizing intravascular
volume that increases venous return (preload) is the most efficient method, as it does not
lead to increased oxygen consumption.
• A dilated, thin-walled ventricle (failing ventricle) has greater wall stress than a thicker-
walled, smaller ventricle. When hydrating patients with heart failure, reducing afterload is
important.
• Hypoxia, acidosis, ischemia, calcium-channel blockers and beta-blockers decrease
contractility.
TACHYCARDIA
BASICS
DESCRIPTION
• Tachycardia is defined as an arrhythmia with a rate >100 beats per minute.
• Tachycardia can be classified in several ways based on the appearance of the QRS complex
(wide- or narrow-QRS complex), origin (supraventricular or ventricular), and regularity
(regular or irregular).
– A narrow-QRS complex (QRS <0.12 seconds) supraventricular tachycardia (SVT)
originates above or within the atrioventricular (AV) node. Examples include (in the order
of observed incidence): sinus tachycardia, atrial fibrillation and flutter, AV nodal reentry,
accessory pathway-mediated tachycardia, atrial tachycardia, multifocal atrial tachycardia
(MFAT), and junctional tachycardia (rare in adults).
– A wide-QRS complex tachycardia (≥0.12 seconds) usually originates outside of the
normal conduction system and may be either ventricular or supraventricular in origin.
Examples include ventricular tachycardia (VT), ventricular fibrillation (VF), preexcited
tachycardia (Wolff–Parkinson–White (WFW) syndrome), ventricular-paced rhythms, and
SVT with aberrancy (the latter represents tachycardia with supraventricular origin).
• Perioperatively, tachycardia may be an early indicator of an underlying condition and
warrants evaluation, treatment of the underlying cause, and possibly symptomatic treatment
of the heart rate, particularly in unstable patients.
EPIDEMIOLOGY
Prevalence
• SVT is common across all age groups
• Regular SVT (or paroxysmal SVT) is more likely to be encountered in the younger patient
with no structural heart disease as compared to atrial fibrillation, which has a 70%
concentration in those older than 65 years of age.
Prevalence
In 1996, the estimated prevalence of all tachycardias in the US was 2.3 million.
Morbidity
• Arise principally from spontaneous degeneration into the more malignant ventricular
rhythms, including VF.
• Can precipitate myocardial ischemia
Mortality
Reported mortality from SVTs is primarily associated with atrial fibrillation and flutter.
• Narrow complex tachycardia
– Sinus tachycardia (enhanced catecholamine release) or reflexively
Hypoxia
Acute coronary ischemia and myocardial infarction
Acidosis
Hypotension and shock
Volume depletion
Anemia
Hypoglycemia
Pain, light anesthesia, awareness, anxiety
Fever, hyperthermia
Bladder distension
Shivering
Sepsis
Pulmonary embolism
Medications: Anticholinergics, beta-agonists (ephedrine, epinephrine), desflurane
Rare causes: Pheochromocytoma, hyperthyroidism, malignant hyperthermia
• Cardiac conduction disease: AV nodal reentry, accessory pathway-mediated, multifocal
tachycardia
• Wide complex tachycardia
– Ischemia
– Bundle branch block
– Tricyclic antidepressant overdose
– Hyperkalemia
• Sinus tachycardia is usually the result of sympathetic nervous system activation in concert
with a decrease in cardiac vagal tone. No specific drug treatment is required. The therapy
should be directed toward identification and treatment of the underlying cause. Concurrent
symptomatic rate reduction may be considered in patients at risk for ischemia from
increased myocardial oxygen consumption or decreased supply (e.g., coronary artery
disease)
• Narrow-QRS complex tachycardia is the most commonly seen arrhythmia during the
perioperative period. The mechanisms of this tachycardia include
– Reentry SVT: Caused by abnormal rhythm circuit that allows a wave of depolarization to
repeatedly travel in a circle in cardiac tissue.
– Abnormal automaticity. Due to rapid repetitive depolarization from a single cell or group
of cells is the basic mechanism for MFAT, focal (ectopic) atrial tachycardia, and junctional
tachycardia. These arrhythmias can be difficult to treat, are not responsive to
cardioversion, and are usually controlled with drugs that slow conduction through the AV
node with subsequent slowing of the ventricular rate.
Aimed at avoidance of causes:
• Avoid hypoxia
• Optimize myocardial oxygen supply and demand
• Maintain fluid hydration
• Transfuse red blood cells, if appropriate
• Provide an adequate depth of anesthesia and analgesia
• Identify patients at risk for DVT and initiate appropriate prophylaxis
• Give anticholinergics slowly, when coadministered with anticholinesterases
• Optimize underlying comorbid conditions
• Continue perioperative antibiotics
• Continue perioperative beta-blockade, as appropriate
• Rule out life-threatening causes of tachycardia: Hypoxia, ischemia, and acidosis.
• Review the EKG to assess wave morphology
– Narrow-QRS complex (SVT) tachycardia has a QRS <0.12 seconds. Assess rate, regularity,
and P-wave presence and morphology.
– Wide-QRS complex tachycardia has a QRS interval ≥0.12 seconds
• Sinus tachycardia
– Review recent events (intubation, blood loss, incision or surgical stimulation, movement,
other vital signs) and medications administered
• Wide complex tachycardia: To distinguish between ventricular and SVT (with aberrations)
origin:
– Maneuvers (i.e., carotid sinus pressure and Valsalva maneuver) – the response of the
arrhythmia to maneuvers may provide insight to the mechanism of the wide complex
tachycardia (SVTs tend to stop with this maneuver while ventricular arrhythmias do not).
– Diagnostic pharmacologic interventions:
SVT: Verapamil, diltiazem, adenosine, or beta-blockers will terminate PSVT and slow
SVT
VT: Procainamide, sotalol, or amiodarone may terminate the rhythm. Adenosine will not
stop or slow down.
Laboratory tests
• Arterial blood gas to assess for hypoxia, acidosis, and anemia
• Plasma potassium and magnesium concentrations. Hypokalemia and hypomagnesemia both
predispose to the development of ventricular tachyarrhythmias. Hyperkalemia can cause a
wide-QRS complex rhythm with the loss of a detectable P-wave, although this usually has a
slow rate (so-called “sinoventricular rhythm”). In patients taking digoxin, quinidine, or
procainamide, consider measuring plasma concentrations to assist in evaluating possible
toxicity.
• Chest x-ray (cardiomegaly or evidence of previous cardiac surgery)
• Narrow complex tachycardia
– Sinus tachycardia
– Atrial fibrillation or flutter
– AV nodal reentry
– Accessory pathway-mediated tachycardia
• Atrial tachycardia
– Multifocal atrial tachycardia
– Junctional tachycardia (rare in adults)
• Wide complex tachycardia
– Ventricular tachycardia
– Ventricular fibrillation
– Supraventricular tachycardia with aberrancy
– Preexcited tachycardia (WPW syndrome)
– Ventricular-paced rhythms
TREATMENT
• If the patient is hemodynamically unstable (hypotension, acutely altered mental status, signs
of shock, chest pain, acute heart failure), proceed immediately to appropriate electrical
shock therapy (synchronized cardioversion or defibrillation for VF):
– Synchronized cardioversion initial recommended dose:
Narrow regular: 50–100 J
Narrow irregular (e.g., atrial fibrillation): 120–200 J biphasic or 200 J monophasic
Wide regular: 100 J
Wide irregular (defibrillation dose – NOT synchronized): 360 J monophasic or 120–200 J
biphasic
Pediatric: Initial dose of 2–4 J/kg. Subsequent energy levels may be considered, but
should not exceed 10 J/kg.
– Not effective for multifocal and focal atrial tachycardia
• Polymorphic VT requires immediate defibrillation with the same strategy used for VF.
Prevention of recurrent polymorphic VT may be performed with magnesium, pacing, and/or
sotalol, amiodarone, or procainamide.
• Stable ST. Treatment should be aimed at the underlying cause. In patients at risk for
myocardial ischemia or demonstrating hemodynamic compromise, consider rate control
with beta-blockers.
• Regular, stable narrow complex tachycardia
– Vagal maneuvers
– Consider: Beta-blockers or calcium channel blockers
– Amiodarone may be considered in patients with congestive heart failure
– Adenosine 6 mg IV followed by a 20 mL saline flush; may repeat with a 12 mg rapid IV
push after 1–2 minutes.
• Stable wide-QRS tachycardia:
– Procainamide, amiodarone, sotalol
FOLLOW-UP
• Patients who develop sustained and/or nonsustained VT during the perioperative period
should be referred to a cardiologist for further evaluation, including an evaluation of their
ventricular function and screening for heart ischemia.
• Several studies suggest beta-blocker therapy can reduce mortality and the incidence of
cardiovascular complications (including the development of arrhythmias) during surgery,
and for up to 2 years afterward.
• For long-term treatment of SVTs: AV nodal blocking agents (e.g., verapamil, diltiazem, beta-
blockers, digoxin), amiodarone, and disopyramide may be started by cardiology.
• Radiofrequency ablation is a safe, effective, and cost-effective method for suppressing SVT.
REFERENCES
1. Neumar Link MS, Atkins DL, Passman RS, et al. Part 6: Electrical therapies: Automated
external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart
Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular
Care. Circulation. 2010;122(18 Suppl 3):S706–S719. Neumar RW, Otto CW, Link MS, et al.
Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association
Circulation. 2010;122(suppl 3):S729–S767. Reising S, Kusumoto F, Goldschlager N. Life-
threatening arrhythmias in the intensive care unit. J Intensive Care Med. 2007;22(1):3–13.
2. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of
patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report
of the American College of Cardiology/American Heart Association Task Force and the
European Society of Cardiology Committee for Practice Guidelines: Developed in
collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
Circulation. 2006;114(10):e385–484.
• Bradycardia
• Anemia
• Atrial tachycardias
CODES
ICD9
• 427.1 Paroxysmal ventricular tachycardia
• 427.89 Other specified cardiac dysrhythmias
• 785.0 Tachycardia, unspecified
ICD10
• R00.0 Tachycardia, unspecified
• I47.1 Supraventricular tachycardia
• I47.2 Ventricular tachycardia
CLINICAL PEARLS
• When the heart rate is <150/min, it is unlikely that symptoms of instability are caused
primarily by the tachycardia unless there is impaired ventricular function or structure (e.g.,
outflow tract obstruction, aortic stenosis, mitral stenosis, etc).
• When cardiac function is poor, cardiac output can be dependent on a rapid heart rate. In
such compensatory sinus tachycardias, stroke volume is limited; thus, decreases in the heart
rate can be detrimental (e.g., induction of general anesthesia with cardiac tamponade).
• If the tachycardia is suspected to be the cause of acute altered mental status, ischemic chest
discomfort, acute heart failure, hypotension, or other signs of shock, the patient should
receive immediate synchronized cardioversion.
• If there is any doubt whether monomorphic or polymorphic VT is present in the unstable
patient, provide high-energy defibrillation without waiting for detailed analysis of the
rhythm.
• Active tachyarrhythmias for which the patient should undergo evaluation and treatment
before noncardiac surgery:
– Symptomatic ventricular arrhythmias
– Supraventricular arrhythmias (including atrial fibrillation) with uncontrolled ventricular
rate (heart rate >100 bpm at rest)
– Newly recognized VT.
TARDIVE DYSKINESIA
Tricia A. Meyer, PharmD, MS, FASHP
BASICS
DESCRIPTION
• Tardive dyskinesia (TD) is a severe, and potentially irreversible, adverse effect of long-term
pharmacologic therapy with dopamine receptor antagonists, primarily in the form of
antipsychotic drugs.
– Characterized by purposeless, involuntary, and repetitive movements in single or multiple
body regions.
– Tardive comes from the French word “tardif,” which means tardy or late. The abnormal
movements usually occur “late” in therapy with antipsychotic medications.
– Dyskinesia comes from the Greek words “dys” and “kinesis” and means difficulty of
movement.
– Antipsychotic medications function mainly as antagonists at postsynaptic dopamine
receptors (primarily dopamine-2 receptor). They are most commonly used in the
treatment of psychiatric disorders such as schizophrenia.
– More than 20% of patients in nursing homes are administered antipsychotics for
behavioral issues associated with dementia; therefore, the perioperative impact of TD
should be expected to increase as our surgical population increases in age.
• TD has an incidence of 2–4% per year of treatment with neuroleptic antipsychotics.
• Acute dystonic reactions (ADRs) differ from TD in that movement-related issues following
administration of antipsychotic or antiemetic agents usually occur within 48 hours of
treatment onset.
– These reactions are rarely life threatening, but frequently anxiety inducing.
– Dystonic reactions are characterized by abnormal contractions of muscle groups in
abnormal positions and frequently lead to tremendous patient discomfort.
ANATOMY
• The orofacial area is mainly affected by classic TD with quick, involuntary movements that
may include
– Blinking
– Grimacing
– Smacking
– Licking
– Sucking
– Puckering
– Chewing
– Tongue movements
• The trunk and limbs may display choreoathetoid movements. This is described as snake like
or twisting movements.
• It is considered to be a disorder of dopamine systems, and evidence suggests that chronic
dopamine blockade results in receptor sensitivity and may be involved in the pathogenesis
of TD.
• The specific pathophysiology of TD is not fully understood but may involve the formation of
free radicals and mitochondrial energy failure.
• Factors that may increase the incidence of TD include
– Advanced age (especially in women; thought to be due to decreased estrogen levels and
increased phenylalanine levels)
– Greater than 6 months duration of use of a first-generation antipsychotic
– History of Parkinsonian side effects
– Previous brain injury
– Phenylketonuria (increased levels of phenylalanine levels).
• Symptoms may first appear around, or after, 6 weeks of antipsychotic therapy but are more
commonly seen with therapy of 2 years or longer.
• The disorder is difficult to treat and prompt withdrawal of the offending drug is
recommended.
Typically, approximately one-third of patients with TD will have resolution within 3 months
of discontinuation of the offending medication. Most will have a remittance within 5 years.
Additionally, TD may actually worsen upon discontinuation or reduction in dose of the
antipsychotic medication following years of therapy.
• Atypical, or second-generation, antipsychotic drugs may have a lower incidence of TD
compared to typical antipsychotics. Clozapine and quetiapine have the lowest incidence.
• Subtypes of TD include:
– Tardive akathisia: Frequent, complex stereotyped movements. Legs are commonly
involved (marching or walking in place, crossing/uncrossing). Additionally, trunk rocking,
respiratory grunting/moaning, and complex hand movements (face rubbing or scratching)
– Tardive dystonia: Involuntary movements that resemble multiple movement disorders
(generally slower and more sustained)
– Tardive tics, myoclonus, stereotypy, and tremor may also be included as subtypes
• A diagnosis of TD is made after exclusion of other movement disorders and is usually
diagnosed by physical exam as well as neuropsychiatric and medication history. Other drug-
induced movement disorders include
– Acute dystonia
– Neuroleptic malignant syndrome
– Neuroleptic-induced Parkinsonism
– Asterixis, chorea
– Serotonin syndrome
• Acute, short-term, perioperative use of antidopaminergic agents will not cause a patient to
develop TD. Additionally, there is no known evidence that administration leads to a quicker
onset of TD symptoms in patients on long-term antidopaminergic therapy. However, in
patients with, or having a history of, TD, it is possible that antidopaminergics can worsen or
cause a remission.
– Anticholinergics and serotonin-specific reuptake inhibitors have antidopaminergic effects.
– Antiemetic drugs
Metoclopramide and prochlorperazine are dopamine-blocking agents. TD may occur after
prolonged use. In 2009, the FDA issued a Black Box Warning for long term and high
dose use of metoclopramide related to the high risk of developing TD.
Haloperidol, perphenazine, and droperidol are antiemetic agents also classified as
antipsychotics. These drugs are used in the perioperative period.
5-hydroxytryptamine-3 receptors (“tron” drugs such as ondansetron and dolasetron) may
be safer choices for the treatment of postoperative nausea and vomiting in patients who
are known to have TD. This class of drugs is not associated with TD or ADRs.
– Calcium channel blockers have also been rarely implicated.
• Respiratory distress may manifest from laryngeal or diaphragmatic dyskinesia.
• ADR that are not classified as TD may present perioperatively with the acute use of
antiemetic medications that have antidopaminergic effects.
– The antihistamine diphenhydramine, due to its anticholinergic properties, has been used
to treat this disorder with good success.
– In addition, benztropine and benzodiazepines have also been used successfully. Effective
doses may vary.
– Routine use of metoclopramide in women prior to Cesarean section may increase the
incidence of ADR. Risks and benefits of metoclopramide should be considered in this
patient population at higher risk for aspiration of gastric contents.
GRAPHS/FIGURES
• Typical (first-generation) antipsychotics
– Chlorpromazine (Thorazine®)
– Droperidol (Inapsine*). Approved indications for droperidol are to reduce incidence of
nausea and vomiting, although it may also be classified as an antipsychotic agent.
– Fluphenazine (Prolixin®)
– Haloperidol (Haldol®)
– Loxapine (Loxitane®)
– Perphenazine (Trilafon®)
– Pimozide (Orap®)
– Thiothixene (Navane®)
– Thioridazine (Mellaril®)
– Trifluoperazine (Stelazine®)
• Atypical (second-generation) antipsychotics
– Aripiprazole (Abilify®)
– Asenapine (Saphris®)
– Clozapine (Clozaril®)
– Iloperidone (Fanapt®)
– Lurasidone (Latuda®)
– Olanzapine (Zyprexa®, Zyprexa, Zydis®)
– Paliperidone (Invega®)
– Quetiapine (Seroquel®)
– Risperidone (Risperdal®, Risperdal Consta®)
– Ziprasidone (Geodon®)
REFERENCES
1. Barak Y, Swartz M, et al. Vitamin E (alpha-tocopherol) in the treatment of tardive
dyskinesia: A statistical meta-analysis. Ann Clin Psychiatry. 1998;10(3):101–105.
2. Burke RE, Kang UJ, Jankovic J, et al. Tardive akathisia: An analysis of clinical features and
response to open therapeutic trials. Mov Disord. 1989;4(2):157–175.
3. Chou K, Friedman J. Tardive syndromes in the elderly. Clin Geriatr Med. 2006;22:915–933.
4. Fauci AS, Braunwald E, Kasper DL, et al. Harrison’s Principles of Internal Medicine, 17th
edn. 2008; New York, NY: McGraw-Hill.
5. Koek RJ, Pi EH. Acute laryngeal dystonic reactions to neuroleptics. Psychosomatics.
1989;30:359–364.
6. Lencz T, Malhorta A. Pharmacogenetics of antipsychotic-induced side effects. Dialogues
Clin Neurosci. 2009;11(11):405–415.
7. Mejia NI, Jankovic J. Tardive dyskinesia and withdrawal emergent syndrome in children.
Expert Rev Neurother. 2010;10(6):893–901.
8. Rao A, Camilleri M. Review article: Metoclopramide and tardive dyskinesia. Aliment
Pharmacol Ther. 2010;31:11–19.
9. Soares-Weiser K, Fernandez H. Tardive dyskinesia. Semin Neurol. 2007;27:159–169.
10. Wemove.org is a website devoted to education regarding movement disorders.
11. Woods SW, Morgenstern H, Saska JR, et al. Incidence of tardive dyskinesia with atypical
versus conventional antipsychotic medications: A prospective cohort study. J Clin
Psychiatry. 2010;71(4):463–474.
• Schizophrenia
CODES
ICD9
333.85 Subacute dyskinesia due to drugs
ICD10
G24.01 Drug induced subacute dyskinesia
CLINICAL PEARLS
• Abrupt withdrawal of the antipsychotic agents (as can occur in the perioperative period) can
lead to withdrawal dyskinesia that may signal the onset of TD.
• No pharmacologic treatment has been shown to be completely effective in treating TD.
Tetrabenazine (Xenazine®) is a dopamine depleting agent and is suggested for treatment of
TD. Tetrabenazine was approved in the US in 2008 as an orphan drug for treatment of
chorea associated with Huntington’s disease. The patient and a provider must complete a
treatment form and send to the company. Once approved, the patient is assigned to one of
four specialty pharmacies for dispensing.
• Reserpine, a catecholamine depleting agent, has been used to treat refractory cases of
choreatic TD.
• Treatment with Vitamin E has been thought to attenuate symptoms of TD when given early
in the course of disease. This effect is thought to be due to the antioxidant properties of
Vitamin E. A 2007 meta-analysis revealed no significant improvement; however, those who
were assigned to the placebo groups showed more deterioration in their symptoms.
• Treatment of TD is usually unsatisfactory and prevention of the disorder is best
accomplished by judicious use of antipsychotic medications known to cause TD. Likewise,
frequent reassessments of the need for these drugs are recommended, and the lowest dose
possible should be used to achieve the desired response.
TETRALOGY OF FALLOT
James D. Boone, MD
BASICS
DESCRIPTION
Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart defect. It is
characterized by
• Right ventricular outflow tract (RVOT) obstruction due to pulmonary valve stenosis or a
dynamic subvalvular (infundibular) obstruction
• Ventricular septal defect (VSD)
• Deviation of the aorta to the right, overriding the right ventricle (RV) and left ventricle (LV)
• Concentric right ventricular hypertrophy
EPIDEMIOLOGY
Prevalence
• Live births: 3 in 10,000
• Occurs equally in males and females
Prevalence
Comprises 3.5–8% of all congenital heart diseases
Morbidity
The morbidity depends on the severity of the right-to-left (R-to-L) shunt and on other organ
dysfunction resulting from chronic heart failure and hypoxemia.
Mortality
• After the first year of life: 25%
• Four years of age: 40%
• Ten years of age: 70%
• Forty years of age: 95%
• Multifactorial
• Untreated maternal diabetes
• Phenylketonuria
• Intake of retinoic acid
• Trisomies 21, 18, 13
• Microdeletion of chromosome 22
• When the LV pressures exceed the RV pressures, flow across the VSD is L-to-R, and patients
can be asymptomatic. However, when the RV pressures exceed the LV pressures,
deoxygenated blood shunts across the intraventricular septum, causing systemic hypoxemia.
The severity of disease is determined by the amount of R-to-L shunting, which is in turn
dependent on ventricular pressure differences and the degree of RVOT obstruction.
– Acidosis, hypoxemia and hypercarbia can all cause an increase in PVR, contributing to a
detrimental increase in RV pressure.
• Newborns are rarely cyanotic at birth unless the RVOT is atretic, leading to a mandatory R-
to-L shunt. R-to-L shunt and cyanosis may not develop for several months; with time, the
increase in pulmonary blood flow (from L-to-R shunting) can lead to significantly increased
pulmonary pressures.
– Can result in myocardial ischemia. This can lead to a drop in cardiac output with possible
circulatory collapse or death.
• Tet spells (hypercyanotic spells) are paroxysmal episodes of arterial hypoxemia that result
from a decrease in SVR or increase in pulmonary vascular resistance (PVR) (favor R-to-L
shunt). It presents as cyanosis, tachypnea, and possibly neurologic compromise. Tet spells:
– Occur in 20–70% of patients and peak at the age of 2–3 months.
– Are usually proceeded by agitation, crying, feeding, defecation, or any increase in physical
activity.
– Can result in transient cerebral ischemia causing paleness, limpness, and even
unconsciousness.
– The squatting (or knee-chest) position is one of the treatments for Tet spells because it
compresses the femoral arteries and increases SVR, reducing the R-to-L shunt.
• The RVOT obstruction can have a dynamic component (muscular) that contracts in response
to inotropic stimuli. Therefore, increased contractility and tachycardia during times of
stimulation or stress can worsen the pulmonary stenosis, causing increased R-to-L shunting
and cyanosis.
• Acidosis, hypoxemia and hypercarbia can all cause an increase in PVR, contributing to a
detrimental increase in RV pressure.
• A clear understanding and appreciation of the patient’s anatomy is crucial in developing a
rational, appropriate plan.
• Avoid agitation, hypovolemia, acidosis, excessive crying, anxiety, and increased airway
pressures.
• Give premedication to ensure sufficient anxiolysis but avoid oversedation and resulting
respiratory acidosis, which can increase PVR.
• Maintain SVR and treat hypotension with phenylephrine and/or volume infusion.
• Avoid drugs with beta-agonist properties as they may worsen infundibular spasm.
• Recognize and treat Tet spells with volume infusion and/or phenylephrine, increasing the
depth of anesthesia, and/or decreasing stimulation.
SYMPTOMS
• Mild-to-moderate cyanosis in the neonatal period without respiratory distress
• Hypercyanotic Tet spells with a sudden decrease in oxygen saturation due to complete or
near complete obstruction of RVOT
• Poor weight gain, failure to thrive in children
History
• Prenatal testing
• Perinatal history
• Other congenital anomalies
• Development/milestones in children
• Ask for signs of cyanosis (Tet spells, clubbing) and frequency of occurrence
Signs/Physical Exam
• Normal S1, single loud S2 (secondary to more anteriorly located aorta)
• Systolic ejection murmur at left upper sternal border (due to RVOT)
• Clubbing, perioral cyanosis
• Check pulse oximetry. A normal saturation should be between 90% and 100% unless the
patient is actively shunting from R-to-L (e.g., Tet spell).
TREATMENT HISTORY
• Surgical correction by closure of the VSD and relief of the RVOT obstruction. RVOT dilation
may result in QRS prolongation and ventricular arrhythmias, as well as pulmonary
regurgitation with resultant RV hypertrophy and dysfunction.
• Palliative surgery with a Blalock–Taussig shunt diverts blood flow from the left subclavian
artery to the pulmonary artery (PA) to bypass the pulmonary stenosis.
MEDICATIONS
• Prostaglandins may be used in neonates to preserve ductal patency postpartum if
infundibular obstruction is severe and stable blood flow to the lungs is needed. Blood then
flows directly from the aorta to the PA, bypassing the pulmonary obstruction.
• Heart failure medications
• Beta-blockers
Labs/Studies
• CBC. Polycythemia may develop from chronic arterial hypoxemia
• Coagulation studies. Liver congestion may result in coagulopathy
• ECG (right axis deviation, RVH)
• Chest x-ray (CXR). Assess for right aortic arch, decreased pulmonary vascular markings,
boot shaped heart
• Echocardiography
• CT angiogram, cardiac MRI
• Cardiac catheterization (not indicated unless multiple VSDs, or abnormalities with the PA or
coronary anatomy are present)
• Cardiac: Severe tricuspid regurgitation, right heart failure, biventricular heart failure
• Pulmonary: Edema, hypoxia, cyanosis, pulmonary hypertension
• Hepatic: Congestion and impaired coagulation
• Hematologic: Polycythemia form chronic hypoxemia; can cause thrombosis, endocarditis,
strokes, and multiorgan dysfunction
• Fulminant heart failure
• Severe dehydration
• Severe hypoxemia
• Arrhythmias
TREATMENT
Premedications
• Benzodiazepines and opioids should be carefully titrated to avoid oversedation and
hypercarbia (can increase PVR). Consider avoiding intramuscular injections, which can lead
to agitation and a possible Tet spell.
• May want to avoid anticholinergics as tachycardia can narrow the RVOT, increase the R-to-L
shunt, and lead to hypoxemia.
• Endocarditis prophylaxis for dental procedures.
• Assess volume status. Hypovolemia can exacerbate the RVOT obstruction. In patients with
polycythemia from chronic hypoxemia, a prolonged NPO period can increase blood
viscosity and lead to sludging. In severe cases, preoperative phlebotomy might be indicated.
Parental consent if a minor
INTRAOPERATIVE CARE
• Individualize based on the patient and surgical procedure.
• May want to avoid spinal anesthesia as this could lead to an undesirable drop in SVR.
Monitors
• In a pediatric patient with a patent ductus arteriosus two pulse oximeters should be placed
to monitor a preductal (right hand) and a postductal (lower extremity) saturation.
• Arterial line may be appropriate to monitor the PaO2
• Consider central line, PA catheter, and/or transesophageal echocardiography for high-risk
surgeries (intraperitoneal and/or intrathoracic cardiac and noncardiac surgeries).
• Prior to induction, ensure euvolemia. Consider IV fluid bolus.
• If an IV is present, etomidate or ketamine induction allows maintenance of the SVR. A mask
induction may be appropriate in patients without an IV in situ or milder degrees of shunting.
Systemic oxygenation and BP must be carefully monitored. High doses of volatile agents can
cause detrimental decreases in SVR.
• Hypotension on induction should be promptly treated with an IV fluid bolus and/or
vasopressors. An alpha agonist such as phenylephrine is preferred because of the beneficial
effects on SVR.
• Opioids can be useful to blunt sympathetic response from intubation or surgical stimulation.
• Nondepolarizing muscle relaxants can be used for paralysis, but histamine releasing muscle
relaxants should be avoided to prevent a drop in the SVR. The chronotropic effects of
pancuronium may be helpful in maintaining cardiac output.
• Avoid a sympathetic surge with intubation (increases contractility) by ensuring that the
patient is deep. The airway should be secured quickly in order to avoid hypoxemia and
hypercarbia.
• Any kind of airway obstruction can trigger a Tet spell. Hypercarbia and hypoxemia increase
PVR and R-to-L shunting. A vicious cycle of further desaturations and decreased pulmonary
blood flow can develop.
Maintenance
• Maintenance can be achieved with any inhalational agent as long as SVR and BP are
maintained.
• Alternatively nitrous oxide can be combined with ketamine; this combination maintains BP
and SVR well.
• Opioids and benzodiazepines can also be used but should be carefully administered to avoid
a decrease in BP and SVR. Morphine should be used with caution due to its potential for
histamine release.
• Controlled ventilation is usually appropriate to maintain normocapnia. Excessive positive
airway pressures can adversely increase the resistance to blood flow through the lungs.
• Take meticulous care to avoid any infusion of air, which can lead to systemic air
embolization (especially if nitrous oxide is used). If infusion of air is suspected, increase the
FiO2 to 1.0 (turn the nitrous oxide off immediately to avoid an increase in bubble size).
• Maintain hemodynamic goals:
– Deep anesthetic state to avoid sympathetic surges
– Normal/high SVR to avoid “emptying” of the heart
– Maintain adequate intravascular volume and treat hypotension aggressively with IV fluid
boluses and vasopressors
– Low PVR to avoid R-to-L shunting
• Avoid hypothermia because this can lead to an increase in PVR and cause a R-to-L shunt.
• Before emergence, ensure adequate analgesia.
• Tachycardia can be treated with short acting beta-blockers such as esmolol.
• Awake extubation can help avoid hypercarbia and hypoxemia; however, coughing and
bucking on the endotracheal tube is also not desired.
FOLLOW-UP
BED ACUITY
• Monitored bed with pulse oximetry
• Consider ICU for high-risk patients
Medication/Lab studies/Consults
COMPLICATIONS
• Right heart failure from volume overload
• Biventricular dysfunction
• Severe hypoxemia
REFERENCES
1. Apitz C, et al.Tetralogy of Fallot. Lancet. 2009;374(9699):1462–1471.
2. Bailliard F, et al.Tetralogy of Fallot, review. Orphanet J Rare Dis. 2009;13(4):2.
3. Fox D, et al.When “blue babies” grow up: What you need to know about tetralogy of Fallot.
Cleve Clin J Med. 2010;77(11):821–828.
4. Schaff H, et al.Anesthetic management for transurethral resection of bladder in a 74-year-
old man with uncorrected tetralogy of Fallot. J Clin Anesth. 2005;17(3):155–157.
5. www.mayoclinic.org/tetralogy-of-fallot
• Pediatric cardiac physiology
• Shunt
• Patent ductus arteriosus
CODES
ICD9
745.2
ICD10
Q21.3 Tetralogy of Fallot
CLINICAL PEARLS
• Minimize R-to-L shunt by keeping the SVR high, maintaining intravascular volume, and
keeping the PVR low (avoid hypercarbia, hypoxia, hypothermia, and acidosis).
• Avoidance and treatment of Tet spells.
THALASSEMIAS
Jeremy Wong, MD
BASICS
DESCRIPTION
• Thalassemia is an autosomal-recessive hemolytic disorder caused by a decrease or absence
of globin chain synthesis. It is classified as either α or β depending on the globin chain that
is affected. Its manifestations are mostly secondary to anemia, iron overload, effects of
chelation therapy, and thrombosis.
• In contrast, sickle cell anemia and other hemoglobinopathies are characterized by the
synthesis of dysfunctional globin proteins.
EPIDEMIOLOGY
Prevalence
Major thalassemia: ∼56,000/year are born with the disease worldwide
Prevalence
• Among the most common genetic disorders, affecting 15 million people worldwide.
Thalassemia trait may provide a degree of protection against malaria, thus explaining its
genetic prevalence in tropical and subtropical regions.
• β-thalassemia: >1% of people in the Mediterranean, India, Southeast Asia, North Africa,
and Indonesia.
• α-thalassemia: Found in 5–10% of people in the Mediterranean, 20–30% in West Africa, and
∼68% in South Pacific.
Morbidity
• Usually related to anemia and its treatment: Splenomegaly, splenectomy, or blood
transfusion.
• Significant morbidity also occurs from liver disease, chronic infection, organ damage from
iron overload, and complications from chelation therapy (cataracts, deafness, infection).
Mortality
Worldwide: 3.4% of deaths in children <5 years
Autosomal-recessive genetic inheritance
• In all thalassemias, imbalanced globin chain synthesis causes a disruption of the normal 1:1
ratio of α and non-α chains. The defective red blood cells (RBCs) and their precursors are
detected by the immune system and destroyed/hemolyzed.
– In β-thalassemias (defect in β chain synthesis), excess α chains precipitate in RBC
precursors, damaging the membrane and leading to cell destruction (disrupted
erythropoiesis). Cells that survive are released into the circulation, but they are subject to
hemolysis. To compensate for the anemia, there is increased production of fetal
hemoglobin (HbF) because the free α chains can bind with γ chains (Note: Has a higher
O2 affinity).
– In α-thalassemias (defect in α chain synthesis), the excess γ chains (early in life) or β
chains (later in life) are relatively soluble and able to form viable, soluble homotetramers.
Hb Bart is comprised of 4γ chains and HbH is comprised of 4β chains.
• Severe anemia stimulates erythropoietin production and expansion of extramedullary
marrow in the thorax, head, and paraspinal regions. This leads to deformations of the face
and skull as well as osteopenia. Neuropathy can be present due to nerve compression by
large extramedullary hematopoietic masses.
• Iron overload is associated with increased bleeding, susceptibility to infection, organ
dysfunction (including left ventricular (LV) dysfunction and myocarditis), and
endocrinopathies (diabetes, thyroid, adrenal disorders). In transfused patients, a heavy iron
turnover is seen. In nontransfused patients, iron overload is the result of increased GI
absorption, possibly to compensate for ineffective erythropoiesis.
• Splenomegaly can result from the unusually large numbers of abnormal RBCs processed by
the spleen.
• Thrombotic tendency, pulmonary hypertension, leg ulcerations, priapism, and stroke may be
a result of endothelial dysfunction due to the decreased bioavailability of nitric oxide (NO).
• Common surgical procedures include splenectomy, cholecystectomy, line placement,
osteotomies for bony deformities, and repair of fractured bones.
• Special care must be taken to anticipate difficult airways in patients with abnormal
maxillofacial anatomy.
• Potential blood loss must be anticipated in the setting of baseline anemia.
• Because of the risk for thrombosis, perioperative prophylaxis should be considered, and
complications recognized and treated as needed.
• In pregnant women with thalassemia, the Hb levels should be maintained above 10 g/dL in
order to reduce the high reported rate of spontaneous abortion, intrauterine growth
restriction, prematurity, as well as suppress hyperactive erythropoiesis in the mother.
• Deferoxamine, if taken, is usually discontinued due to possible teratogenic effects. Of note,
pregnancy, itself, may be an iron chelator due to hemodilution and fetal consumption of
free iron.
• Caesarean delivery is usually planned in order to reduce the cardiovascular stress associated
with labor (especially in patients with compromised LV function) and to avoid
complications of cephalopelvic disproportion due to small stature that is commonly seen in
thalassemics.
SYMPTOMS
Fatigue, weakness, fevers, loss of appetite/weight loss, shortness of breath
History
• α-thalassemia: Mild or moderate forms demonstrate hematologic abnormalities at birth
• β-thalassemia major is usually diagnosed in the latter part of the first year of life (but can
appear as late as age 3–5 years) after the body converts from HbF to HbA production (γ
chain production stops).
Signs/Physical Exam
Pallor, jaundice, hepatosplenomegaly, failure to thrive, bony deformities including frontal
bossing, prominent facial bones, dental malocclusion (“chipmunk facies”), neuropathy, heart
murmur, signs of congestive heart failure.
TREATMENT HISTORY
• Patients with severe thalassemia require regular blood transfusion in combination with well-
monitored chelation therapy. The goal is to maintain an Hb value of at least 9–9.5 g/dL.
Units should be leukocyte poor.
• Splenectomy may be indicated for those with hypersplenism who require excessive blood
transfusions or who develop bleeding due to thrombocytopenia
• For select patients, stem cell transplantation is indicated. This is the only curative therapy
available. If successful, no blood transfusions are required, but patients may still require
chelation therapy.
MEDICATIONS
• Deferoxamine (chelating agent). Delays or prevents onset of cardiac disease. 30–40
mg/kg/day by subcutaneous infusion over 8–12 hours for 5 days/week, with IV
supplementation as needed. Usually started 1–2 years after transfusions are initiated.
• Vitamin E (antioxidant given for iron overload)
• Folic acid to replenish stores that may be depleted from high cell turnover.
• Aspirin for thromboprophylaxis.
Labs/Studies
• CBC. In severe thalassemia, Hb often ranges from 2 to 8 g/dL, and MCV and MCH are
usually very low. WBC count is often elevated in β-thalassemia major. Platelet count is
usually normal unless there is marked splenomegaly. Peripheral blood smear shows marked
hypochromasia and microcytosis.
• Serum iron levels are elevated, with saturation as high as 80%. Serum ferritin level is high.
• Skeletal imaging may show classic bone changes, osteopenia, and fractures.
• MRI and CT can be used to evaluate large extramedullary tumor-like masses, or iron
overload in the liver and heart (monitor response to chelation therapy). Liver biopsy may
also be performed.
• ECG and echocardiogram may be indicated to evaluate cardiac function and iron overload.
• Cardiopulmonary: Arrhythmias, pericarditis, CHF, pulmonary hypertension
• GI: Hepatomegaly, cirrhosis
• Hematologic: Infection, splenomegaly, thrombosis
• Endocrine: Diabetes, thyroid dysfunction, adrenal dysfunction
• Skeletal: Osteoporosis, fractures, osteonecrosis, maxillary hyperplasia, hypertelorism
• Neurologic: Paresthesia, paralysis, hearing loss, vision loss
Evidence of cardiopulmonary compromise or significant endocrine dysfunction should delay
elective procedures to allow for further workup and optimization.
CLASSIFICATIONS
• α-thalassemias result from a deficiency or deletion of one or more of the 4α genes (2 from
each parent).
– Clinically silent carrier state: No symptoms, but may have mild microcytic, hypochromic
anemia.
– α-thalassemia trait: Deletion of 2α genes causes a mild hypochromic anemia.
– α-thalassemia intermedia (Hemoglobin H disease): Deletion of 3α genes leads to
moderately severe hemolytic anemia, hepatosplenomegaly, jaundice, and vasculopathy;
patients may require occasional or frequent transfusions depending on severity of disease.
– α-thalassemia major: Deletion of all 4α genes causes HbF Bart’s disease (hydrops fetalis
syndrome, unless intrauterine blood transfusions given).
• β-thalassemias result from a deficiency or deletion of one or more of the 4β genes (2 from
each parent)
– Clinically silent carrier state: No symptoms, but can have a mild microcytic, hypochromic
anemia
– β-thalassemia trait: Deletion of 2β genes causes anemia, marked hypochromia and
microcytosis, elevated Hb A2, HbF, or both.
– β-thalassemia intermedia: Deletion of 3β genes leads to severe anemia, but are not
typically transfusion dependent due to a compound heterozygote state.
– β-thalassemia major: Deletion of all 4β genes causes Cooley’s anemia (transfusion
dependent anemia, massive splenomegaly, craniofacial abnormalities, growth
retardation).
• β-thalassemia associated with β chain structural variants: Coinheritance with HbE results in
HbE/β thalassemia, which may cause clinical anemia varying in severity from thalassemia
intermedia to thalassemia major.
TREATMENT
Premedications
• Prophylactic antibiotics, particularly in patients who have had a splenectomy.
• RBC transfusion, if appropriate
• Thromboprophylaxis, as appropriate.
Blood consent should be discussed given the higher likelihood of anemia and need for
transfusion.
INTRAOPERATIVE CARE
• Anesthetic literature is scant, but both regional and general anesthesia are probably safe as
long as thrombocytopenia is not present.
• Spine abnormalities due to osteoporosis may make neuraxial anesthesia more difficult.
Monitors
• Invasive monitoring may be indicated, depending on the operation and presence of cardiac
dysfunction.
Bony abnormalities of the maxillofacial area may make intubation difficult. Have difficult
airway equipment nearby and/or ready.
Maintenance
• Balanced anesthetic techniques that minimize cardiovascular depression are especially
important. Cardiac output should be maintained to ensure optimal peripheral oxygen
delivery in patients with significant anemia.
• Blood transfusion should be performed with leukocyte reduced red cells.
• Cell salvage has been successfully used to manage blood loss. Successful cardiopulmonary
bypass in patients with Hemoglobin H has also been described.
No specific considerations, unless difficult airway is present.
FOLLOW-UP
BED ACUITY
Depending on the degree of organ dysfunction and nature of surgery, an ICU bed may be
warranted.
• Restart deferoxamine as soon as possible if discontinued preoperatively.
• Transfusion-dependent patients should have frequent blood counts and transfusions as
needed to maintain target values.
• Serum ferritin levels are often used as a marker for hepatic and macrophage iron stores in
order to guide chelation therapy.
• For patients with severe disease, a hematology consultation is recommended to aid with
perioperative management.
COMPLICATIONS
Primarily involves airway complications, congestive heart failure, transfusion reactions, and
thrombosis.
REFERENCES
1. Butwick A, Findley I, Wonke B. Management of pregnancy in a patient with thalassemia
major. Int J Obstet Anesth. 2005;14(4):351–354.
2. Firth P. Anesthesia and hemoglobinopathies. Anesthesiology Clin. 2009;27:321–336.
3. Morris CR. Mechanisms of vasculopathy in sickle cell disease and thalassemia. Hematology.
2008;1:177–185.
4. Vichinsky E. Changing patterns of thalassemia worldwide. Cooley’s Anemia: Eighth
Symposium. Annals of the New York Academy of Sciences. 2005;1054:18–24.
5. http://emedicine.medscape.com/article/958850-overview\
• Hemoglobin
• Anemia
• Hemolytic anemia
CODES
ICD9
• 282.40
• 282.43 α thalassemia
• 282.44 β thalassemia
ICD10
• D56.0 α thalassemia
• D56.1 β thalassemia
• D56.9 Thalassemia, unspecified
CLINICAL PEARLS
• Patients with thalassemia may have concomitant organ dysfunction that can complicate
anesthetic management, including heart failure, arrhythmia, pulmonary hypertension, and
splenomegaly.
• Extramedullary bone expansion may lead to changes in airway anatomy that can make
intubation difficult.
• Patients with thalassemia may have increased risk for thrombosis, especially if
splenectomized.
• Chelation therapy and regular blood transfusions are important tools in the management of
significant thalassemias.
THE ADDICTED ANESTHESIA CARE PROVIDER
Ethan O. Bryson, MD
BASICS
DESCRIPTION
• Opioid addiction represents a major issue in the anesthesia workplace, so much so that some
have called it an occupational hazard.
• Alcoholism and addiction to other substances impact anesthesia care providers at rates
similar to other professions.
• The drug of choice for anesthesia care providers entering treatment is typically an opioid,
usually fentanyl.
• There is an association between chemical dependence and mental illness. Successful
treatment for addiction requires treatment of comorbid psychopathology.
• Participation in self-help groups is considered a vital component in the therapy of the
impaired healthcare provider.
EPIDEMIOLOGY
Incidence
• The incidence of drug abuse among anesthesia care providers as indicated by referral to
treatment centers is between 1% (for attending physicians) and 2% (for residents and
cRNAs).
• The incidence of drug abuse as indicated by anonymous self-reporting is upwards of 10%.
Prevalence
• Drug abuse is at least as prevalent among anesthesia care providers as it is among the
general population, and tends to mirror the community prevalence.
• The prevalence of alcohol and other drug abuse over the course of the anesthesia care
provider’s career is 12–15%.
Morbidity
• The addicted anesthesia care provider may develop hypersensitivity to physical stimuli
including allodynia in addition to developing tolerance.
• These individuals are at increased risk for developing blood-borne viral infections such as
HIV, hepatitis C virus (HCV) and hepatitis B virus (HBV).
• Chronic injection can lead to soft tissue infections.
• They are also at risk for drug overdose and drug dependence, and may also have associated
mental health problems.
Mortality
The risk of drug-related death among anesthesia care providers is highest in the first 5 years
after training and remains increased over that of other healthcare providers.
• Occupational exposures to drugs of abuse that sensitize the reward pathways in the brain
may promote substance use by physically altering the brain’s chemistry.
• Many genes have been identified as being associated with the susceptibility to drug
addiction and traits associated with risk taking behavior.
• While most individuals who experiment with drugs do not become dependent; individuals
who exhibit traits such as novelty-seeking and antisocial behavior are at higher risk for
developing addiction.
• In some cases self-administration of drugs of abuse may indicate an attempt to self-medicate
the symptoms associated with psychiatric illness.
• Emotional stress coupled with physical exhaustion and access to drugs of abuse may trigger
addiction in susceptible individuals.
• Dopamine release in the mesolimbic system of the brain reinforces drug-seeking behaviors
associated with several drugs of abuse.
• Drugs of abuse physically alter the chemistry of the addicted brain. Alterations in the
relative levels of GABA, dopamine, and serotonin (neurotransmitters associated with reward
pathways) favor drug-seeking behavior.
• A contributing cause of addiction in anesthesia care providers is the easy access to opioids
and other psychoactive medications. Tighter control allows for earlier detection and
documentation in suspected cases of abuse.
• Anesthesia information management systems can be used to identify patterns suspicious for
diversion among anesthesia personnel.
• Wasted medications should be returned to the pharmacy and analyzed to verify content.
• Random drug screening has been proposed as a deterrent, but most nonmilitary hospitals do
not employ such practices.
• Education regarding the risk for addiction in anesthesia care providers as well as the signs
and symptoms associated with the disease is very important.
DIAGNOSIS
• Because the addicted anesthesia care provider needs to remain close to their drug of choice,
they may appear quite functional until late in the disease.
• There is no specific pattern of behavior that suggests addiction; it can be as minimal as a
change in behavior over a short period of time. Changes typically seen in the addicted
anesthesia care provider include the following:
– Withdrawal from family, friends, and leisure activities
– Mood swings, with periods of depression alternating with periods of euphoria
– Increased episodes of anger, irritability, and hostility
– Spending more time at the hospital, even when off duty
– Volunteering for extra call
– Refusing relief for lunch or coffee breaks
– Requesting frequent bathroom breaks
– Signing out increasing amounts of narcotics or quantities inappropriate for the given case
– Weight loss and pale skin
• The addicted individual is often the last to recognize that a problem exists.
• It is important that relatives, friends, and coworkers gain a clear understanding of the
disease and understand what to do if they suspect addiction.
• The anesthesia care provider who exhibits some of the signs and symptoms above may not,
in fact, be diverting and abusing drugs.
• Other possibilities include
– Trying to establish oneself in the group practice
– Attempting to increase personal income
– Coexisting mental illness
TREATMENT
Once an anesthesia care provider has been identified as requiring treatment for addiction, a
referral is made to an inpatient facility that specializes in the treatment of healthcare
providers.
• It is important for recovery that the affected individual develops the support of other
similarly affected healthcare providers.
• Treatment involves detoxification, monitored abstinence, intensive education, exposure to
self-help groups, and psychotherapy.
• Individual and group therapy sessions attempt to alter addictive behaviors. The length of
inpatient stay for this initial treatment lasts anywhere from 8 weeks to 3 months and in
cases of relapse may require a 12-month stay.
FOLLOW-UP
• State medical societies are allowed to enroll addicted healthcare providers into diversion
programs designed to rehabilitate the affected individual and return them to practice. The
addicted anesthesia care provider is allowed to return to clinical practice only under close
supervision.
• The length of post-treatment monitoring contracts are at least 5 years. The contracts
mandate regular random collection of urine and/or hair samples for evidence of drug use as
well as participation in facilitated group and individual therapy and anonymous 12-step
programs.
• Return to work should be in a graded fashion so that the anesthesia care provider has
adequate time to attend to recovery-related obligations and is not overwhelmed by clinical
duties. Duties may be gradually increased on a set schedule that can be adjusted after
consulting with the worksite monitor and therapist.
• The risk of relapse is increased in individuals with a family history of addiction or coexisting
mental illness. Such persons should be advised to strongly consider retraining in another
medical field with less access to the major opioids.
CLOSED CLAIMS DATA
In a review of 2,715 claims in the database, only 7 mention substance abuse as possibly
playing a role in malpractice litigation against anesthesiologists.
REFERENCES
1. Booth JV, Grossman D, Moore J, et al. Substance abuse among physicians: A survey of
academic anesthesiology programs. Anesth Analg. 2002;(95):1024–1030.
2. Bryson EO, Silverstein JH. Addiction and substance abuse in anesthesiology. Anesthesiology.
2008;109(5):905–917.
3. Bryson EO, Hamza H. The drug seeking anesthesia provider. Int Anesthesiol Clin.
2011;49(1):157–171.
4. Bryson EO, Frost EAM (Eds). Perioperative Addiction. New York, NY: Springer Science and
Business Media, 2011.
• Alcohol abuse
CLINICAL PEARLS
• The most common drug abused by anesthesia care providers is fentanyl.
• If a colleague is suspected of abusing drugs or alcohol, the issue should be taken to the
state’s physician or nursing health program.
• Addiction is a chronic, relapsing disease. There is no cure but patients can be successfully
managed with a variety of treatment modalities.
• Legal issues
– Not bringing an affected individual to the attention of those who can help may leave
people open to legal liability if the impaired anesthesia care provider subsequently injures
a patient.
– Not all states have mandatory reporting laws; familiarization with the state’s specific
expectations should be made.
– In the event that the state does not mandate that impaired providers are reported, this
should not preclude one from filing a complaint.
– If you have first-hand knowledge of provider impairment, you have an ethical obligation
to report it in order to protect the public and to get the individual the help that they need.
THORACIC ANEURYSM REPAIR
Alina M. Grigoire, MD, MHS, FASE
Ileana Gheorghiu, MD
BASICS
DESCRIPTION
General
• A thoracic aortic aneurysm (TAA) is a permanent, localized dilation that is at least 1.5 times
the diameter of the expected normal value. Classifications are based on the anatomic
location and extent of involvement (Crawford, Debakey, and Stanford).
• Surgical repair often implements partial left heart bypass (LHBP) or femoral-femoral (fem-
fem) cardiopulmonary bypass (with selective cerebral perfusion and deep hypothermic
circulatory arrest [DHCA]) when the aneurysm is located at the ascending aorta or arch;
there is proximal involvement of structures (aortic valve, annulus, sinuses of Valsalva, etc.);
it is large in size; or repair is anticipated to be complex or require a long cross-clamp time.
These techniques decrease hemodynamic stability and spinal cord ischemia/ paralysis. In
select cases (e.g., descending aneurysms), repair may be considered without LHBP or fem-
fem bypass.
• Following surgical exposure, partial or full heparinization is administered, bypass techniques
are implemented, and the aorta is cross-clamped both distal and proximal to the aneurysm.
The aneurysm is opened and repaired typically with a Dacron graft. This is followed by
declamping, reperfusion, adequate hemostasis, and closure.
• Open surgical repair involves surgical exposure, followed by partial or full heparinization
and partial left heart bypass (LHBP) or femoral-femoral (fem-fem) cardiopulmonary bypass
(CPB). The aorta is cross-clamped both proximal and distal to the aneurysmal segment, the
aneurysm opened and repaired with Dacron graft. This is followed by declamping,
reperfusion, adequate hemostasis, and closure.
• Endovascular repair has become a popular approach; it provides the benefit of a less
invasive surgical technique with faster recovery and better short-term outcomes.
Position
Right (R) lateral decubitus with hips rotated toward a more supine position.
Incision
• Left (L) lateral thoracic
• Median sternotomy for CPB with deep hypothermic circulatory arrest (DHCA) technique
Approximate Time
4–5 hours average, depending on surgical experience
EBL Expected
500–1,500 mL blood loss, dependent on surgical experience
Hospital Stay
5–10 days
• Partial LHBP with selective organ perfusion.
• Fem-fem CPB with DHCA and selective cerebral perfusion.
EPIDEMIOLOGY
Prevalence
• No current feasible screening technique
• 10.4/100,000 person/years; equal in both sexes
• Ascending aorta 51%, aortic arch 11%, descending aorta 38%
• Average growth of 0.07 cm/year in ascending aorta and 0.19 cm/year in descending aorta.
Growth rate >1 cm/year is an indication for elective surgical repair.
Prevalence
400/100,000 autopsies by the age of 65.
Morbidity
• Cumulative risk of rupture is 20% at 5 years.
• Risk factors for rupture: Female, elevated diastolic pressure, aneurysm >5 cm, obstructive
pulmonary disease.
Mortality
• 27.4% overall in-hospital mortality for acute aortic dissection
• Type A: 26% surgical management and 58% medical management. Type B: 31.4% surgical
management and 10.7% medical management
• Hemodynamic (HD) instability is very common in the presence of dissecting aneurysms
(cardiac tamponade, ongoing hemorrhage, myocardial ischemia, organ malperfusion).
• Repair involves significant HD changes such as massive blood loss, drop in preload, acute
increase in afterload with cross-clamping, and myocardial depression.
• Neuroprotection techniques can include a spinal drain, neurophysiologic monitoring, and
electroencephalogram (EEG) for DHCA technique.
SYMPTOMS
• Enlargement: Hoarseness (recurrent laryngeal nerve compression), dysphagia, plethora and
edema, congestive heart failure (CHF), pain (neck, jaw, precordial, interscapular).
• Dissection/rupture: Hemiparesis, hemiplegia, HD instability, tamponade, respiratory
distress, cardiogenic shock.
History
Most frequently diagnosed incidentally
Signs/Physical Exam
Hypertension (HTN) or hypotension, syncope, altered mental status, superior vena cava
syndrome, cardiac tamponade (pulsus paradoxus, jugular venous distension, Kussmaul’s sign),
limb ischemia
MEDICATIONS
• Beta-blockers: Decrease aortic wall tension and myocardial oxygen consumption, decrease
perioperative morbidity and mortality, could augment preexisting left ventricular (LV)
dysfunction.
• Anticoagulant and antiplatelet medication: Impact the placement of spinal drains
• Antihypertensives: Sodium nitroprusside and nitroglycerine (both have negative impact of
spinal cord perfusion pressure (SCPP)); nicardipine is the drug of choice
Labs/Studies
• Hg, WBC, platelet count/function, PT/PTT, INR, BUN/creatinine
• CT/MRI angiography: 100% sensitivity, as well as assessment of the extension of aneurysms
and airway involvement (distortion of L main stem bronchus).
• Angiogram: Accurate diagnosis of the tear points, involvement of the artery of Adamkiewicz,
dissection into other major arteries (great vessels, renal, mesenteric, common iliac arteries).
• Carotid Doppler: Evaluate the extent of dissection into carotid arteries, rule out
atherosclerotic plaques with potential risk for stroke during selective antegrade cerebral
perfusion.
• Pulmonary function tests for preexisting pulmonary disease, COPD, restrictive lung disease,
previous lung resection to assess the feasibility of one lung ventilation.
• Echocardiogram and dobutamine stress test for preexisting ischemic cardiomyopathy,
coronary stents, pulmonary hypertension (PHTN), right ventricular dysfunction.
Cerebrovascular, coronary artery, pulmonary, renal, peripheral vascular disease
TREATMENT
Premedications
• Antihypertensive and antianginal medication should be continued, as appropriate.
• Anxiolytics can minimize HTN and rupture.
• Emergency intervention for unstable cases/altered mental status
• Consent for blood transfusion
• Potential for spinal cord injury and paralysis
Wide coverage of both gram (+) and (–) germs; Staphylococcus aureus, most common,
followed by Salmonella.
INTRAOPERATIVE CARE
• General anesthesia with endotracheal tube (ETT)
• Epidural anesthesia may also be used; however, it poses a higher risk for spinal cord
hematoma and makes postoperative neurotesting more challenging.
Monitors
• Standard monitors and Foley catheter.
• Preinduction radial arterial line (R side for descending aortic procedures, L side for
ascending aorta and arch); femoral line after induction (R side for L thoracotomy with
LHBP, L side for fem-fem CPB with DHCA technique).
• Large-bore peripheral IVs and multiport central line. A rapid infusion system should be
primed and connected. Consider a pulmonary artery catheter for preexisting LV dysfunction,
pulmonary HTN.
• Nasopharyngeal temperature (NPT) for brain temperature and bladder temperature (BT) for
visceral temperature.
• Spinal drain for monitoring CSF pressure and spinal cord protection.
• Regional cerebral oximetry: Assessment of adequate, bilateral brain oxygenation during CPB
with DHCA and selective cerebral perfusion.
• BIS may be considered, particularly for LHBP or fem-fem bypass.
• TEE: Confirmation of the extent and severity of aortic pathology, assessment of volume
status, myocardial function, aortic valve function, adequate LV decompression during CPB
with DHCA.
• Neuromonitoring: MEP, SSEP, EEG for CPB with DHCA.
• Maintain HD stability and volume status
• Double lumen tubes (DLT) are used to improve visualization for descending aneurysms;
usually left-sided (consider a right DLT if the left mainstem bronchus is compressed or
distorted).
• Single lumen ETT for ascending aortic and arch surgery.
Maintenance
• LHBP technique is used for partial redistribution of blood from the upper to the lower body,
reduction in afterload and myocardial O2 consumption, and improved SCPP. Heparinize to
an activated clotting time of 300 s and maintain flows at 1,000–2,000 mL/min.
• Fem-fem CPB with DHCA. Full heparinization, cool to 18°C, initiate DHCA after 20 min of
18°C core temperature, rewarm slowly with NPT-BT gradient ≤2°C
• Spinal cord protection
– Steroids can decrease spinal cord edema; mannitol can enhance free radical scavenging.
– Lumbar drains may be placed for spinal cord protection when bypass techniques are not
used. Spinal cord perfusion pressure is equal to the mean arterial pressure minus the
intracranial pressure. CSF is drained in 10 mL aliquots when the lumbar CSF pressure
exceeds 10 mm Hg; avoid draining >20 mL/hour.
– Neuromonitoring.
Avoid high levels of volatile agents and consider TIVA (propofol, fentanyl, remifentanil).
Boluses should be avoided, particularly at critical times to avoid false positives.
Avoid muscle relaxation, if possible; alternatively maintain 2–3 twitches when MEP
monitoring is used (this should be discussed with the surgical and neuromonitoring
team).
• Avoid muscle relaxation, if possible; alternatively, maintain 2–3 twitches when MEP
monitoring is used.
• Spinal cord protection: SCPP = MAP – ICP. CSF is drained for lumbar CSF pressure >10
mm Hg in 10 mL aliquots; avoid draining >20 mL/hour. Steroids and mannitol decrease
spinal cord edema and free radical scavenging.
• Aortic clamping is associated with an acute increase in afterload, preload (secondary to
volume redistribution), myocardial oxygen consumption, and ICP
• Aortic unclamping is associated with hypotension from hypovolemia, accumulation of
vasoactive substances, acidosis, hypocalcemia.
• Coagulopathy is commonly encountered as the result of dilution, hypothermia, quantitative
and qualitative platelet dysfunction, heparin effect, and fibrinolysis. Antifibrinolytic use is
recommended.
If a DLT was utilized, should be carefully changed to a single lumen ETT (patient may have
significant facial and laryngeal edema).
FOLLOW-UP
BED ACUITY
• Intensive care unit
• Maintain systolic blood pressure (SBP) >140 mm Hg for adequate SCPP
• Avoid anticoagulants and antiplatelet medication for the first 48 hours.
ANALGESIA
• Significant pain
• Local anesthetic infiltration at the incision site
• Opioid/dexmedetomidine drip
COMPLICATIONS
• Bleeding, graft infection, heart attack, stroke, renal failure, bowel ischemia, respiratory
failure.
• Spinal cord injury is multifactorial in etiology: Interruption of blood flow, spasm of the
microcirculation, increased CSF, inadequate revascularization of the spinal arteries.
– Increase SBP to >140 mm Hg or a MAP >90 mm Hg using vasopressors
– Drain CSF to achieve a CSF pressure ≤10 mm Hg (maximum 20 mL/hr)
– Consider steroids and magnesium.
PROGNOSIS
5-year overall survival is 56%.
REFERENCES
1. Coselli JS,Conklin LD, LeMaire SA. Thoracoabdominal aortic aneurysms repair: Review and
update of current strategies. Ann Thorac Surg. 2002;74:S1881–1884.
2. Coselli JS, Moreno PL. Descending and thoracoabdominal aneurysm. In Cohn LH, Edmunds
LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:1169–1190.
3. Crawfors ES, Coselli JS. Thoracoabdominal aneurysm surgery. Semin Thorac Cardiovasc
Surg. 1991;3:300–322.
4. Davies RR, Gallo A, et al. Novel measurement of relative aortic size predicts rupture of
thoracic aortic aneurysm. Ann Thorac Surg. 2008;85:S1–41.
5. Khan RD, Stone ME, et al. Anesthetic considerations for descending thoracic aortic
aneurysms repair. Semin Cardiothorac Vasc Anesth. 2007;11:205–223.
• Somatosensory- and Motored-evoked potentials (SSEPs/MEPs)
CODES
ICD9
• 441.2 Thoracic aneurysm without mention of rupture
• 747.29 Other anomalies of aorta
ICD10
• I71.2 Thoracic aortic aneurysm, without rupture
• Q25.4 Other congenital malformations of aorta
CLINICAL PEARLS
• Maintain a low preload prior to cross-clamping.
• If acute hypoxia occurs during one lung ventilation and aortic cross-clamp, consider asking
the surgeon to partially cross-clamp the left pulmonary artery to minimize blood being
shunted to the unventilated left lung.
• If the BP drops during LHBP and the TEE confirms normal LV function with an underfilled
LV, decrease the LHBP flow to increase LV preload.
• Acute HD instability could occur during aortic cross-clamping due to blood loss from the
collateral circulation.
THROMBOCYTOPENIA
Mona G. Sarkiss, MD, PhD
BASICS
DESCRIPTION
• Thrombocytopenia is defined as a platelet count <150,000/μL; it can result from decreased
production, increased destruction, dilution, and errors with measurement. The platelet
count is not, by itself, a predictor of platelet function and perioperative bleeding.
• Occasionally thrombocytopenia is associated with hypercoagulability and an increased risk
of thrombosis.
EPIDEMIOLOGY
Prevalence
• Pseudothrombocytopenia: 0.2% in the general population, 1.9% in hospitalized patients,
and 2% in patients taking abciximab.
• Autoimmune thrombocytopenia (in the US): Adults less than 10 per 100,000 and children 1–
4 per 100,000.
• Heparin-induced thrombocytopenia (HIT): Up to 8% of patients receiving heparin are at risk
of developing antibodies to platelets; only 1–5% will progress to develop HIT with
thrombocytopenia and one-third may suffer from arterial and/or venous thrombosis.
• Gestational thrombocytopenia: Occurs in 5.8% of pregnancies and is not associated with
increased risk of bleeding.
• Preeclampsia related thrombocytopenia occurs in 50% of preeclamptic patients but clinical
hemorrhage is uncommon.
• Impaired production:
– Congenital
– Acute leukemia, myelodysplasia
– Osteoporosis
– Toxins: Chemotherapy, alcohol
– Infections: HIV
– Radiotherapy
• Increased intravascular destruction:
– Autoimmune:
Primary causes: Idiopathic thrombocytopenia, systemic lupus erythematous
Secondary causes: Drug-induced (HIT), post-transfusion, neonatal autoimmune
thrombocytopenia
– Non-autoimmune:
Disseminated intravascular coagulopathy (DIC)
Thrombotic thrombocytopenic purpura (TTP)
Hemolytic uremic syndrome (HUS)
Infection
Preeclampsia/HELLP syndrome
• Increased extravascular destruction:
– Hypersplenism
• Dilutional:
– Massive transfusion
• Pseudothrombocytopenia
• Idiopathic thrombocytopenia: Attachment of antibodies or immune complexes to platelets
resulting in their premature removal from the circulation by the reticuloendothelial system.
• Systemic lupus erythematous: Antiplatelet antibodies or circulating immune complexes bind
to platelets.
• HIT
– HIT type 1: A benign, non-autoimmune condition. Mild thrombocytopenia occurs within
1–2 days after heparin therapy and resolves spontaneously within a few days even with
continued heparin therapy.
– HIT type II: IgG antibodies bind to heparin bound to platelet factor 4. Together, this IgG–
heparin–PF4 complex binds to platelet receptors and activates them. Venous thrombosis
occurs more commonly than arterial thrombosis. Occurs 5–10 days after the initiation of
therapy.
• Post-transfusion thrombocytopenia occurs about 10 days after a blood transfusion and is due
to antibodies in the recipient against human platelet antigen 1a (HPA–1a) on transfused
platelets.
• Neonatal alloimmune thrombocytopenia (NAIT) results from transfer of maternal IgG
antiplatelet antibodies across the placenta to the fetus. The antibody attaches to the HPA-1a
inherited from the father and is lacking in the mother. Severe thrombocytopenia during the
early phase of the second trimester can occur and may cause intracranial hemorrhage (20%
incidence).
• DIC results from an abnormal, systemic activation of the coagulation cascade. This leads to
deposition of fibrin in the microcirculation and aggregation and "consumption" of platelets
with consequent thrombosis causing ischemia and organ necrosis. The blood becomes
“unclottable" and severe hemorrhage occurs.
• TTP is due to an inability to cleave large multimers of von Willebrand factor (vWF). These
large multimers bind to platelets and cause thrombosis of the small vessels. TTP may result
in renal failure and impaired neurological function.
• HUS is similar to TTP in that there is a failure of cleavage of large multimers of vWF. It is
characterized by the acute onset of microangiopathic hemolytic anemia, renal injury, and a
low platelet count. HUS can be triggered by infection (e.g., Escherichia coli and HIV),
genetic predisposition, medication, and systemic diseases that cause microvascular injury
(e.g., systemic lupus).
• HELLP syndrome results in microvascular injury with endothelial cell damage along with
progressive platelet activation and consumptive thrombocytopenia.
• Infection. Viral (e.g., HIV, EBV, and CMV), rickettsial, and parasitic infections (e.g., malaria)
can reduce platelet production causing thrombocytopenia. Also sepsis in the critically ill is
associated with an increase in macrophage colony-stimulating factor; it is responsible for
histiocyte engulfment of megakaryocytes.
• Splenomegaly. Up to 90% of platelets may be sequestered in the spleen but it is not usually
associated with bleeding.
• Dilutional thrombocytopenia can occur in patients who have received multiple units of
whole blood or packed RBCs (pRBCs). Blood stored at 4°C for 24 hours has few viable
functioning platelets (after 6 hours storage at 4%C, platelets lose 50–70% of their activity.
• Pseudothrombocytopenia. Occurs due to in vitro agglutination of platelets by EDTA
anticoagulant and can result in falsely low platelet counts being recorded with automated
measurements.
• Pregnancy associated thrombocytopenia is mild, asymptomatic, and present in 5% of
pregnant women at term.
• A thrombocytopenic patient should be evaluated for the underlying cause, the possibility of
qualitative platelet dysfunction, other coagulation defects, and signs and symptoms of
impaired hemostasis.
• Each unit of transfused platelets increases the platelet count by 10,000/μL assuming that
there is no immediate sequestration and destruction by hypersplenism or dilution by IV
fluids and pRBCs.
• Ensure that the blood bank has a recent type and cross-match with pRBCs and platelets
available and ready for immediate transfusion, if needed. Of note, cross-matching the
recipient’s platelets with those of the donor is not necessary; however incompatibility can
reduce post-transfusion counts.
SYMPTOMS
Hematemesis, hemoptysis, hematochezia, melena
History
• Easy bruising or bleeding gums
• Medications that can cause impaired or decreased platelet counts
• Malignancies and radiation
Signs/Physical Exam
• Bruising, petechiae, purpura of the skin conjunctiva or oral mucosa
• Bleeding at venipuncture sites or petechiae at the BP cuff site.
TREATMENT HISTORY
Dependent on the etiology and severity
• ITP: Steroids, IV immunoglobulin (IVIG), splenectomy
• TTP, HUS: IVIG, plasmapheresis
• HIT: Discontinue heparin, consider alternative anticoagulant if blood thinning is still needed
• Hypersplenism: Splenectomy
Labs/Studies
• A manual platelet count is more accurate and reliable in patients with recent
thrombocytopenia.
• When pseudothrombocytopenia is suspected, counts should be repeated in citrate-
anticoagulated or heparin-anticoagulated blood samples.
• Platelet function tests include
– PFA-100
– Plateletworks analyzer
– Thromboelastogram (TEG). Assesses the entire process of clot formation including platelet
and coagulation factor function.
– Aggregometry
– Con and plate analyzer
Depends on underlying cause and can include
• Renal failure
• Liver cirrhosis
• Bone marrow failure
• Anemia and hypovolemia
• Thrombocytopenic thrombotic disorders may result in deep venous thrombosis (DVT),
pulmonary embolism (PE), myocardial infarction (MI), and cerebrovascular accident (CVA)
• For complex causes of thrombocytopenia, a hematology consult may be warranted to
optimize the patient preoperatively and continue appropriate therapy intraoperatively and
postoperatively.
• Spontaneous bleeding occurs with platelet counts <20,000/μL (1).
• Neurosurgery and ophthalmic surgery, where even minimal bleeding can have a deleterious
effect, should be performed only with a platelet count ≥100,000/μL.
• Major invasive surgery including cardiac surgery can be safely performed with platelet
counts of 50,000/μL only if platelet function is normal and no other coagulation
abnormalities exist (2).
• Obstetrics patients with HELLP syndrome. Platelet transfusions should be considered when
the count is <30,000/μL for vaginal delivery or <50,000/μL for Cesarean section (2).
• Lumbar puncture for intrathecal chemotherapy should not be performed with platelet counts
<20,000/μL (4).
CLASSIFICATIONS
• Impaired production
• Increased destruction (intravascular or extravascular)
• Dilutional
• Pseudothrombocytopenia
TREATMENT
Premedications
• Preoperative platelet transfusion if the platelet count is <50,000/μL or active hemorrhage is
present and surgery must be performed.
• DDAVP 0.3 μg/kg IV in patients with renal failure or von Willebrand’s disease
• A temporary increase in platelet count can be achieved with IVIG, plasma exchange, or
corticosteroids, when appropriate.
Discuss the possibility of blood product transfusion
INTRAOPERATIVE CARE
Spinal anesthesia requires a minimal platelet count of 50,000/μL while epidural anesthesia
requires a minimal platelet count of 80,000/μL (2). When weighing the risks and benefits,
coagulation profile should also be considered.
Monitors
• Central line placement. Oozing from the site may occur if the platelet count is <50,000/μL
(5).
Airway instrumentation should be performed gently due to the risk of mucosal bleeding.
Consider lubricating the ETT and laryngoscope. Nasal intubation is relatively contraindicated.
Maintenance
• Nasogastric tube placement should be avoided.
• Volume status. Should be continuously assessed, due to the risk of bleeding.
• Transfusion. pRBC and platelet transfusion, as needed.
• Vigilance with airway bleeding during extubation
• Avoid nasal trumpet placement
FOLLOW-UP
BED ACUITY
Depends on the surgical procedure, comorbidities, and intraoperative events (e.g., massive
transfusion and ongoing bleeding).
• Corticosteroids, when appropriate, should be continued in the postoperative period.
• Follow-up platelet counts
• Hematology consult may be required
COMPLICATIONS
• Thrombocytopenia related
– Postoperative bleeding
– Bleeding or hematoma at IV, central line, and arterial line sites
– Postoperative thrombosis: DVT, PE, MI, CVA
• Platelet transfusion related
– Alloimmunization can be minimized by using leukocyte-depleted platelet concentrates or
HLA-matched platelets.
– Graft-versus-host disease can be prevented by gamma-irradiation of platelet concentrates
prior to transfusion in patients with immunodeficiencies (6).
– Increased risk of disease transmission
• Perioperative thrombosis: DVT, PE, MI, CVA.
REFERENCES
1. obas M.Preoperative assessment of coagulation disorders. Int Anesthesiol Clin.
2001;39(1):1–15.
2. Samama CM, Djoudi R, Lecompte T, et al. Perioperative platelet transfusion.
Recommendations of the French Health Products Safety Agency (AFSSAPS) 2003. Minerva
Anestesiol. 2006;72(6):447–452.
3. Spahn DR. Strategies for transfusion therapy. Best Pract Res Clin Anaesthesiol.
2004;18(4):661–673.
4. Howard SC, Gajjar AJ, Cheng C, et al. Risk factors for traumatic and bloody lumbar
puncture in children with acute lymphoblastic leukemia. JAMA. 2002;288(16):2001–2007.
5. Fisher NC, Mutimer DJ. Central venous cannulation in patients with liver disease and
coagulopathy–A prospective audit. Intensive Care Med. 1999;25(5):481–485.
6. Kam PC. Anaesthetic management of a patient with thrombocytopenia. Curr Opin
Anaesthesiol. 2008;21(3):369–374.
• Platelets
• Heparin-induced thrombocytopenia
• Preeclampsia
• von Willebrand’s disease
CODES
ICD9
• 287.30 Primary thrombocytopenia,unspecified
• 287.49 Other secondary thrombocytopenia
• 287.5
ICD10
• D69.49 Other primary thrombocytopenia
• D69.59 Other secondary thrombocytopenia
• D69.6 Thrombocytopenia, unspecified
CLINICAL PEARLS
• Bleeding time does not correlate with the risk of intraoperative bleeding.
• Avoid platelet transfusion before the spleen is removed during splenectomy.
THYROIDECTOMY
BASICS
DESCRIPTION
General
• Thyroidectomy describes the complete or partial excision of the thyroid gland.
• Indications include
– Hyperthyroidism due to autoimmune or multinodular thyroid disease
– Thyroid malignancy
– Thyroid nodules with growth potential
– Goiter causing tracheal compromise, swallowing difficulty, or other discomfort
• Exposure. Following a horizontal incision (lower neck, usually in skin crease if present) into
the first three layers (skin, subcutaneous fat, and superficial fascia), the upper flap is
elevated until it reaches the thyroid cartilage and the lower flap is pulled downward. The
deep fascia is incised in a vertical, midline manner and the infrahyoid muscle is laterally
retracted.
• Identification of the parathyroid glands, recurrent laryngeal nerve (RLN), and superior
laryngeal nerve (SLN) are performed to protect them from injury.
• Devascularization to the thyroid gland involves clamping and ligating the
– Superior thyroid artery; a branch of the external carotid. Ligation is typically made
proximal to the gland to avoid injury to the external laryngeal nerve.
– Inferior thyroid artery; a branch of the thyrocervical trunk. Ligation is performed distal to
the superior and inferior parathyroid arteries to preserve the blood supply to the
parathyroid glands.
• The thyroid is dissected off the trachea (pretracheal fascia) to avoid damage prior to
removal of the gland.
• Endoscopic removal has been described but is not commonly performed.
Position
• Supine
• Arms tucked to facilitate the surgeon’s access to the neck.
• Shoulder rolled to hyperextend the neck and optimized exposure.
Incision
• Generally involves a small incision across the anterior neck at the level of the thyroid
cartilage.
• Dissection may be complicated in patients with aggressive cancer, prior surgery, or a history
of radiation.
• In rare cases, the thyroid gland extends into the mediastinum (retrosternal goiter) and a
sternotomy incision is required.
Approximate Time
1–3 hours
EBL Expected
Minimal
Hospital Stay
• Unilateral lobectomy is generally an outpatient procedure.
• Total thyroidectomy is generally associated with a short inpatient admission.
• Intraoperative neuromonitoring may be performed in select cases (endotracheal tube with
monitoring electrodes [e.g., NIM tube]).
• Ultrasound for anatomic confirmation of lesion location (select cases).
EPIDEMIOLOGY
Morbidity
• RLN damage.
– RLN is a branch of the vagus nerve (CN X) and provides sensation to the trachea and
innervation to all the muscles of the larynx (vocal cord adductors and the single abductor
posterior cricoarytenoid), except the cricothyroid muscle.
– Unilateral RLN damage leads to hoarseness.
– Bilateral partial RLN damage (to the abductor) leads to stridor and respiratory distress
(from unopposed adduction by the RLN and the SLN’s cricothyroid muscle).
• SLN damage.
– SLN is a branch of the vagus nerve and provides sensation to the larynx and innervation to
the cricothyroid muscle.
– Unilateral SLN damage has minimal effects.
– Bilateral SLN damage leads to hoarseness and easy tiring of the voice.
• Hypoparathyroidism. Inadvertent removal of the parathyroid glands can lead to acute
hypocalcemia with spasticity/tetany.
– If removal of parathyroid glands is recognized, they can be surgically reimplanted.
• Hematoma leads to airway compromise.
• Hypothyroidism (iatrogenic).
Mortality
Rare
• Preoperative assessment of the indication for surgery, physiologic status, and size/location
of mass. If the mass is extending into the mediastinum, a review of the CT scan and a
discussion with the surgeon should be performed; the need for pulmonary function testing
(flow-volume loops) or other imaging may be necessary to assess the extent of airway
obstruction or potential for post-induction cardiovascular collapse due to impingement on
central vascular structures.
• Hyperthyroidism should be aggressively treated prior to surgery unless emergency surgery is
required.
• Consult with the surgeon regarding the need for nerve monitoring. EMG monitoring
necessitates avoidance of long-acting neuromuscular blockage.
• Significant impingement on the trachea by thyrooid tissue can produce tracheomalacia with
resultant dynamic collapse of the airway after removal (results in a variable, extrathoracic
obstructive lesion).
SYMPTOMS
• Compression of local structures
– Dysphagia from esophageal compression
– Dyspnea secondary to tracheal compromise
– Hoarseness caused by compression of RLN or SLN
• Hyperthyroidism. Palpitations, heat intolerance, weight loss, fatigue, hair loss, tremor,
muscle weakness.
History
Patients typically present for surgery after a thyroid mass/nodule is found on incidental
exam. The majority of patients are asymptomatic.
Signs/Physical Exam
• Thyroid goiter
• Tachypnea and/or stridor from airway compression
• Hyperparathyroidism is associated with tachycardia, tremors, and perspiration
• Exophthalmos/periorbital edema is associated with Grave’s disease.
• Inability to lie flat on exam (air hunger).
• Inability to produce a forceful cough during valsalva.
MEDICATIONS
• Beta-blockers (especially propranolol) treat the sympathetic response associated with
elevated thyroid levels.
• Propylthiouracil (PTU) or methimazole (MMZ) blocks the production of thyroid hormone.
Labs/Studies
• Thyroid function tests: Thyroid stimulating hormone (TSH), T4 (free + total), T3
• CBC (mild anemia is common)
• Electrolytes (including ionized calcium)
• Flow-volume loops. Evaluate for airway obstruction in the sitting, reclining, and supine
positions if anterior mediastinal mass is suspected or present.
• ECG. Assess for normal rhythm, QT interval, and presence of other disease.
• CXR. Evaluate for active infection, tracheal deviation, and extension into mediastinum.
• CT. Further assessment of mediastinal involvement and tracheal impingement.
• Consider preoperative otorhinolaryngology consultation and functional vocal cord
evaluation in patients with hoarseness or in high-risk procedures (cancer, reoperation, post-
radiation thyroid procedure). This is primarily a surgical issue to facilitate postoperative
assessment of nerve injury.
• Cardiac. Cardiomyopathy and/or atrial fibrillation if long-standing, untreated
hyperthyroidism.
• Neurologic. Grave’s disease is associated with ocular symptoms; neuropsychiatric symptoms
can occur in severe hyperthyroidism.
TREATMENT
Premedications
Anxiolytics as appropriate; use with caution if airway compression is suspected.
None
INTRAOPERATIVE CARE
• General endotracheal anesthesia is the most common approach.
– LMAs can be considered in select patients.
• Local/regional block with sedation can be considered in select patients (not common).
– Cervical plexus block with local infiltration.
– Not optimal for monitoring cases or procedures involving large goiters and invasive
disease.
Monitors
• Neuromonitoring (select cases).
• Invasive arterial monitoring in patients with significant risk of thyrotoxicosis.
• In most patients, the thyroid goiter has minimal impingement on the airway and no special
measures are required.
• Patients with a significant tracheal impingement should undergo topicalized, awake
fiberoptic intubation.
– Tracheal compromise is suggested by CT findings, an obstructive pattern on flow-volume
loops, or the presence of severe dysphagia, hoarseness/stridor, or difficulty lying flat.
– Consider using a small ETT if tracheal compression is suspected.
• Videolaryngoscopy (GlideScope, etc.) can facilitate placement of the EMG’s electrode sensors
at the vocal cords.
– Allows the surgeon and neurophysiologist to confirm placement of the tube and avoid
repeated laryngoscopy.
– Used intraoperatively to reevaluate the position of electrodes if the signal is lost.
Maintenance
• General anesthesia with volatile anesthetics or total IV anesthetic.
• Muscle relaxant is not necessary for surgical exposure. Avoid long-acting relaxant if
monitoring the RLN.
• Consider dexamethasone for postoperative nausea and vomiting prophylaxis and modulation
of airway edema.
• Carefully consider the need for postoperative intubation. Tracheomalacia, leading to
dynamic airway obstruction, can occur in patients with significant preoperative tracheal
involvement by the thyroid mass. Acute airway obstruction is a concern in the setting of
intraoperative RLN injury.
– Functional evaluation of vocal cord function can be performed at emergence via fiberoptic
assessment. Performed as the ETT is withdrawn at emergence or via an LMA placed prior
to emergence.
– Continuous real-time monitoring for vocal cord movement during surgery with fiberoptic
bronchoscopy through an LMA has been proposed.
– Low-dose remifentanil infusion (0.02–0.05 μg/kg/min) may facilitate tolerance of the ETT
and functional vocal assessment, while minimizing coughing.
• Avoid coughing at emergence. Straining against the ETT may promote suture disruption and
hematoma formation. Postoperative hematoma formation can cause airway compromise.
– Resumption of spontaneous ventilation during closure may facilitate prompt extubation on
emergence.
– Suctioning of the airway should be done before extubation and while the patient is “deep”
to remove any accumulated blood or secretions that can stimulate coughing.
FOLLOW-UP
BED ACUITY
• Routine nursing care
• In complicated procedures, there is significant concern for RLN injury and respiratory
symptoms; consider prolonged PACU stay and monitored floor bed.
ANALGESIA
• Acetaminophen
• Opioid
• Local infiltration
• Cough lozenges
COMPLICATIONS
• Hypoparathyroidism with acute hypocalcemia and tetany
• Recurrent laryngeal nerve injury with hoarseness or obstruction
• Tracheomalacia with dynamic airway obstruction
• Neck hematoma from post-surgical bleeding that may occur suddenly after an episode of
wretching or coughing
– This is a surgical emergency. Airway management can be exceptionally challenging due to
compression from the hematoma.
– The most effective intervention is surgical decompression of the neck hematoma at the
bedside prior to induction of anesthesia or attempted intubation.
REFERENCES
1. Dillon FX.Electromyographic (EMG) neuromonitoring in otolaryngology-head and neck
surgery. Anesthesiol Clin. 2010;28(3):423–442.
2. Murkin JM.Anesthesia and hypothyroidism: A review of thyroxine physiology,
pharmacology, and anesthetic implications. Anesth Analg. 1982;61(4):371–383.
3. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin N.
2006;35:663–686.
4. Yerzingatsian KL. Thyroidectomy under local analgesia: The anatomical basis of cervical
blocks. Ann Roy Coll Surg Eng. 1989;71:207–210.
• Electromyelography (EMG)
• Hyperthyroidism
CODES
ICD9
• 193 Malignant neoplasm of thyroid gland
• 242.90 Thyrotoxicosis without mention of goiter or other cause, and without mention of
thyrotoxic crisis or storm
ICD10
• C73 Malignant neoplasm of thyroid gland
• E05.90 Thyrotoxicosis, unsp without thyrotoxic crisis or storm
CLINICAL PEARLS
• Enlargement of the thyroid gland can cause compression of the trachea, esophagus, and
RLN.
• Patient should be euthyroid before proceeding with an elective thyroidectomy.
• Thyroid storm is a medical emergency that may present in a patient with hyperthyroidism.
– Common manifestations include arrhythmias (SVT and Afib) and hyperthermia.
– Acute treatment includes beta-blockade, corticosteroids, PTU, and antipyretics.
• Neuromonitoring is generally reserved for more invasive thyroid masses.
• Smooth emergence minimizes the risk of hematoma formation and airway compromise.
TIDAL VOLUME
Quinn L. Johnson, MD
BASICS
DESCRIPTION
• The principal function of respiration is to exchange oxygen and carbon dioxide with
circulating blood at the level of the alveoli (takes place during inspiration and expiration).
• Tidal volume (TV) refers to the amount of air that is involved in one half of respiration,
either the volume of expiration or the volume of inspiration. In addition to being used to
calculate minute ventilation (respiratory rate times TV), it serves as a major component of
several lung capacities:
– Total lung capacity (TLC)
– Inspiratory capacity (IC)
– Forced vital capacity (FVC)
• The concept of the TV is utilized when discussing:
– Spontaneous ventilation: An average measure of inspiration or expiration volumes that
occurs for an individual, typically during normal breathing. Direct measurement of the TV
occurs using a spirometer or through a variety of lesser-utilized dilutional techniques.
– Mechanical ventilation: The amount of air delivered or returned into the breathing circuit.
Volume modes allow for the TV to be set; they are often pressure limited to avoid
barotrauma. Conversely, pressure modes have variable tidal volumes and depend on the
lung’s compliance.
• Normal values
– Spontaneous ventilation: ∼6–7 cc/kg; for an average 70 kg adult, this equates to roughly
500 cc of volume.
– Mechanical ventilation: ∼7–15 cc/kg are programmed for delivery secondary to
compliance of the circuit, chest wall resistance, and increased apparatus dead space.
• Components of TV. Not all of the TV is involved in air exchange. Dead space describes the
portion of the volume not involved in actual gas exchange.
– Anatomic dead space: Involves passageways such as the trachea and upper bronchioles.
Typically around 30%.
– Alveolar dead space: Alveoli that are not being perfused (contributes a negligible amount
in healthy patients).
– Physiologic dead space: The combined volume of the anatomic and pathologic dead space.
This is roughly equivalent to 2 cc/kg or 150 cc in an adult.
– Apparatus, mechanical, or equipment dead space describes the additional TV that does not
participate in air exchange (endotracheal tube, laryngeal mask airway, corrugated
extendors, humidifiers, etc.). Clinically, this is often minor in adults, but can become
significant in pediatrics, particularly neonates.
• Movement of air
– Spontaneous ventilation at rest. Inspiration, at rest, results primarily from contraction of
the diaphragm and the external intercostal muscles. This causes an increase in the
thoracic cavity volume and the development of negative pressure compared to the
atmosphere. The pressure difference that is created allows the flow of air into the
pulmonary system. Expiration, at rest, is normally passive. As the muscles of inspiration
relax, the thoracic cavity decreases in volume and the elastic recoil of the lungs act in
concert to create a positive pressure compared with the atmosphere; air flows out of the
pulmonary system. Not all of the air is expelled from the lungs; the volume left behind is
referred to as the functional residual capacity (comprises the expiratory reserve volume
and residual volume).
– Spontaneous ventilation during disease states or distress. Adequate oxygenation requires
the use of accessory muscles. Inspiration can involve the scalene, sternocleidomastoid, or
pectoralis muscles. Expiration becomes an active process and involves the abdominal
muscles or internal intercostals.
– Mechanical ventilation. Inspiration is dependent on the generation of positive pressure.
Two general modes for controlled ventilation are commonly used: Volume control and
pressure control. Volume control will attempt to deliver a preset volume of gas to the
patient using a variable, but limited, amount of pressure. Pressure-dependant ventilation
utilizes a set pressure and, therefore, results in variable TVs to the patient. Volumes and
pressures then can be adjusted based on clinical and laboratory values to optimize
ventilation. Expiration remains a passive process; occurs after the removal of positive
pressure ventilation due to chest wall recoil and peritoneal cavity contents.
• Measurements of TV
– Spirometry: A device that measures the volume of air for both inspiration and expiration
breathed by a patient. The rate of volume movement is also recorded. Overall, it provides
a means to identify possible pulmonary pathology (e.g., COPD, pulmonary fibrosis).
– Ventilator. TV can be measured directly using a respirometer, usually found in the
expiratory limb of the ventilator circuit. A unidirectional microvane or a bidirectional
volumeter is physically spun by the gas flow as it leaves the patient; the number of
rotations correlate (are calibrated) to a specified TV. A second indirect measure of TV is a
gas flow rate meter found in newer equipment. Ultrasound techniques measure the
volume of air moving past the transducers and the TV is calculated based on this
relationship.
• Position
– Spontaneous ventilation. In the supine position, the relaxed diaphragm is located higher in
the thoracic cavity compared to when the patient is in a standing or upright position.
Because of this height difference, the diaphragm will have more space to contract and
results in a larger volume being moved for a given amount of energy (work).
– Mechanical ventilation. Often performed in the supine position. Neuromuscular blockade
and/or general anesthesia result in the diaphragm rising high into the thoracic cavity from
abdominal contents pushing against a “weakened" diaphragm. This will result in
decreased lung volumes, and therefore, larger pressures are necessary to expand the
alveoli when ventilating a patient.
– Prone and, to a lesser degree, lateral positioning can improve respiratory mechanics
secondary to the effects of gravity (shifting of abdominal contents and improved
diaphragm excursion). Similarly, a patient in reverse Trendelenburg has improved
respiratory mechanics compared to the supine and Trendelenburg position.
• Impaired oxygenation or ventilation in the spontaneously ventilating patient often results in
the recruitment of accessory muscles during inspiration and expiration to increase the TV
and compensate for increases in dead space or shunting. However, not all pathological
processes are limited to the pulmonary system, and may include cardiac and metabolic
disease.
• Dead space increases in either mechanical ventilation or spontaneous breathing in the
following situations:
– Rapid, shallow breathing as may be seen from abdominal or thoracic incisional pain. The
smaller TVs result in an increased fraction of dead space (can exceed 50%).
– Pulmonary embolism prevents perfusion to alveolar units being ventilated, thus increasing
pathological dead space. The location of the embolism will determine the extent of the
increase in dead space.
– Cardiac arrest/severe hypotension results in alveolar units that continue to be ventilated
but now have decreased or absent perfusion.
• Obesity. Pulmonary compliance may decrease by 35% in morbidly obese patients secondary
to reductions in both pulmonary and chest wall compliance. This results in an increased
respiratory rate, but smaller TVs. This breathing pattern creates a preferential ventilation of
poorly perfused lung tissue and leads to hypoxemia and/or hypercapnia particularly while
under anesthesia (1) unless TVs are augmented.
• Geriatrics. Lung volumes decrease; however, the volume solely attributable to age is difficult
to predict because smoking history, occupational illnesses, environmental conditions, and
exposure to lung pollutants also factor into the decrease. The loss of height associated with
spinal osteoporosis can affect thoracic volumes (2). In addition, the internal structure of the
lungs is affected; TV begins to decrease in the mid-40’s secondary to an increasing closing
volume. The encroachment of closing volume on TV increases with age such that by age 65
they are equal in the sitting position. In general, respiratory rates remain unchanged and
there is a diminished response to correct hypercapnia or hypoxia.
• Changes begin early as the uterus increases in size; they become more clinically obvious and
peak during the 3rd trimester. The gravid uterus will displace the diaphragm superiorly, by
up to 4 cm, and the thoracic cavity will increase both the transverse and anteroposterior
diameters in part due to the effects of the hormone relaxin. As a result, respiration becomes
more dependent on the diaphragm (3). While several lung volumes are decreased during
pregnancy (expiratory reserve volume, residual volume, and functional residual volume),
the TV component increases by up to 40%. Oxygen consumption and carbon dioxide
production will increase in large part due to the growing fetus, but this is matched with an
increase in minute ventilation by 30–50%. The increase in minute ventilation is attributable
to progesterone, known to stimulate increased ventilation directly at the respiratory center
found in the medulla. The increase in minute ventilation will cause the arterial partial
pressure of CO2 to decrease to between 26 and 32 mm Hg.
• Both dead space and TV estimations per kilogram remain constant in the pediatric
population. However, accurate estimation and then delivery of that TV becomes more
difficult for mechanical ventilation. Because the volume being delivered is very small, even
minor issues can have an unexpectedly large impact on the actual volume that is delivered.
Volume can be lost secondary to the compliance of the breathing circuit, or a leak in the
ventilator circuit due to the number of accessory items (humidifiers or heaters). To that
extent, specialized pediatric circuits can be utilized (less compliant, smaller ventilation
bags) and pediatric ventilators can improve TV delivery. Despite these improvements,
vigilance is necessary to avoid inadequate ventilation leading to hypoxia and hypercapnia
(4).
• Obesity. Initial interventions include increasing TV and/or adding PEEP. However, the
dangers of a greatly increased TV include hyperventilation, hypocapnia, high airway
pressures, and increased risk of parenchyma damage due to the combination of volume and
pressure. Frequently, while normalizing oxygen levels, hypocapnia results. The respiratory
alkalosis can cause a shift in the oxyhemoglobin curve that increases affinity of the heme
molecule for oxygen and results in worsening of tissue oxygenation (5). The strategy for
maintaining oxygenation and normocapnia for obese patients is complex, particularly
during laparoscopic surgery. Despite multiple studies, no single method has been
demonstrated to improve ventilation.
• Acute lung injury. Recent studies have indicated that patients who have acute lung injury
such as ARDS may benefit from low TVs (6 cc/kg) when utilizing mechanical ventilation.
These lower volumes have been associated with lower serum concentrations of
inflammatory mediators. Overall, this is correlated with a decrease in mortality in patients
who have ARDS and other acute lung injury (6).
• The geriatric patient is at increased risk of hypoxia, particularly when sedated and the use of
supplementary oxygen is warranted even for simple procedures (7).
EQUATIONS
• IC = TV + IRV, where IC is inspiratory capacity, TV is tidal volume, and IRV is inspiratory
reserve volume.
• FVC = IRV + TV + ERV, where FVC is forced vital capacity and ERV is expiratory reserve
volume.
• TLC = IRV + TV + ERV + RV, where TLC is total lung capacity and RV is residual
volume.
REFERENCES
1. Sprung J, Whalley DG, Falcone T, et al. The effects of tidal volume and respiratory rate on
oxygenation and respiratory mechanics during laparoscopy in morbidly obese patients.
Anesth Analg. 2003;97:1.
2. eleznik J. Normative aging of the respiratory system. Clin Geriatr Med. 2003;19:1.
3. obrowski RA. Pulmonary physiology in pregnancy. Clin Obstet Gynecol. 2010;53:285–300.
4. amel RRT, Cheifetz MD. Measuring pediatric tidal volumes. RT: For Decision Makers in
Respiratory Care. 2002.
5. ardoczky GI, Yernault JC, Houben JJ, et al. Large tidal volume ventilation does not
improve oxygenation in morbidly obese patients during anesthesia. Anesth Analg.
1995;81:385–388.
6. Parsons PE, Eisner MD, Thompson BT, et al. Lower tidal volume ventilation and plasma
cytokine markers of inflammation in patients with acute lung injury. Crit Care Med.
2005;33(1):1–6.
7. Bailey PL, Wilbrink J, Zwanikke

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